It’s unfortunate that medical organizations such as SHM do not have the equivalent of a national championship or a Super Bowl. If there was, given what SHM has accomplished in the past 13 years, there is no question that SHM would have won it.

­­So as my first act as SHM president, I hereby declare the Society of Hospital Medicine the national champions of physician organizations.

With that out of the way, now comes the hard part: because the only thing harder than winning a championship is keeping it. For with success comes the temptation to rest. The struggle to achieve success is about outward comparisons. But having achieved success, the perspective of the champion must shift if it is to be sustained. For in the mind of the champion, the perspective is internal, and the measure of competition is about besting oneself. For a champion such as SHM, future success will be measured solely upon an internal inventory of what we do well . . . and what could be done better. Allow me to make this more tangible.

Continued Growth and Inclusion

Our membership continues to grow. And with 10,000 members, it would be easy to rest. But given that there are 30,000 hospitalists, it would be convenient to ignore the question we have to answer: “Where are the other 20,000?”

Would they not benefit from our attention to quality and patient safety? SHM, like no other organization, has built an infrastructure of empowerment, particularly with respect to advancing the goals of quality and patient safety. It is not merely a self-serving goal to recruit these 20,000 hospitalists to SHM; in your heart, you have to believe that their time with SHM would improve the care of their patients. I am confident that Brian Curtis, Manoj Matthews, and their respective Membership and Chapter Support committees will be instrumental as we work toward this goal.

As we grow, for our colleagues in pediatrics, family medicine, the nonphysician providers, and practice administrators, will we make the right decision to maintain the “big tent” that has defined SHM’s success? Quality is quality, regardless of specialty, and the principles of improving a healthcare system that is safe and patient-centered apply to us all.

But as we continue to grow, sustaining the big tent will become increasingly difficult to maintain. Even so, it must remain our priority. Erin Stucky, Bob Harrington, Jeannette Kalupa, Ajay Kharbanda, and their respective teams will be central in preserving this important goal.

At HM10, our annual meeting, attendance topped out at more than 2,500 participants, and the quality of the programming has never been stronger. But there are new challenges that come with this success. Can we sustain the intimacy—the personal attention—necessary for networking and collaboration as the annual meeting continues to grow? There are homogenous messages that do, and will continue to, speak to us all.

But heterogeneity persists in hospitalist systems, and the ability to network with other hospitalists around these unique issues has been an incredibly valuable service of the national meeting. Yet as the meeting grows, it will become increasingly difficult to network hospitalists with similar needs. Preserving the intimacy of the annual meeting, despite its growing size, must be our goal. Dan Dressler, Jeff Glasheen, Mike Pistoria, and the Annual Meeting Committee will be tasked with finding creative solutions to achieving this goal.

Technology = Solutions

At the heart of the solution to both challenges is Kendall Rogers and his Information Technology team. IT sustains meaningful communication in the face of growth, and I believe this to be a central solution. However, the tasks for our IT team are not merely internal. Our profession is at the very beginning of a sharp upward slope on the IT curve, and IT will play an increasing role in patient care.

Technology should be the servant of the people, not the other way around. The unanticipated consequence of more IT has been the temptation to depersonalize patient care in lieu of practicing medicine via computer. IT unquestionably makes healthcare more efficient, but it has the equal prospect of making it less patient-centered; no efficiency is worth that.

Our goal as a society must be to take a leadership role in ensuring that the efficiencies brought about by IT leverage more time to spend with our patients, and empower systems solutions that prevent medical errors. SHM must be positioned so that we have a meaningful voice in advocating for health IT solutions that enable the hospitalist to meet PQRI standards, and to empower the hospitalist to be a leader in the advocacy of appropriate IT solutions that advance, not deter, our mission of quality care. At no time should a computer screen replace the provider’s time at the bedside with the patient; we must be the leaders in preserving this central tenet of patient-centered care.

One Voice—Credible, Unified, Patient-Focused

Hospitalists have spent a decade trying to a get a voice in the legislative discussion. Now that we have a voice in the national healthcare conversation, we must speak with credibility. And the measure of our credibility will be grounded in fidelity to our core mission: preserving what is best for the patient. We cannot succumb, as so many other organizations have done, to merely advocating what is best for SHM. If we do, our time at the table will be short.

Finding the balance between what is best for hospitalists without compromising what is best for the patient will be our challenge. Eric Siegal, Pat Torcson, Kirk Matthews, and their respective Advocacy, Practice Analysis, and Performance and Standards committees will be at the heart of this solution. But through it all, we must not be afraid of confronting the tough issues. Whatever might come with value-based purchasing, bundling, or PQRI, we must have a voice in designing legislation that not only ensures the welfare of the hospitalized patient, but also the sustainability of the hospitalist who is central to that care.

For if we are who we say we are, one is synonymous with the other.

Quality Remains Job No. 1

Perhaps the biggest challenge facing us is heterogeneity. Thanks to SHM’s mentored implementation programs, there is an increasing number of high-performance hospitalist teams. But we are only as strong as our weakest link, and our success will be ignored in light of our weakness until we can ensure, from a quality perspective, homogeneity across all hospital groups. Tex Landis, Steve Deitelzweig, and their respective Practice Management and Practice Analysis committees will be central to finding this solution.

SHM’s biannual hospitalist survey has partnered with industry leader MGMA, and as such, we have gained great credibility in leveraging the results of the survey with the C-suite. But surveys are only as good as the questions that are asked, and SHM must continue its role in collaborating with MGMA to ensure that we are asking the right questions. We need to know what defines the highest-performing teams, and we must find creative solutions to bring every hospitalist team to that same standard of quality by adopting the best practices of our strongest groups.

But at the heart of it all is quality: SHM’s universal mandate is that hospitalists ensure safe, timely, efficient, equitable, and patient-centered care. The leadership of Vikas Parekh and the Education Committee, and Nasim Afsarmanesh, Andrew Dunn, Kevin O’Leary, Greg Maynard and their respective Quality committees, will be central to the advancement of this mandate.

But this mandate must not go unsupported. Each hospitalist group must not be tasked with reinventing the wheel with each QI project, and each hospitalist group must not suffer from the same mistakes. Imagine a day when SHM becomes the repository of QI projects, enabling one hospitalist group to search a database to find QI projects designed and executed by other groups of similar size and character. It is an ambitious goal, but it is a measure that will ensure that all hospitalists can prosper from the success of our colleagues. It will close the heterogeneity gap and ensure that in five years’ time, if there is a hospitalist who does not engage in QI, it is not because they didn’t know how.

Properly designed, such a database could enable hospitalists to create and complete the Practice Improvement Module (PIM) for the American Board of Internal Medicine’s Focused Practice in Hospital Medicine Maintenance of Certification, and empower hospitalists to meet PQRI requirements.

Train Generation Next

As we make all of these advances, we must not lose sight of the importance of a balance between “production” and “production capacity.” For SHM to be a true leader in hospital quality, we must become more than reactionary. Via “user-inspired research,” we must produce new knowledge that improves the practice of us all. And we must address the “hole in the boat.”

Despite our success in improving the understanding of quality with our current membership, I fear we are losing ground: Each year, 10,000 new practitioners leave their residency having been inadequately trained in the principles of quality and patient safety. To make meaningful changes in healthcare quality, we have to fulfill our call to become the stewards of this training, ensuring that the next generations of physicians will be more adept in the fundamentals of quality and patient safety than we were. Jeff Glasheen, David Meltzer, Lorenz DiFrancesco, Paul Grant, Greg Seymann, and the Academic, Research, Pipeline, and Early Career Hospitalists teams will be tasked with this important legacy.

And so we come to a defining moment in SHM’s history. Will SHM be a one-and-done champion? Or will it be defined as a legacy?

Less ambitious goals and visions are certainly more comfortable, but it is not the spirit that has brought us this far. I doubt that the legendary figures of hospital medicine—John Nelson, Win Whitcomb, Bob Wachter, Larry Wellikson, et al—dreamed of a day when SHM would be “OK.” I suspect even our success as an organization is not enough for them, and personally, it’s not enough for me, either.

So digest this as an ambitious strategy that only a champion would be brave enough to design. No team wins without coaching, but no team wins on coaching alone. It will take all of us to make meaningful execution of this strategy a reality. Yes, we are the champions. Now, let’s play like it. TH

Dr. Wiese is president of SHM.

It’s unfortunate that medical organizations such as SHM do not have the equivalent of a national championship or a Super Bowl. If there was, given what SHM has accomplished in the past 13 years, there is no question that SHM would have won it.

­­So as my first act as SHM president, I hereby declare the Society of Hospital Medicine the national champions of physician organizations.

With that out of the way, now comes the hard part: because the only thing harder than winning a championship is keeping it. For with success comes the temptation to rest. The struggle to achieve success is about outward comparisons. But having achieved success, the perspective of the champion must shift if it is to be sustained. For in the mind of the champion, the perspective is internal, and the measure of competition is about besting oneself. For a champion such as SHM, future success will be measured solely upon an internal inventory of what we do well . . . and what could be done better. Allow me to make this more tangible.

Continued Growth and Inclusion

Our membership continues to grow. And with 10,000 members, it would be easy to rest. But given that there are 30,000 hospitalists, it would be convenient to ignore the question we have to answer: “Where are the other 20,000?”

Would they not benefit from our attention to quality and patient safety? SHM, like no other organization, has built an infrastructure of empowerment, particularly with respect to advancing the goals of quality and patient safety. It is not merely a self-serving goal to recruit these 20,000 hospitalists to SHM; in your heart, you have to believe that their time with SHM would improve the care of their patients. I am confident that Brian Curtis, Manoj Matthews, and their respective Membership and Chapter Support committees will be instrumental as we work toward this goal.

As we grow, for our colleagues in pediatrics, family medicine, the nonphysician providers, and practice administrators, will we make the right decision to maintain the “big tent” that has defined SHM’s success? Quality is quality, regardless of specialty, and the principles of improving a healthcare system that is safe and patient-centered apply to us all.

But as we continue to grow, sustaining the big tent will become increasingly difficult to maintain. Even so, it must remain our priority. Erin Stucky, Bob Harrington, Jeannette Kalupa, Ajay Kharbanda, and their respective teams will be central in preserving this important goal.

At HM10, our annual meeting, attendance topped out at more than 2,500 participants, and the quality of the programming has never been stronger. But there are new challenges that come with this success. Can we sustain the intimacy—the personal attention—necessary for networking and collaboration as the annual meeting continues to grow? There are homogenous messages that do, and will continue to, speak to us all.

But heterogeneity persists in hospitalist systems, and the ability to network with other hospitalists around these unique issues has been an incredibly valuable service of the national meeting. Yet as the meeting grows, it will become increasingly difficult to network hospitalists with similar needs. Preserving the intimacy of the annual meeting, despite its growing size, must be our goal. Dan Dressler, Jeff Glasheen, Mike Pistoria, and the Annual Meeting Committee will be tasked with finding creative solutions to achieving this goal.

Technology = Solutions

At the heart of the solution to both challenges is Kendall Rogers and his Information Technology team. IT sustains meaningful communication in the face of growth, and I believe this to be a central solution. However, the tasks for our IT team are not merely internal. Our profession is at the very beginning of a sharp upward slope on the IT curve, and IT will play an increasing role in patient care.

Technology should be the servant of the people, not the other way around. The unanticipated consequence of more IT has been the temptation to depersonalize patient care in lieu of practicing medicine via computer. IT unquestionably makes healthcare more efficient, but it has the equal prospect of making it less patient-centered; no efficiency is worth that.

Our goal as a society must be to take a leadership role in ensuring that the efficiencies brought about by IT leverage more time to spend with our patients, and empower systems solutions that prevent medical errors. SHM must be positioned so that we have a meaningful voice in advocating for health IT solutions that enable the hospitalist to meet PQRI standards, and to empower the hospitalist to be a leader in the advocacy of appropriate IT solutions that advance, not deter, our mission of quality care. At no time should a computer screen replace the provider’s time at the bedside with the patient; we must be the leaders in preserving this central tenet of patient-centered care.

One Voice—Credible, Unified, Patient-Focused

Hospitalists have spent a decade trying to a get a voice in the legislative discussion. Now that we have a voice in the national healthcare conversation, we must speak with credibility. And the measure of our credibility will be grounded in fidelity to our core mission: preserving what is best for the patient. We cannot succumb, as so many other organizations have done, to merely advocating what is best for SHM. If we do, our time at the table will be short.

Finding the balance between what is best for hospitalists without compromising what is best for the patient will be our challenge. Eric Siegal, Pat Torcson, Kirk Matthews, and their respective Advocacy, Practice Analysis, and Performance and Standards committees will be at the heart of this solution. But through it all, we must not be afraid of confronting the tough issues. Whatever might come with value-based purchasing, bundling, or PQRI, we must have a voice in designing legislation that not only ensures the welfare of the hospitalized patient, but also the sustainability of the hospitalist who is central to that care.

For if we are who we say we are, one is synonymous with the other.

Quality Remains Job No. 1

Perhaps the biggest challenge facing us is heterogeneity. Thanks to SHM’s mentored implementation programs, there is an increasing number of high-performance hospitalist teams. But we are only as strong as our weakest link, and our success will be ignored in light of our weakness until we can ensure, from a quality perspective, homogeneity across all hospital groups. Tex Landis, Steve Deitelzweig, and their respective Practice Management and Practice Analysis committees will be central to finding this solution.

SHM’s biannual hospitalist survey has partnered with industry leader MGMA, and as such, we have gained great credibility in leveraging the results of the survey with the C-suite. But surveys are only as good as the questions that are asked, and SHM must continue its role in collaborating with MGMA to ensure that we are asking the right questions. We need to know what defines the highest-performing teams, and we must find creative solutions to bring every hospitalist team to that same standard of quality by adopting the best practices of our strongest groups.

But at the heart of it all is quality: SHM’s universal mandate is that hospitalists ensure safe, timely, efficient, equitable, and patient-centered care. The leadership of Vikas Parekh and the Education Committee, and Nasim Afsarmanesh, Andrew Dunn, Kevin O’Leary, Greg Maynard and their respective Quality committees, will be central to the advancement of this mandate.

But this mandate must not go unsupported. Each hospitalist group must not be tasked with reinventing the wheel with each QI project, and each hospitalist group must not suffer from the same mistakes. Imagine a day when SHM becomes the repository of QI projects, enabling one hospitalist group to search a database to find QI projects designed and executed by other groups of similar size and character. It is an ambitious goal, but it is a measure that will ensure that all hospitalists can prosper from the success of our colleagues. It will close the heterogeneity gap and ensure that in five years’ time, if there is a hospitalist who does not engage in QI, it is not because they didn’t know how.

Properly designed, such a database could enable hospitalists to create and complete the Practice Improvement Module (PIM) for the American Board of Internal Medicine’s Focused Practice in Hospital Medicine Maintenance of Certification, and empower hospitalists to meet PQRI requirements.

Train Generation Next

As we make all of these advances, we must not lose sight of the importance of a balance between “production” and “production capacity.” For SHM to be a true leader in hospital quality, we must become more than reactionary. Via “user-inspired research,” we must produce new knowledge that improves the practice of us all. And we must address the “hole in the boat.”

Despite our success in improving the understanding of quality with our current membership, I fear we are losing ground: Each year, 10,000 new practitioners leave their residency having been inadequately trained in the principles of quality and patient safety. To make meaningful changes in healthcare quality, we have to fulfill our call to become the stewards of this training, ensuring that the next generations of physicians will be more adept in the fundamentals of quality and patient safety than we were. Jeff Glasheen, David Meltzer, Lorenz DiFrancesco, Paul Grant, Greg Seymann, and the Academic, Research, Pipeline, and Early Career Hospitalists teams will be tasked with this important legacy.

And so we come to a defining moment in SHM’s history. Will SHM be a one-and-done champion? Or will it be defined as a legacy?

Less ambitious goals and visions are certainly more comfortable, but it is not the spirit that has brought us this far. I doubt that the legendary figures of hospital medicine—John Nelson, Win Whitcomb, Bob Wachter, Larry Wellikson, et al—dreamed of a day when SHM would be “OK.” I suspect even our success as an organization is not enough for them, and personally, it’s not enough for me, either.

So digest this as an ambitious strategy that only a champion would be brave enough to design. No team wins without coaching, but no team wins on coaching alone. It will take all of us to make meaningful execution of this strategy a reality. Yes, we are the champions. Now, let’s play like it. TH

Dr. Wiese is president of SHM.

It’s unfortunate that medical organizations such as SHM do not have the equivalent of a national championship or a Super Bowl. If there was, given what SHM has accomplished in the past 13 years, there is no question that SHM would have won it.

­­So as my first act as SHM president, I hereby declare the Society of Hospital Medicine the national champions of physician organizations.

With that out of the way, now comes the hard part: because the only thing harder than winning a championship is keeping it. For with success comes the temptation to rest. The struggle to achieve success is about outward comparisons. But having achieved success, the perspective of the champion must shift if it is to be sustained. For in the mind of the champion, the perspective is internal, and the measure of competition is about besting oneself. For a champion such as SHM, future success will be measured solely upon an internal inventory of what we do well . . . and what could be done better. Allow me to make this more tangible.

Continued Growth and Inclusion

Our membership continues to grow. And with 10,000 members, it would be easy to rest. But given that there are 30,000 hospitalists, it would be convenient to ignore the question we have to answer: “Where are the other 20,000?”

Would they not benefit from our attention to quality and patient safety? SHM, like no other organization, has built an infrastructure of empowerment, particularly with respect to advancing the goals of quality and patient safety. It is not merely a self-serving goal to recruit these 20,000 hospitalists to SHM; in your heart, you have to believe that their time with SHM would improve the care of their patients. I am confident that Brian Curtis, Manoj Matthews, and their respective Membership and Chapter Support committees will be instrumental as we work toward this goal.

As we grow, for our colleagues in pediatrics, family medicine, the nonphysician providers, and practice administrators, will we make the right decision to maintain the “big tent” that has defined SHM’s success? Quality is quality, regardless of specialty, and the principles of improving a healthcare system that is safe and patient-centered apply to us all.

But as we continue to grow, sustaining the big tent will become increasingly difficult to maintain. Even so, it must remain our priority. Erin Stucky, Bob Harrington, Jeannette Kalupa, Ajay Kharbanda, and their respective teams will be central in preserving this important goal.

At HM10, our annual meeting, attendance topped out at more than 2,500 participants, and the quality of the programming has never been stronger. But there are new challenges that come with this success. Can we sustain the intimacy—the personal attention—necessary for networking and collaboration as the annual meeting continues to grow? There are homogenous messages that do, and will continue to, speak to us all.

But heterogeneity persists in hospitalist systems, and the ability to network with other hospitalists around these unique issues has been an incredibly valuable service of the national meeting. Yet as the meeting grows, it will become increasingly difficult to network hospitalists with similar needs. Preserving the intimacy of the annual meeting, despite its growing size, must be our goal. Dan Dressler, Jeff Glasheen, Mike Pistoria, and the Annual Meeting Committee will be tasked with finding creative solutions to achieving this goal.

Technology = Solutions

At the heart of the solution to both challenges is Kendall Rogers and his Information Technology team. IT sustains meaningful communication in the face of growth, and I believe this to be a central solution. However, the tasks for our IT team are not merely internal. Our profession is at the very beginning of a sharp upward slope on the IT curve, and IT will play an increasing role in patient care.

Technology should be the servant of the people, not the other way around. The unanticipated consequence of more IT has been the temptation to depersonalize patient care in lieu of practicing medicine via computer. IT unquestionably makes healthcare more efficient, but it has the equal prospect of making it less patient-centered; no efficiency is worth that.

Our goal as a society must be to take a leadership role in ensuring that the efficiencies brought about by IT leverage more time to spend with our patients, and empower systems solutions that prevent medical errors. SHM must be positioned so that we have a meaningful voice in advocating for health IT solutions that enable the hospitalist to meet PQRI standards, and to empower the hospitalist to be a leader in the advocacy of appropriate IT solutions that advance, not deter, our mission of quality care. At no time should a computer screen replace the provider’s time at the bedside with the patient; we must be the leaders in preserving this central tenet of patient-centered care.

One Voice—Credible, Unified, Patient-Focused

Hospitalists have spent a decade trying to a get a voice in the legislative discussion. Now that we have a voice in the national healthcare conversation, we must speak with credibility. And the measure of our credibility will be grounded in fidelity to our core mission: preserving what is best for the patient. We cannot succumb, as so many other organizations have done, to merely advocating what is best for SHM. If we do, our time at the table will be short.

Finding the balance between what is best for hospitalists without compromising what is best for the patient will be our challenge. Eric Siegal, Pat Torcson, Kirk Matthews, and their respective Advocacy, Practice Analysis, and Performance and Standards committees will be at the heart of this solution. But through it all, we must not be afraid of confronting the tough issues. Whatever might come with value-based purchasing, bundling, or PQRI, we must have a voice in designing legislation that not only ensures the welfare of the hospitalized patient, but also the sustainability of the hospitalist who is central to that care.

For if we are who we say we are, one is synonymous with the other.

Quality Remains Job No. 1

Perhaps the biggest challenge facing us is heterogeneity. Thanks to SHM’s mentored implementation programs, there is an increasing number of high-performance hospitalist teams. But we are only as strong as our weakest link, and our success will be ignored in light of our weakness until we can ensure, from a quality perspective, homogeneity across all hospital groups. Tex Landis, Steve Deitelzweig, and their respective Practice Management and Practice Analysis committees will be central to finding this solution.

SHM’s biannual hospitalist survey has partnered with industry leader MGMA, and as such, we have gained great credibility in leveraging the results of the survey with the C-suite. But surveys are only as good as the questions that are asked, and SHM must continue its role in collaborating with MGMA to ensure that we are asking the right questions. We need to know what defines the highest-performing teams, and we must find creative solutions to bring every hospitalist team to that same standard of quality by adopting the best practices of our strongest groups.

But at the heart of it all is quality: SHM’s universal mandate is that hospitalists ensure safe, timely, efficient, equitable, and patient-centered care. The leadership of Vikas Parekh and the Education Committee, and Nasim Afsarmanesh, Andrew Dunn, Kevin O’Leary, Greg Maynard and their respective Quality committees, will be central to the advancement of this mandate.

But this mandate must not go unsupported. Each hospitalist group must not be tasked with reinventing the wheel with each QI project, and each hospitalist group must not suffer from the same mistakes. Imagine a day when SHM becomes the repository of QI projects, enabling one hospitalist group to search a database to find QI projects designed and executed by other groups of similar size and character. It is an ambitious goal, but it is a measure that will ensure that all hospitalists can prosper from the success of our colleagues. It will close the heterogeneity gap and ensure that in five years’ time, if there is a hospitalist who does not engage in QI, it is not because they didn’t know how.

Properly designed, such a database could enable hospitalists to create and complete the Practice Improvement Module (PIM) for the American Board of Internal Medicine’s Focused Practice in Hospital Medicine Maintenance of Certification, and empower hospitalists to meet PQRI requirements.

Train Generation Next

As we make all of these advances, we must not lose sight of the importance of a balance between “production” and “production capacity.” For SHM to be a true leader in hospital quality, we must become more than reactionary. Via “user-inspired research,” we must produce new knowledge that improves the practice of us all. And we must address the “hole in the boat.”

Despite our success in improving the understanding of quality with our current membership, I fear we are losing ground: Each year, 10,000 new practitioners leave their residency having been inadequately trained in the principles of quality and patient safety. To make meaningful changes in healthcare quality, we have to fulfill our call to become the stewards of this training, ensuring that the next generations of physicians will be more adept in the fundamentals of quality and patient safety than we were. Jeff Glasheen, David Meltzer, Lorenz DiFrancesco, Paul Grant, Greg Seymann, and the Academic, Research, Pipeline, and Early Career Hospitalists teams will be tasked with this important legacy.

And so we come to a defining moment in SHM’s history. Will SHM be a one-and-done champion? Or will it be defined as a legacy?

Less ambitious goals and visions are certainly more comfortable, but it is not the spirit that has brought us this far. I doubt that the legendary figures of hospital medicine—John Nelson, Win Whitcomb, Bob Wachter, Larry Wellikson, et al—dreamed of a day when SHM would be “OK.” I suspect even our success as an organization is not enough for them, and personally, it’s not enough for me, either.

So digest this as an ambitious strategy that only a champion would be brave enough to design. No team wins without coaching, but no team wins on coaching alone. It will take all of us to make meaningful execution of this strategy a reality. Yes, we are the champions. Now, let’s play like it. TH

Dr. Wiese is president of SHM.

In case you haven’t seen it, the latest national survey data on hospitalist production, compensation, and other metrics was released in June.

Just as the Masters golf tournament is promoted as “a tradition like no other,” the combined SHM-MGMA (Medical Group Management Association) survey is without peer. Prior to this year, MGMA and SHM conducted separate surveys annually and biannually, respectively. The organizations chose to do a combined survey to take advantage of MGMA’s size and expertise in survey work (they’ve been conducting an annual survey of every specialty in medicine for decades) as well as SHM’s database of hospitalists and knowledge of the issues unique to HM.

If you want the most reliable data, this is the source you should use. I freely acknowledge my potential conflict of interest, which stems from my history with SHM (as a cofounder of SHM, I feel like a proud parent eager to trumpet all its accomplishments), and my consulting partner, Leslie Flores, was in charge of the survey process and data analysis for SHM. You should consider other sources of hospitalist data that might be available to you, but unless you have an unusually robust local or regional survey, the SHM-MGMA data will be the most valuable.

It’s Just a Survey

This survey provides the best national data, but like all such surveys, it has limitations. First, survey respondents vary in their diligence and accuracy in reporting their own data. It is even likely that some might “sanitize” or adjust the data they report in an effort, usually misguided, to provide a more accurate picture of their practice or cover up what might be for them an embarrassing issue. There is a process in place to catch outlier and inconsistent data submitted by a practice, and such practices are questioned to ensure accurate reporting and clear up any confusion or errors. But even that process is imperfect. There isn’t a team of auditors sent to “look at the books” to independently verify the accuracy of the data reported by each practice; that would be too costly, time-consuming, and even intimidating or annoying to be practical. So keep in mind that there is clearly some unavoidable “noise” or contamination in the data.

People sometimes say “SHM [or MGMA] says that ‘X’ is the right number of encounters for a hospitalist in a year,” where X is a number taken from the survey. Don’t make this mistake. I think it is misleading to think of the survey as establishing optimal or “right” benchmarks for any metric.

In fact, I think of benchmarks being something other than just survey numbers; instead, they’re well-considered data points derived from research showing what is optimal. The average glycohemoglobin of diabetics in the U.S. isn’t a desirable benchmark or goal, but the glycohemoglobin shown by research to be associated with the lowest risk of diabetic complications is. Keep this in mind when thinking about the survey results. There are little or no robust and generalizable research data regarding hospitalist productivity and compensation targets associated with the best performance.

click for large version

Hospitalist Incomes Surge

Let’s look at one data point: mean salary. The data points in Figure 1 (left) are the average salary going back to the first year the SHM survey was conducted. Note that all historical data points are from the SHM survey only, and thus represent a different population of respondents than the 2010 SHM-MGMA data point. It is important to remember this when looking at any trended hospitalist data.

Perhaps most importantly, previous SHM survey numbers included a significant proportion of academic hospitalist practices, which were largely unrepresented in the new SHM-MGMA survey data because SHM and MGMA will be conducting a separate survey of academic hospitalist practices in the fall.

Since academic hospitalists tend to earn less—and have lower overall productivity—than hospitalists in other settings, their absence from this survey likely results in greater increases in average compensation and production than would otherwise have been the case.

Beginning in about 2001, MGMA began reporting hospitalist compensation, but I have left those numbers off of this figure. And since about 2002, SHM has separated data for hospitalists who care for adults versus those that care for children; when separate data were available, this figure shows the compensation for hospitalists who care for adults and excludes pediatric hospitalists.

Note that the compensation figures include all salary elements, including a “base” or fixed component, productivity component, quality bonus, etc. The numbers exclude such benefits as the cost of health insurance or matching retirement plan contributions.

Inflation and a trend of increased hospitalist productivity are two reasons that hospitalist compensation has been increasing, but neither explains more than a portion of the increase in salary. (According to computational-knowledge engine WolframAlpha.com, inflation in the U.S. averaged 2.3% per year from 1997 to 2002. I’ll talk more about trends in hospitalist productivity in a future column.) I think the principal reason for the rising trend in our pay is “market forces,” primarily demand for hospitalists that has exceeded the supply.

What the Future Holds

It is interesting to speculate whether the historical trend line will accurately predict future increases in salary. At some point, forces will have to “bend the curve” so that it climbs more slowly. It could look like a curve reaching asymptote.

It is anyone’s guess when that might start to happen, but there are two developments over the last couple of years that suggest it might be coming: In some markets, the demand for hospitalists has been met and new candidates can’t find positions, so salaries in those markets might start to level off. And, unlike a few years ago, hospitalists are now competing with nearly every other physician specialty to get financial support from their hospitals, so hospitalists might find their hospital has less money available for them.

But the really big—and unknown—variable that could increase or decrease future hospitalist salaries is the effect of any further national healthcare reform legislation. TH

Dr. Nelson has been a practicing hospitalist since 1988 and is cofounder and past president of SHM. He is a principal in Nelson Flores Hospital Medicine Consultants, a national hospitalist practice management consulting firm (www.nelson flores.com). He is course co-director and faculty for SHM’s “Best Practices in Managing a Hospital Medicine Program” course. This column represents his views and is not intended to reflect an official position of SHM.

In case you haven’t seen it, the latest national survey data on hospitalist production, compensation, and other metrics was released in June.

Just as the Masters golf tournament is promoted as “a tradition like no other,” the combined SHM-MGMA (Medical Group Management Association) survey is without peer. Prior to this year, MGMA and SHM conducted separate surveys annually and biannually, respectively. The organizations chose to do a combined survey to take advantage of MGMA’s size and expertise in survey work (they’ve been conducting an annual survey of every specialty in medicine for decades) as well as SHM’s database of hospitalists and knowledge of the issues unique to HM.

If you want the most reliable data, this is the source you should use. I freely acknowledge my potential conflict of interest, which stems from my history with SHM (as a cofounder of SHM, I feel like a proud parent eager to trumpet all its accomplishments), and my consulting partner, Leslie Flores, was in charge of the survey process and data analysis for SHM. You should consider other sources of hospitalist data that might be available to you, but unless you have an unusually robust local or regional survey, the SHM-MGMA data will be the most valuable.

It’s Just a Survey

This survey provides the best national data, but like all such surveys, it has limitations. First, survey respondents vary in their diligence and accuracy in reporting their own data. It is even likely that some might “sanitize” or adjust the data they report in an effort, usually misguided, to provide a more accurate picture of their practice or cover up what might be for them an embarrassing issue. There is a process in place to catch outlier and inconsistent data submitted by a practice, and such practices are questioned to ensure accurate reporting and clear up any confusion or errors. But even that process is imperfect. There isn’t a team of auditors sent to “look at the books” to independently verify the accuracy of the data reported by each practice; that would be too costly, time-consuming, and even intimidating or annoying to be practical. So keep in mind that there is clearly some unavoidable “noise” or contamination in the data.

People sometimes say “SHM [or MGMA] says that ‘X’ is the right number of encounters for a hospitalist in a year,” where X is a number taken from the survey. Don’t make this mistake. I think it is misleading to think of the survey as establishing optimal or “right” benchmarks for any metric.

In fact, I think of benchmarks being something other than just survey numbers; instead, they’re well-considered data points derived from research showing what is optimal. The average glycohemoglobin of diabetics in the U.S. isn’t a desirable benchmark or goal, but the glycohemoglobin shown by research to be associated with the lowest risk of diabetic complications is. Keep this in mind when thinking about the survey results. There are little or no robust and generalizable research data regarding hospitalist productivity and compensation targets associated with the best performance.

click for large version

Hospitalist Incomes Surge

Let’s look at one data point: mean salary. The data points in Figure 1 (left) are the average salary going back to the first year the SHM survey was conducted. Note that all historical data points are from the SHM survey only, and thus represent a different population of respondents than the 2010 SHM-MGMA data point. It is important to remember this when looking at any trended hospitalist data.

Perhaps most importantly, previous SHM survey numbers included a significant proportion of academic hospitalist practices, which were largely unrepresented in the new SHM-MGMA survey data because SHM and MGMA will be conducting a separate survey of academic hospitalist practices in the fall.

Since academic hospitalists tend to earn less—and have lower overall productivity—than hospitalists in other settings, their absence from this survey likely results in greater increases in average compensation and production than would otherwise have been the case.

Beginning in about 2001, MGMA began reporting hospitalist compensation, but I have left those numbers off of this figure. And since about 2002, SHM has separated data for hospitalists who care for adults versus those that care for children; when separate data were available, this figure shows the compensation for hospitalists who care for adults and excludes pediatric hospitalists.

Note that the compensation figures include all salary elements, including a “base” or fixed component, productivity component, quality bonus, etc. The numbers exclude such benefits as the cost of health insurance or matching retirement plan contributions.

Inflation and a trend of increased hospitalist productivity are two reasons that hospitalist compensation has been increasing, but neither explains more than a portion of the increase in salary. (According to computational-knowledge engine WolframAlpha.com, inflation in the U.S. averaged 2.3% per year from 1997 to 2002. I’ll talk more about trends in hospitalist productivity in a future column.) I think the principal reason for the rising trend in our pay is “market forces,” primarily demand for hospitalists that has exceeded the supply.

What the Future Holds

It is interesting to speculate whether the historical trend line will accurately predict future increases in salary. At some point, forces will have to “bend the curve” so that it climbs more slowly. It could look like a curve reaching asymptote.

It is anyone’s guess when that might start to happen, but there are two developments over the last couple of years that suggest it might be coming: In some markets, the demand for hospitalists has been met and new candidates can’t find positions, so salaries in those markets might start to level off. And, unlike a few years ago, hospitalists are now competing with nearly every other physician specialty to get financial support from their hospitals, so hospitalists might find their hospital has less money available for them.

But the really big—and unknown—variable that could increase or decrease future hospitalist salaries is the effect of any further national healthcare reform legislation. TH

Dr. Nelson has been a practicing hospitalist since 1988 and is cofounder and past president of SHM. He is a principal in Nelson Flores Hospital Medicine Consultants, a national hospitalist practice management consulting firm (www.nelson flores.com). He is course co-director and faculty for SHM’s “Best Practices in Managing a Hospital Medicine Program” course. This column represents his views and is not intended to reflect an official position of SHM.

In case you haven’t seen it, the latest national survey data on hospitalist production, compensation, and other metrics was released in June.

Just as the Masters golf tournament is promoted as “a tradition like no other,” the combined SHM-MGMA (Medical Group Management Association) survey is without peer. Prior to this year, MGMA and SHM conducted separate surveys annually and biannually, respectively. The organizations chose to do a combined survey to take advantage of MGMA’s size and expertise in survey work (they’ve been conducting an annual survey of every specialty in medicine for decades) as well as SHM’s database of hospitalists and knowledge of the issues unique to HM.

If you want the most reliable data, this is the source you should use. I freely acknowledge my potential conflict of interest, which stems from my history with SHM (as a cofounder of SHM, I feel like a proud parent eager to trumpet all its accomplishments), and my consulting partner, Leslie Flores, was in charge of the survey process and data analysis for SHM. You should consider other sources of hospitalist data that might be available to you, but unless you have an unusually robust local or regional survey, the SHM-MGMA data will be the most valuable.

It’s Just a Survey

This survey provides the best national data, but like all such surveys, it has limitations. First, survey respondents vary in their diligence and accuracy in reporting their own data. It is even likely that some might “sanitize” or adjust the data they report in an effort, usually misguided, to provide a more accurate picture of their practice or cover up what might be for them an embarrassing issue. There is a process in place to catch outlier and inconsistent data submitted by a practice, and such practices are questioned to ensure accurate reporting and clear up any confusion or errors. But even that process is imperfect. There isn’t a team of auditors sent to “look at the books” to independently verify the accuracy of the data reported by each practice; that would be too costly, time-consuming, and even intimidating or annoying to be practical. So keep in mind that there is clearly some unavoidable “noise” or contamination in the data.

People sometimes say “SHM [or MGMA] says that ‘X’ is the right number of encounters for a hospitalist in a year,” where X is a number taken from the survey. Don’t make this mistake. I think it is misleading to think of the survey as establishing optimal or “right” benchmarks for any metric.

In fact, I think of benchmarks being something other than just survey numbers; instead, they’re well-considered data points derived from research showing what is optimal. The average glycohemoglobin of diabetics in the U.S. isn’t a desirable benchmark or goal, but the glycohemoglobin shown by research to be associated with the lowest risk of diabetic complications is. Keep this in mind when thinking about the survey results. There are little or no robust and generalizable research data regarding hospitalist productivity and compensation targets associated with the best performance.

click for large version

Hospitalist Incomes Surge

Let’s look at one data point: mean salary. The data points in Figure 1 (left) are the average salary going back to the first year the SHM survey was conducted. Note that all historical data points are from the SHM survey only, and thus represent a different population of respondents than the 2010 SHM-MGMA data point. It is important to remember this when looking at any trended hospitalist data.

Perhaps most importantly, previous SHM survey numbers included a significant proportion of academic hospitalist practices, which were largely unrepresented in the new SHM-MGMA survey data because SHM and MGMA will be conducting a separate survey of academic hospitalist practices in the fall.

Since academic hospitalists tend to earn less—and have lower overall productivity—than hospitalists in other settings, their absence from this survey likely results in greater increases in average compensation and production than would otherwise have been the case.

Beginning in about 2001, MGMA began reporting hospitalist compensation, but I have left those numbers off of this figure. And since about 2002, SHM has separated data for hospitalists who care for adults versus those that care for children; when separate data were available, this figure shows the compensation for hospitalists who care for adults and excludes pediatric hospitalists.

Note that the compensation figures include all salary elements, including a “base” or fixed component, productivity component, quality bonus, etc. The numbers exclude such benefits as the cost of health insurance or matching retirement plan contributions.

Inflation and a trend of increased hospitalist productivity are two reasons that hospitalist compensation has been increasing, but neither explains more than a portion of the increase in salary. (According to computational-knowledge engine WolframAlpha.com, inflation in the U.S. averaged 2.3% per year from 1997 to 2002. I’ll talk more about trends in hospitalist productivity in a future column.) I think the principal reason for the rising trend in our pay is “market forces,” primarily demand for hospitalists that has exceeded the supply.

What the Future Holds

It is interesting to speculate whether the historical trend line will accurately predict future increases in salary. At some point, forces will have to “bend the curve” so that it climbs more slowly. It could look like a curve reaching asymptote.

It is anyone’s guess when that might start to happen, but there are two developments over the last couple of years that suggest it might be coming: In some markets, the demand for hospitalists has been met and new candidates can’t find positions, so salaries in those markets might start to level off. And, unlike a few years ago, hospitalists are now competing with nearly every other physician specialty to get financial support from their hospitals, so hospitalists might find their hospital has less money available for them.

But the really big—and unknown—variable that could increase or decrease future hospitalist salaries is the effect of any further national healthcare reform legislation. TH

Dr. Nelson has been a practicing hospitalist since 1988 and is cofounder and past president of SHM. He is a principal in Nelson Flores Hospital Medicine Consultants, a national hospitalist practice management consulting firm (www.nelson flores.com). He is course co-director and faculty for SHM’s “Best Practices in Managing a Hospital Medicine Program” course. This column represents his views and is not intended to reflect an official position of SHM.

Registration for the Focused Practice in Hospital Medicine (FPHM) Maintenance of Certification (MOC) through the American Board of Internal Medicine (ABIM) opened March 15. Since then, hundreds of board-certified IM physicians have registered to complete their MOC through the FPHM. For those of you who haven’t gone through MOC yet, it is required every 10 years in order to maintain your board certification.

As a member of the committee tasked with helping ABIM develop the FPHM, as well as write the FPHM examination, I’m frequently asked questions about this process, especially since FPHM was featured on the May 2010 cover of this magazine. Some of the questions stem from the perplexity associated with this significant change to the MOC process. Others arise from misinformation and apprehension, and could rightly be called urban legends. Here is a sample of those questions, with their respective veracity.

Does This Certification Mean I’ll No Longer be an Internist?

No. I clearly remember the day I found out I passed the ABIM certification exam; it represented the culmination of years of work, the pinnacle. All those long hours of study, late-night admissions, and exam preparation had finally paid off. I was a board-certified internist! I cherish my board certification and hold it out as recognition of my mastery of the field of IM. As such, I certainly understand the concern that entering the FPHM will somehow result in “losing” IM certification. However, this just isn’t true.

First, all diplomates—ABIM terminology for those enrolled in the board (re)certification process—in the FPHM are certified as internists. This is simply, as the name suggests, recognition of focused practice in HM—the core certification is still in IM. We are still internists—just internists who have focused our practice to hospital care. The formal board designation will read: ABIM Board Certified in Internal Medicine with a Focused Practice in Hospital Medicine.

Will Hospital Credentialing Boards Recognize This Certification?

Yes. The FPHM is certification in IM by the ABIM. This carries the same weight and meaning as the regular IM MOC. All credentialing boards that recognize the ABIM MOC in IM will recognize the FPHM.

Is the FPHM MOC More Rigorous Than the Regular IM MOC?

Yes, and it was intentional. It is recognized that hospitalists do things that make them “special” by acquiring and refining skills learned experientially outside of a supervised training program. Thus, one can attain FPHM board designation only after three years of practice as a hospitalist. The problem is that this is largely unsupervised time (unlike a fellowship), so the threshold to ensure we have achieved a level of competency has to be established through the MOC process.

As such, the bar for the MOC for FPHM has been set higher. The upshot is that to maintain designation of FPHM, hospitalists are required to achieve 60 self-evaluation points every three years, compared with 100 points every 10 years for IM MOC. Forty of those 60 points must come in the form of Practice Improvement Modules, or PIMs. While more rigorous, it only makes sense that a group committed to the improvement of healthcare quality would commit to higher levels of quality assurance.

Will the FPHM Confer Subspecialty Status to Hospitalists?

No. This is where there has been the greatest deal of controversy surrounding the FPHM program. FPHM is not a subspecialty certification. Rather, it is MOC for IM physicians who focus their practice in the hospital setting. The American Board of Medical Specialties (ABMS), the group that oversees the ABIM, is very clear that only training-based subspecialties can be deemed board-certified subspecialties.

Still, the new FPHM will differentiate hospitalists from nonhospitalists. To me, this is semantics, and the recognition that comes with the FPHM is enough to recognize what I do as “special.”

Will the Examination for the FPHM Reflect What I Do?

Yes. I’ve had several colleagues tell me they’ve heard that the examination will contain elements not found on the standard MOC test. This is true, but it also is the major benefit of the new test. As reported on the ABIM website, the FPHM MOC exam will consist of roughly 45% inpatient medicine, 15% consultative and comanagement work, 15% transitions and ambulatory medicine, 15% patient safety/quality improvement, 5% epidemiology, and 5% ethics and end-of-life care. In this respect, it better reflects what most of us spend most of our time doing—inpatient care, consultative medicine, and transitions of care. Those three areas comprise nearly 75% of the examination. The one area that is new is the focus on patient safety and quality. However, for a field built on the promise of improving the quality, safety, and efficiency of healthcare, this is a welcome change.

Will I Be Able to Prepare for the FPHM Exam?

Yes. Because the FPHM utilizes a different exam than the standard IM MOC, some physicians are concerned that they there are no avenues for preparation, but this is not true. While the exam will weigh various portions of the test differently (e.g., less ambulatory and more inpatient content), the inpatient content will be similar to what is currently on the standard MOC test. After all, heart failure, cellulitis, and pulmonary embolism are the same, regardless of the test it shows up on.

The difference is that there will be more of it—a good thing for the practicing hospitalist. Many of the standard IM test preparation options will help you prepare for the FPHM exam. The ABIM also offers HM knowledge modules as part of the enrollment fee, which, while not meant to be preparation for the exam, can help you identify gaps in your knowledge. The blueprint for the exam is on the ABIM website and can give you clues to areas in which to prepare.

It is true that there will be patient safety and QI content on the HM test, which might not be available for study in typical board review books. However, much of this is the kind of information hospitalists live every day, such as handoffs, transitions of care, and infection control.

Should I Fear the Change?

Humans are intrinsically wired to dislike change. It’s that old saw about choosing the devil we know rather than the devil we don’t. My guess is that much of the concern around the new process stems from this human sentiment—it’s just easier to not do the FPHM and go down the standard IM MOC route. We must avoid this temptation.

The FPHM is a key step in solidifying HM’s status in the healthcare milieu. It gives us credibility in a way no other designation can. It also allows those of us who are serious about an HM career to differentiate ourselves from those who masquerade as hospitalists. And, most importantly, it allows us to demonstrate to our patients our sincere commitment to improving the quality of the inpatient systems that envelop them at their sickest moments.

For that reason alone, I’m enrolling in the FPHM MOC. TH

Dr. Glasheen is physician editor of The Hospitalist.

Registration for the Focused Practice in Hospital Medicine (FPHM) Maintenance of Certification (MOC) through the American Board of Internal Medicine (ABIM) opened March 15. Since then, hundreds of board-certified IM physicians have registered to complete their MOC through the FPHM. For those of you who haven’t gone through MOC yet, it is required every 10 years in order to maintain your board certification.

As a member of the committee tasked with helping ABIM develop the FPHM, as well as write the FPHM examination, I’m frequently asked questions about this process, especially since FPHM was featured on the May 2010 cover of this magazine. Some of the questions stem from the perplexity associated with this significant change to the MOC process. Others arise from misinformation and apprehension, and could rightly be called urban legends. Here is a sample of those questions, with their respective veracity.

Does This Certification Mean I’ll No Longer be an Internist?

No. I clearly remember the day I found out I passed the ABIM certification exam; it represented the culmination of years of work, the pinnacle. All those long hours of study, late-night admissions, and exam preparation had finally paid off. I was a board-certified internist! I cherish my board certification and hold it out as recognition of my mastery of the field of IM. As such, I certainly understand the concern that entering the FPHM will somehow result in “losing” IM certification. However, this just isn’t true.

First, all diplomates—ABIM terminology for those enrolled in the board (re)certification process—in the FPHM are certified as internists. This is simply, as the name suggests, recognition of focused practice in HM—the core certification is still in IM. We are still internists—just internists who have focused our practice to hospital care. The formal board designation will read: ABIM Board Certified in Internal Medicine with a Focused Practice in Hospital Medicine.

Will Hospital Credentialing Boards Recognize This Certification?

Yes. The FPHM is certification in IM by the ABIM. This carries the same weight and meaning as the regular IM MOC. All credentialing boards that recognize the ABIM MOC in IM will recognize the FPHM.

Is the FPHM MOC More Rigorous Than the Regular IM MOC?

Yes, and it was intentional. It is recognized that hospitalists do things that make them “special” by acquiring and refining skills learned experientially outside of a supervised training program. Thus, one can attain FPHM board designation only after three years of practice as a hospitalist. The problem is that this is largely unsupervised time (unlike a fellowship), so the threshold to ensure we have achieved a level of competency has to be established through the MOC process.

As such, the bar for the MOC for FPHM has been set higher. The upshot is that to maintain designation of FPHM, hospitalists are required to achieve 60 self-evaluation points every three years, compared with 100 points every 10 years for IM MOC. Forty of those 60 points must come in the form of Practice Improvement Modules, or PIMs. While more rigorous, it only makes sense that a group committed to the improvement of healthcare quality would commit to higher levels of quality assurance.

Will the FPHM Confer Subspecialty Status to Hospitalists?

No. This is where there has been the greatest deal of controversy surrounding the FPHM program. FPHM is not a subspecialty certification. Rather, it is MOC for IM physicians who focus their practice in the hospital setting. The American Board of Medical Specialties (ABMS), the group that oversees the ABIM, is very clear that only training-based subspecialties can be deemed board-certified subspecialties.

Still, the new FPHM will differentiate hospitalists from nonhospitalists. To me, this is semantics, and the recognition that comes with the FPHM is enough to recognize what I do as “special.”

Will the Examination for the FPHM Reflect What I Do?

Yes. I’ve had several colleagues tell me they’ve heard that the examination will contain elements not found on the standard MOC test. This is true, but it also is the major benefit of the new test. As reported on the ABIM website, the FPHM MOC exam will consist of roughly 45% inpatient medicine, 15% consultative and comanagement work, 15% transitions and ambulatory medicine, 15% patient safety/quality improvement, 5% epidemiology, and 5% ethics and end-of-life care. In this respect, it better reflects what most of us spend most of our time doing—inpatient care, consultative medicine, and transitions of care. Those three areas comprise nearly 75% of the examination. The one area that is new is the focus on patient safety and quality. However, for a field built on the promise of improving the quality, safety, and efficiency of healthcare, this is a welcome change.

Will I Be Able to Prepare for the FPHM Exam?

Yes. Because the FPHM utilizes a different exam than the standard IM MOC, some physicians are concerned that they there are no avenues for preparation, but this is not true. While the exam will weigh various portions of the test differently (e.g., less ambulatory and more inpatient content), the inpatient content will be similar to what is currently on the standard MOC test. After all, heart failure, cellulitis, and pulmonary embolism are the same, regardless of the test it shows up on.

The difference is that there will be more of it—a good thing for the practicing hospitalist. Many of the standard IM test preparation options will help you prepare for the FPHM exam. The ABIM also offers HM knowledge modules as part of the enrollment fee, which, while not meant to be preparation for the exam, can help you identify gaps in your knowledge. The blueprint for the exam is on the ABIM website and can give you clues to areas in which to prepare.

It is true that there will be patient safety and QI content on the HM test, which might not be available for study in typical board review books. However, much of this is the kind of information hospitalists live every day, such as handoffs, transitions of care, and infection control.

Should I Fear the Change?

Humans are intrinsically wired to dislike change. It’s that old saw about choosing the devil we know rather than the devil we don’t. My guess is that much of the concern around the new process stems from this human sentiment—it’s just easier to not do the FPHM and go down the standard IM MOC route. We must avoid this temptation.

The FPHM is a key step in solidifying HM’s status in the healthcare milieu. It gives us credibility in a way no other designation can. It also allows those of us who are serious about an HM career to differentiate ourselves from those who masquerade as hospitalists. And, most importantly, it allows us to demonstrate to our patients our sincere commitment to improving the quality of the inpatient systems that envelop them at their sickest moments.

For that reason alone, I’m enrolling in the FPHM MOC. TH

Dr. Glasheen is physician editor of The Hospitalist.

Registration for the Focused Practice in Hospital Medicine (FPHM) Maintenance of Certification (MOC) through the American Board of Internal Medicine (ABIM) opened March 15. Since then, hundreds of board-certified IM physicians have registered to complete their MOC through the FPHM. For those of you who haven’t gone through MOC yet, it is required every 10 years in order to maintain your board certification.

As a member of the committee tasked with helping ABIM develop the FPHM, as well as write the FPHM examination, I’m frequently asked questions about this process, especially since FPHM was featured on the May 2010 cover of this magazine. Some of the questions stem from the perplexity associated with this significant change to the MOC process. Others arise from misinformation and apprehension, and could rightly be called urban legends. Here is a sample of those questions, with their respective veracity.

Does This Certification Mean I’ll No Longer be an Internist?

No. I clearly remember the day I found out I passed the ABIM certification exam; it represented the culmination of years of work, the pinnacle. All those long hours of study, late-night admissions, and exam preparation had finally paid off. I was a board-certified internist! I cherish my board certification and hold it out as recognition of my mastery of the field of IM. As such, I certainly understand the concern that entering the FPHM will somehow result in “losing” IM certification. However, this just isn’t true.

First, all diplomates—ABIM terminology for those enrolled in the board (re)certification process—in the FPHM are certified as internists. This is simply, as the name suggests, recognition of focused practice in HM—the core certification is still in IM. We are still internists—just internists who have focused our practice to hospital care. The formal board designation will read: ABIM Board Certified in Internal Medicine with a Focused Practice in Hospital Medicine.

Will Hospital Credentialing Boards Recognize This Certification?

Yes. The FPHM is certification in IM by the ABIM. This carries the same weight and meaning as the regular IM MOC. All credentialing boards that recognize the ABIM MOC in IM will recognize the FPHM.

Is the FPHM MOC More Rigorous Than the Regular IM MOC?

Yes, and it was intentional. It is recognized that hospitalists do things that make them “special” by acquiring and refining skills learned experientially outside of a supervised training program. Thus, one can attain FPHM board designation only after three years of practice as a hospitalist. The problem is that this is largely unsupervised time (unlike a fellowship), so the threshold to ensure we have achieved a level of competency has to be established through the MOC process.

As such, the bar for the MOC for FPHM has been set higher. The upshot is that to maintain designation of FPHM, hospitalists are required to achieve 60 self-evaluation points every three years, compared with 100 points every 10 years for IM MOC. Forty of those 60 points must come in the form of Practice Improvement Modules, or PIMs. While more rigorous, it only makes sense that a group committed to the improvement of healthcare quality would commit to higher levels of quality assurance.

Will the FPHM Confer Subspecialty Status to Hospitalists?

No. This is where there has been the greatest deal of controversy surrounding the FPHM program. FPHM is not a subspecialty certification. Rather, it is MOC for IM physicians who focus their practice in the hospital setting. The American Board of Medical Specialties (ABMS), the group that oversees the ABIM, is very clear that only training-based subspecialties can be deemed board-certified subspecialties.

Still, the new FPHM will differentiate hospitalists from nonhospitalists. To me, this is semantics, and the recognition that comes with the FPHM is enough to recognize what I do as “special.”

Will the Examination for the FPHM Reflect What I Do?

Yes. I’ve had several colleagues tell me they’ve heard that the examination will contain elements not found on the standard MOC test. This is true, but it also is the major benefit of the new test. As reported on the ABIM website, the FPHM MOC exam will consist of roughly 45% inpatient medicine, 15% consultative and comanagement work, 15% transitions and ambulatory medicine, 15% patient safety/quality improvement, 5% epidemiology, and 5% ethics and end-of-life care. In this respect, it better reflects what most of us spend most of our time doing—inpatient care, consultative medicine, and transitions of care. Those three areas comprise nearly 75% of the examination. The one area that is new is the focus on patient safety and quality. However, for a field built on the promise of improving the quality, safety, and efficiency of healthcare, this is a welcome change.

Will I Be Able to Prepare for the FPHM Exam?

Yes. Because the FPHM utilizes a different exam than the standard IM MOC, some physicians are concerned that they there are no avenues for preparation, but this is not true. While the exam will weigh various portions of the test differently (e.g., less ambulatory and more inpatient content), the inpatient content will be similar to what is currently on the standard MOC test. After all, heart failure, cellulitis, and pulmonary embolism are the same, regardless of the test it shows up on.

The difference is that there will be more of it—a good thing for the practicing hospitalist. Many of the standard IM test preparation options will help you prepare for the FPHM exam. The ABIM also offers HM knowledge modules as part of the enrollment fee, which, while not meant to be preparation for the exam, can help you identify gaps in your knowledge. The blueprint for the exam is on the ABIM website and can give you clues to areas in which to prepare.

It is true that there will be patient safety and QI content on the HM test, which might not be available for study in typical board review books. However, much of this is the kind of information hospitalists live every day, such as handoffs, transitions of care, and infection control.

Should I Fear the Change?

Humans are intrinsically wired to dislike change. It’s that old saw about choosing the devil we know rather than the devil we don’t. My guess is that much of the concern around the new process stems from this human sentiment—it’s just easier to not do the FPHM and go down the standard IM MOC route. We must avoid this temptation.

The FPHM is a key step in solidifying HM’s status in the healthcare milieu. It gives us credibility in a way no other designation can. It also allows those of us who are serious about an HM career to differentiate ourselves from those who masquerade as hospitalists. And, most importantly, it allows us to demonstrate to our patients our sincere commitment to improving the quality of the inpatient systems that envelop them at their sickest moments.

For that reason alone, I’m enrolling in the FPHM MOC. TH

Dr. Glasheen is physician editor of The Hospitalist.

Click here to listen to Dr. Vidyarthi

Click here to listen to Dr. Dalal

Click here to listen to Dr. Kripalani

Click here to listen to Dr. Vidyarthi

Click here to listen to Dr. Dalal

Click here to listen to Dr. Kripalani

Click here to listen to Dr. Vidyarthi

Click here to listen to Dr. Dalal

Click here to listen to Dr. Kripalani

Few medical students receive formal training in how to perform patient handoffs effectively and efficiently, says Vineet Arora, MD, FHM, who chairs an SHM task force on improving handoffs. Most pick it up on the job, but Dr. Arora and her colleagues at the University of Chicago—where she is associate director of the internal-medicine residency program—and at the University of Michigan have been exploring ways to improve the process through education.¹ Handoffs and care transitions are a major focus for hospital quality-improvement (QI) efforts nationally.

Dr. Arora’s group created an “observed simulation handoff experience” for medical students and residents, “offering an air of authenticity to the experience without the high-risk environment of learning on live patients,” she explains. Students who have completed an interactive training session perform the simulation at a computer station. They are provided with two types of information: static data about the mock patient—including such information as diagnosis, primary-care physician, and code status from a history and physical report—and video clips offering “a virtual, real-time barrage of constant updates” about the patient’s changing clinical status.

“They are given some time to extract and synthesize the important data for a handoff, and then they go in and perform the handoff in person to a ‘standardized receiver,’ ” Dr. Arora explains. The receiver is a resident or other clinician familiar both with the case and how the handoff should go, and who then provides a standardized evaluation, grade, and feedback.

“The goal is to teach students the triggers that need to be incorporated into an effective handoff,” Dr. Arora says. Her group also reviewed concepts of good handoffs from the medical literature and worked with a psychology expert in human communication.

“How do you teach people to give good handoffs? We don’t know all of the answers, but we think you have to start somewhere,” she says. “Technology can be a great facilitator to make handoffs go better. It’s not a perfect substitute for face-to-face, interactive handoffs, but it can dramatically inform care transitions.”

Larry Beresford is a freelance writer based in Oakland, Calif.

Few medical students receive formal training in how to perform patient handoffs effectively and efficiently, says Vineet Arora, MD, FHM, who chairs an SHM task force on improving handoffs. Most pick it up on the job, but Dr. Arora and her colleagues at the University of Chicago—where she is associate director of the internal-medicine residency program—and at the University of Michigan have been exploring ways to improve the process through education.¹ Handoffs and care transitions are a major focus for hospital quality-improvement (QI) efforts nationally.

Dr. Arora’s group created an “observed simulation handoff experience” for medical students and residents, “offering an air of authenticity to the experience without the high-risk environment of learning on live patients,” she explains. Students who have completed an interactive training session perform the simulation at a computer station. They are provided with two types of information: static data about the mock patient—including such information as diagnosis, primary-care physician, and code status from a history and physical report—and video clips offering “a virtual, real-time barrage of constant updates” about the patient’s changing clinical status.

“They are given some time to extract and synthesize the important data for a handoff, and then they go in and perform the handoff in person to a ‘standardized receiver,’ ” Dr. Arora explains. The receiver is a resident or other clinician familiar both with the case and how the handoff should go, and who then provides a standardized evaluation, grade, and feedback.

“The goal is to teach students the triggers that need to be incorporated into an effective handoff,” Dr. Arora says. Her group also reviewed concepts of good handoffs from the medical literature and worked with a psychology expert in human communication.

“How do you teach people to give good handoffs? We don’t know all of the answers, but we think you have to start somewhere,” she says. “Technology can be a great facilitator to make handoffs go better. It’s not a perfect substitute for face-to-face, interactive handoffs, but it can dramatically inform care transitions.”

Larry Beresford is a freelance writer based in Oakland, Calif.

Few medical students receive formal training in how to perform patient handoffs effectively and efficiently, says Vineet Arora, MD, FHM, who chairs an SHM task force on improving handoffs. Most pick it up on the job, but Dr. Arora and her colleagues at the University of Chicago—where she is associate director of the internal-medicine residency program—and at the University of Michigan have been exploring ways to improve the process through education.¹ Handoffs and care transitions are a major focus for hospital quality-improvement (QI) efforts nationally.

Dr. Arora’s group created an “observed simulation handoff experience” for medical students and residents, “offering an air of authenticity to the experience without the high-risk environment of learning on live patients,” she explains. Students who have completed an interactive training session perform the simulation at a computer station. They are provided with two types of information: static data about the mock patient—including such information as diagnosis, primary-care physician, and code status from a history and physical report—and video clips offering “a virtual, real-time barrage of constant updates” about the patient’s changing clinical status.

“They are given some time to extract and synthesize the important data for a handoff, and then they go in and perform the handoff in person to a ‘standardized receiver,’ ” Dr. Arora explains. The receiver is a resident or other clinician familiar both with the case and how the handoff should go, and who then provides a standardized evaluation, grade, and feedback.

“The goal is to teach students the triggers that need to be incorporated into an effective handoff,” Dr. Arora says. Her group also reviewed concepts of good handoffs from the medical literature and worked with a psychology expert in human communication.

“How do you teach people to give good handoffs? We don’t know all of the answers, but we think you have to start somewhere,” she says. “Technology can be a great facilitator to make handoffs go better. It’s not a perfect substitute for face-to-face, interactive handoffs, but it can dramatically inform care transitions.”

Larry Beresford is a freelance writer based in Oakland, Calif.

Supplement Editor:
Marc S. Penn, MD, PhD

Contents

Introduction: Heart-brain medicine: Update 2009
Marc S. Penn, MD, PhD, and Earl E. Bakken, MD (HonC), DSc (3 Hon), DHL (2 Hon)

Depression and Heart Disease

Depression and heart failure: An overview of what we know and don't know
Marc A. Silver, MD

The American Heart Association science advisory on depression and coronary heart disease: An exploration of the issues raised
J. Thomas Bigger, MD, and Alexander H. Glassman, MD

Depression and cardiovascular disease: Selected findings, controversies, and clinical implications from 2009
Karina W. Davidson, PhD, and Maya Rom Korin, PhD

Pioneer Lecture

Recovery of consciousness after severe brain injury: The role of arousal regulation mechanisms and some speculation on the heart-brain interface
Nicholas D. Schiff, MD

Heart-Brain Medicine Publications: The Year in Review

Neuroscience and heart-brain medicine: The year in review
David S. Goldstein, MD, PhD

Pathophysiologic mechanisms linking impaired cardiovascular health and neurologic dysfunction: The year in review
Ki E. Park, MD, and Carl J. Pepine, MD

Biomedical engineering in heart-brain medicine: A review
Peter G. Katona, ScD

Novel Findings in Heart-Brain Medicine

Sudden death in epilepsy, surgery, and seizure outcomes: The interface between heart and brain
Lara Jehi, MD

Biofeedback in the Treatment of Disease

Biofeedback in the treatment of heart failure
Michael G. McKee, PhD, and Christine S. Moravec, PhD

Biofeedback in the treatment of epilepsy
M. Barry Sterman, PhD

The effects of biofeedback in diabetes and essential hypertension
Angele McGrady, PhD, MEd, LPCC

Biofeedback in headache: An overview of approaches and evidence
Frank Andrasik, PhD

Device-Based Therapies

Use of deep brain stimulation in treatment-resistant depression
Donald A. Malone, Jr, MD

Poster Abstracts

Abstract 1: Potential role of the cardiac protease corin in energy metabolism
Jingjing Jiang, Yujie Cui, Wei Wang, and Qingyu Wu

Abstract 2: Anxiety and type D personality in ICD patients: Impact of shocks
Mina K. Chung, MD; Melanie Panko, RN; Tina Gupta; Scott Bea, PhD; Karen Broer, PhD; Diana Bauer; Denise Kosty-Sweeney, RN; Betty Ching, RN; Suzanne Pedersen, PhD; Sam Sears, PhD; and Leo Pozuelo, MD

Abstract 3: Microglia activation and neuroprotection during CNS preconditioning
Walid Jalabi, Ranjan Dutta, Yongming Jin, Gerson Criste, Xinghua Yin, Grahame J. Kidd, and Bruce D. Trapp

Abstract 4: Brain MRI correlates of atrial fibrillation
Stephen E. Jones, MD, PhD; Thomas Callahan, MD; Kamal Chémali, MD; Michael Phillips, MD; David Van Wagoner, PhD; and Walid Saliba, MD

Abstract 5: Identification and characterization of autonomic dysfunction in migraineurs with and without auras: Phase I
Mark Stillman, MD

Abstract 6: Sudden unexpected death in epilepsy: Finding the missing cardiac links
Lara Jehi, MD; Kanjana Unnongswe, MD; Thomas Callahan, MD; Liang Li, PhD; and Imad Najm, MD

Abstract 7: Cardiomyopathy after subarachnoid hemorrhage is mediated by neutrophils
J. Javier Provencio, Shari Moore, and Saksith Smithason

Abstract 8: Mindfulness, yoga, and cardiovascular disease
Didier Allexandre, Emily Fox, Mladen Golubic, Tom Morledge, and Joan E.B. Fox

Abstract 9: Multidisciplinary research in biofeedback
Christine S. Moravec, PhD; Michael G. McKee, PhD; James B. Young, MD; Betul Hatipoglu, MD; Leopoldo Pozuelo, MD; Leslie Cho, MD; Gordon Blackburn, MD; Francois Bethoux, MD; Mary Rensel, MD; Katherine Hoercher, RN; J. Javier Provencio, MD; and Marc S. Penn, MD

Abstract 10: Complex regional pain syndrome (CRPS I): A systemic disease of the autonomic nervous system
Kamal Chemali, MD; Robert Shields, MD; Lan Zhou, MD, PhD; Salim Hayek, MD, PhD; and Thomas Chelimsky, MD

Abstract 11: Biofeedback in the treatment of heart failure
Dana L. Frank, BA; Lamees Khorshid, PsyD; Jerome Kiffer, MA; Christine S. Moravec, PhD; and Michael G. McKee, PhD

Abstract 12: Change in depressive symptom status predicts health-related quality of life in patients with heart failure
Rebecca L. Dekker, MSN, RN, PhD candidate; Terry A. Lennie, PhD, RN; Nancy Albert, PhD, CCNS; Barbara Riegel, DNSc, RN; Misook L. Chung, PhD, RN; Seongkum Heo, PhD, RN; Eun Kyeung Song, PhD, RN; Jia-Rong Wu, PhD, RN; and Debra K. Moser, DNSc, RN

Abstract 13: Entropy of EKG time series distinguishes epileptic from nonepileptic patients
Rebecca O’Dwyer, Ulrich Zurcher, Brian Vyhnalek, Miron Kaufman, and Richard Burgess

Abstract 14: Evaluation of cardiac autonomic balance in major depression treated with different antidepressant therapies: A study with heart rate variability measures
K. Udupa, K.R. Kishore, J. Thirthalli, B.N. Gangadhar, T.R. Raju, and T.N. Sathyaprabha

Abstract 15: Proinflammatory status in major depression: Effects of escitalopram
John Piletz, PhD; Angelos Halaris, MD; Erin Tobin, MS; Edwin Meresh, MD; Jawed Fareed, PhD; Omer Iqbal, MD; Debra Hoppenstead, PhD; and James Sinacore, PhD

Abstract 16: Heart rate variability in depression: Effect of escitalopram
Angelos Halaris, MD; John Piletz, PhD; Erin Tobin, MA; Edwin Meresh, MD; James Sinacore, PhD; and Christopher Lowden

Abstract 17: Effects of omega-3/6 dietary ratio variation after a myocardial infarction in a rat model
Guy Rousseau, Isabelle Rondeau, Sandrine Picard, Thierno Madjou Bah, Louis Roy, and Roger Godbout

Abstract 18: The effects of tai chi on the heart and the brain
Qian Luo, Xi Cheng, and Xi Zha

Abstract 19: A randomized controlled trial of the effect of hostility reduction on cardiac autonomic regulation
Richard P. Sloan, PhD; Peter A. Shapiro, MD; Ethan E. Gorenstein, PhD; Felice A. Tager, PhD; Catherine E. Monk, PhD; Paula S. McKinley, PhD; Michael M. Myers, PhD; Emilia Bagiella, PhD; Ivy Chen, MST; Richard Steinman, BA; and J. Thomas Bigger, Jr., MD

Supplement Editor:
Marc S. Penn, MD, PhD

Contents

Introduction: Heart-brain medicine: Update 2009
Marc S. Penn, MD, PhD, and Earl E. Bakken, MD (HonC), DSc (3 Hon), DHL (2 Hon)

Depression and Heart Disease

Depression and heart failure: An overview of what we know and don't know
Marc A. Silver, MD

The American Heart Association science advisory on depression and coronary heart disease: An exploration of the issues raised
J. Thomas Bigger, MD, and Alexander H. Glassman, MD

Depression and cardiovascular disease: Selected findings, controversies, and clinical implications from 2009
Karina W. Davidson, PhD, and Maya Rom Korin, PhD

Pioneer Lecture

Recovery of consciousness after severe brain injury: The role of arousal regulation mechanisms and some speculation on the heart-brain interface
Nicholas D. Schiff, MD

Heart-Brain Medicine Publications: The Year in Review

Neuroscience and heart-brain medicine: The year in review
David S. Goldstein, MD, PhD

Pathophysiologic mechanisms linking impaired cardiovascular health and neurologic dysfunction: The year in review
Ki E. Park, MD, and Carl J. Pepine, MD

Biomedical engineering in heart-brain medicine: A review
Peter G. Katona, ScD

Novel Findings in Heart-Brain Medicine

Sudden death in epilepsy, surgery, and seizure outcomes: The interface between heart and brain
Lara Jehi, MD

Biofeedback in the Treatment of Disease

Biofeedback in the treatment of heart failure
Michael G. McKee, PhD, and Christine S. Moravec, PhD

Biofeedback in the treatment of epilepsy
M. Barry Sterman, PhD

The effects of biofeedback in diabetes and essential hypertension
Angele McGrady, PhD, MEd, LPCC

Biofeedback in headache: An overview of approaches and evidence
Frank Andrasik, PhD

Device-Based Therapies

Use of deep brain stimulation in treatment-resistant depression
Donald A. Malone, Jr, MD

Poster Abstracts

Abstract 1: Potential role of the cardiac protease corin in energy metabolism
Jingjing Jiang, Yujie Cui, Wei Wang, and Qingyu Wu

Abstract 2: Anxiety and type D personality in ICD patients: Impact of shocks
Mina K. Chung, MD; Melanie Panko, RN; Tina Gupta; Scott Bea, PhD; Karen Broer, PhD; Diana Bauer; Denise Kosty-Sweeney, RN; Betty Ching, RN; Suzanne Pedersen, PhD; Sam Sears, PhD; and Leo Pozuelo, MD

Abstract 3: Microglia activation and neuroprotection during CNS preconditioning
Walid Jalabi, Ranjan Dutta, Yongming Jin, Gerson Criste, Xinghua Yin, Grahame J. Kidd, and Bruce D. Trapp

Abstract 4: Brain MRI correlates of atrial fibrillation
Stephen E. Jones, MD, PhD; Thomas Callahan, MD; Kamal Chémali, MD; Michael Phillips, MD; David Van Wagoner, PhD; and Walid Saliba, MD

Abstract 5: Identification and characterization of autonomic dysfunction in migraineurs with and without auras: Phase I
Mark Stillman, MD

Abstract 6: Sudden unexpected death in epilepsy: Finding the missing cardiac links
Lara Jehi, MD; Kanjana Unnongswe, MD; Thomas Callahan, MD; Liang Li, PhD; and Imad Najm, MD

Abstract 7: Cardiomyopathy after subarachnoid hemorrhage is mediated by neutrophils
J. Javier Provencio, Shari Moore, and Saksith Smithason

Abstract 8: Mindfulness, yoga, and cardiovascular disease
Didier Allexandre, Emily Fox, Mladen Golubic, Tom Morledge, and Joan E.B. Fox

Abstract 9: Multidisciplinary research in biofeedback
Christine S. Moravec, PhD; Michael G. McKee, PhD; James B. Young, MD; Betul Hatipoglu, MD; Leopoldo Pozuelo, MD; Leslie Cho, MD; Gordon Blackburn, MD; Francois Bethoux, MD; Mary Rensel, MD; Katherine Hoercher, RN; J. Javier Provencio, MD; and Marc S. Penn, MD

Abstract 10: Complex regional pain syndrome (CRPS I): A systemic disease of the autonomic nervous system
Kamal Chemali, MD; Robert Shields, MD; Lan Zhou, MD, PhD; Salim Hayek, MD, PhD; and Thomas Chelimsky, MD

Abstract 11: Biofeedback in the treatment of heart failure
Dana L. Frank, BA; Lamees Khorshid, PsyD; Jerome Kiffer, MA; Christine S. Moravec, PhD; and Michael G. McKee, PhD

Abstract 12: Change in depressive symptom status predicts health-related quality of life in patients with heart failure
Rebecca L. Dekker, MSN, RN, PhD candidate; Terry A. Lennie, PhD, RN; Nancy Albert, PhD, CCNS; Barbara Riegel, DNSc, RN; Misook L. Chung, PhD, RN; Seongkum Heo, PhD, RN; Eun Kyeung Song, PhD, RN; Jia-Rong Wu, PhD, RN; and Debra K. Moser, DNSc, RN

Abstract 13: Entropy of EKG time series distinguishes epileptic from nonepileptic patients
Rebecca O’Dwyer, Ulrich Zurcher, Brian Vyhnalek, Miron Kaufman, and Richard Burgess

Abstract 14: Evaluation of cardiac autonomic balance in major depression treated with different antidepressant therapies: A study with heart rate variability measures
K. Udupa, K.R. Kishore, J. Thirthalli, B.N. Gangadhar, T.R. Raju, and T.N. Sathyaprabha

Abstract 15: Proinflammatory status in major depression: Effects of escitalopram
John Piletz, PhD; Angelos Halaris, MD; Erin Tobin, MS; Edwin Meresh, MD; Jawed Fareed, PhD; Omer Iqbal, MD; Debra Hoppenstead, PhD; and James Sinacore, PhD

Abstract 16: Heart rate variability in depression: Effect of escitalopram
Angelos Halaris, MD; John Piletz, PhD; Erin Tobin, MA; Edwin Meresh, MD; James Sinacore, PhD; and Christopher Lowden

Abstract 17: Effects of omega-3/6 dietary ratio variation after a myocardial infarction in a rat model
Guy Rousseau, Isabelle Rondeau, Sandrine Picard, Thierno Madjou Bah, Louis Roy, and Roger Godbout

Abstract 18: The effects of tai chi on the heart and the brain
Qian Luo, Xi Cheng, and Xi Zha

Abstract 19: A randomized controlled trial of the effect of hostility reduction on cardiac autonomic regulation
Richard P. Sloan, PhD; Peter A. Shapiro, MD; Ethan E. Gorenstein, PhD; Felice A. Tager, PhD; Catherine E. Monk, PhD; Paula S. McKinley, PhD; Michael M. Myers, PhD; Emilia Bagiella, PhD; Ivy Chen, MST; Richard Steinman, BA; and J. Thomas Bigger, Jr., MD

Supplement Editor:
Marc S. Penn, MD, PhD

Contents

Introduction: Heart-brain medicine: Update 2009
Marc S. Penn, MD, PhD, and Earl E. Bakken, MD (HonC), DSc (3 Hon), DHL (2 Hon)

Depression and Heart Disease

Depression and heart failure: An overview of what we know and don't know
Marc A. Silver, MD

The American Heart Association science advisory on depression and coronary heart disease: An exploration of the issues raised
J. Thomas Bigger, MD, and Alexander H. Glassman, MD

Depression and cardiovascular disease: Selected findings, controversies, and clinical implications from 2009
Karina W. Davidson, PhD, and Maya Rom Korin, PhD

Pioneer Lecture

Recovery of consciousness after severe brain injury: The role of arousal regulation mechanisms and some speculation on the heart-brain interface
Nicholas D. Schiff, MD

Heart-Brain Medicine Publications: The Year in Review

Neuroscience and heart-brain medicine: The year in review
David S. Goldstein, MD, PhD

Pathophysiologic mechanisms linking impaired cardiovascular health and neurologic dysfunction: The year in review
Ki E. Park, MD, and Carl J. Pepine, MD

Biomedical engineering in heart-brain medicine: A review
Peter G. Katona, ScD

Novel Findings in Heart-Brain Medicine

Sudden death in epilepsy, surgery, and seizure outcomes: The interface between heart and brain
Lara Jehi, MD

Biofeedback in the Treatment of Disease

Biofeedback in the treatment of heart failure
Michael G. McKee, PhD, and Christine S. Moravec, PhD

Biofeedback in the treatment of epilepsy
M. Barry Sterman, PhD

The effects of biofeedback in diabetes and essential hypertension
Angele McGrady, PhD, MEd, LPCC

Biofeedback in headache: An overview of approaches and evidence
Frank Andrasik, PhD

Device-Based Therapies

Use of deep brain stimulation in treatment-resistant depression
Donald A. Malone, Jr, MD

Poster Abstracts

Abstract 1: Potential role of the cardiac protease corin in energy metabolism
Jingjing Jiang, Yujie Cui, Wei Wang, and Qingyu Wu

Abstract 2: Anxiety and type D personality in ICD patients: Impact of shocks
Mina K. Chung, MD; Melanie Panko, RN; Tina Gupta; Scott Bea, PhD; Karen Broer, PhD; Diana Bauer; Denise Kosty-Sweeney, RN; Betty Ching, RN; Suzanne Pedersen, PhD; Sam Sears, PhD; and Leo Pozuelo, MD

Abstract 3: Microglia activation and neuroprotection during CNS preconditioning
Walid Jalabi, Ranjan Dutta, Yongming Jin, Gerson Criste, Xinghua Yin, Grahame J. Kidd, and Bruce D. Trapp

Abstract 4: Brain MRI correlates of atrial fibrillation
Stephen E. Jones, MD, PhD; Thomas Callahan, MD; Kamal Chémali, MD; Michael Phillips, MD; David Van Wagoner, PhD; and Walid Saliba, MD

Abstract 5: Identification and characterization of autonomic dysfunction in migraineurs with and without auras: Phase I
Mark Stillman, MD

Abstract 6: Sudden unexpected death in epilepsy: Finding the missing cardiac links
Lara Jehi, MD; Kanjana Unnongswe, MD; Thomas Callahan, MD; Liang Li, PhD; and Imad Najm, MD

Abstract 7: Cardiomyopathy after subarachnoid hemorrhage is mediated by neutrophils
J. Javier Provencio, Shari Moore, and Saksith Smithason

Abstract 8: Mindfulness, yoga, and cardiovascular disease
Didier Allexandre, Emily Fox, Mladen Golubic, Tom Morledge, and Joan E.B. Fox

Abstract 9: Multidisciplinary research in biofeedback
Christine S. Moravec, PhD; Michael G. McKee, PhD; James B. Young, MD; Betul Hatipoglu, MD; Leopoldo Pozuelo, MD; Leslie Cho, MD; Gordon Blackburn, MD; Francois Bethoux, MD; Mary Rensel, MD; Katherine Hoercher, RN; J. Javier Provencio, MD; and Marc S. Penn, MD

Abstract 10: Complex regional pain syndrome (CRPS I): A systemic disease of the autonomic nervous system
Kamal Chemali, MD; Robert Shields, MD; Lan Zhou, MD, PhD; Salim Hayek, MD, PhD; and Thomas Chelimsky, MD

Abstract 11: Biofeedback in the treatment of heart failure
Dana L. Frank, BA; Lamees Khorshid, PsyD; Jerome Kiffer, MA; Christine S. Moravec, PhD; and Michael G. McKee, PhD

Abstract 12: Change in depressive symptom status predicts health-related quality of life in patients with heart failure
Rebecca L. Dekker, MSN, RN, PhD candidate; Terry A. Lennie, PhD, RN; Nancy Albert, PhD, CCNS; Barbara Riegel, DNSc, RN; Misook L. Chung, PhD, RN; Seongkum Heo, PhD, RN; Eun Kyeung Song, PhD, RN; Jia-Rong Wu, PhD, RN; and Debra K. Moser, DNSc, RN

Abstract 13: Entropy of EKG time series distinguishes epileptic from nonepileptic patients
Rebecca O’Dwyer, Ulrich Zurcher, Brian Vyhnalek, Miron Kaufman, and Richard Burgess

Abstract 14: Evaluation of cardiac autonomic balance in major depression treated with different antidepressant therapies: A study with heart rate variability measures
K. Udupa, K.R. Kishore, J. Thirthalli, B.N. Gangadhar, T.R. Raju, and T.N. Sathyaprabha

Abstract 15: Proinflammatory status in major depression: Effects of escitalopram
John Piletz, PhD; Angelos Halaris, MD; Erin Tobin, MS; Edwin Meresh, MD; Jawed Fareed, PhD; Omer Iqbal, MD; Debra Hoppenstead, PhD; and James Sinacore, PhD

Abstract 16: Heart rate variability in depression: Effect of escitalopram
Angelos Halaris, MD; John Piletz, PhD; Erin Tobin, MA; Edwin Meresh, MD; James Sinacore, PhD; and Christopher Lowden

Abstract 17: Effects of omega-3/6 dietary ratio variation after a myocardial infarction in a rat model
Guy Rousseau, Isabelle Rondeau, Sandrine Picard, Thierno Madjou Bah, Louis Roy, and Roger Godbout

Abstract 18: The effects of tai chi on the heart and the brain
Qian Luo, Xi Cheng, and Xi Zha

Abstract 19: A randomized controlled trial of the effect of hostility reduction on cardiac autonomic regulation
Richard P. Sloan, PhD; Peter A. Shapiro, MD; Ethan E. Gorenstein, PhD; Felice A. Tager, PhD; Catherine E. Monk, PhD; Paula S. McKinley, PhD; Michael M. Myers, PhD; Emilia Bagiella, PhD; Ivy Chen, MST; Richard Steinman, BA; and J. Thomas Bigger, Jr., MD

Hypogonadism is a highly prevalent condition that is under-diagnosed and under-treated despite available effective therapies. Low levels of testosterone result in losses of lean body mass and bone mass, decreases in libido and sexual function and is associated with insulin resistance, metabolic syndrome, diabetes, and other chronic comorbid conditions. It is important for physicians to be aware of how testosterone levels can be related to these conditions, which are seen in primary care practices on a daily basis.

This CME supplement discusses the definition, epidemiology and key signs and symptoms of late-onset hypogonadism, the role of lab measurements, factors to consider in selecting patients for testosterone replacement therapy, and how to identify the best treatment strategy for each patient.

Hypogonadism is a highly prevalent condition that is under-diagnosed and under-treated despite available effective therapies. Low levels of testosterone result in losses of lean body mass and bone mass, decreases in libido and sexual function and is associated with insulin resistance, metabolic syndrome, diabetes, and other chronic comorbid conditions. It is important for physicians to be aware of how testosterone levels can be related to these conditions, which are seen in primary care practices on a daily basis.

This CME supplement discusses the definition, epidemiology and key signs and symptoms of late-onset hypogonadism, the role of lab measurements, factors to consider in selecting patients for testosterone replacement therapy, and how to identify the best treatment strategy for each patient.

Hypogonadism is a highly prevalent condition that is under-diagnosed and under-treated despite available effective therapies. Low levels of testosterone result in losses of lean body mass and bone mass, decreases in libido and sexual function and is associated with insulin resistance, metabolic syndrome, diabetes, and other chronic comorbid conditions. It is important for physicians to be aware of how testosterone levels can be related to these conditions, which are seen in primary care practices on a daily basis.

This CME supplement discusses the definition, epidemiology and key signs and symptoms of late-onset hypogonadism, the role of lab measurements, factors to consider in selecting patients for testosterone replacement therapy, and how to identify the best treatment strategy for each patient.

Coenzyme Q10 supplements have been purported to be effective for treating a variety of disorders,^1,2 in particular hypertension and statin-induced myalgia.

Several studies^3–7 found that coenzyme Q10 supplementation significantly lowered blood pressure in hypertensive patients. Moreover, some trials have demonstrated that statin therapy reduces serum or muscle levels of coenzyme Q10,^8–14 prompting investigations to determine whether coenzyme Q10 deficiency is related to statin-induced muscle pain.^15–17

In this review, we discuss the efficacy and safety of coenzyme Q10 supplementation in patients with hypertension and those taking statins, and some of the caveats about using supplements that are not approved by the US Food and Drug Administration (FDA), as well as the bioavailability and quality of available formulations.

WHAT IS COENZYME Q10?

Coenzyme Q10, also known as coenzyme Q, ubidecarenone, and ubiquinone, is found in all human cells, with the highest concentrations in the heart, liver, kidney, and pancreas.^1,2 It is a potent antioxidant, a membrane stabilizer, and an integral cofactor in the mitochondrial respiratory chain, helping to generate adenosine triphosphate, the major cellular energy source.^1,2,18 It may also regulate genes associated with cell metabolism.¹⁹

RATIONALE FOR SUPPLEMENTATION

Coenzyme Q10 supplementation has been used, recommended, or studied in heart failure, hypertension, parkinsonism, mitochondrial encephalomyopathies, and other ailments.

In hypertension

Depending on the class, various antihypertensive drugs can have adverse effects such as depression, cough, and cardiac and renal dysfunction. ^20,21 Furthermore, many patients need to take more than one drug to control their blood pressure, increasing their risk of side effects. Some researchers believe coenzyme Q10 supplementation may reduce the need to take multiple antihypertensive drugs.⁵

Coenzyme Q10 appears to lower blood pressure. The exact mechanism is not known, but one theory is that it reduces peripheral resistance by preserving nitric oxide.²¹ Nitric oxide relaxes peripheral arteries, lowering blood pressure. In some forms of hypertension, superoxide radicals that inactivate nitric oxide are overproduced; coenzyme Q10, with its antioxidant effects, may prevent the inactivation of nitric oxide by these free radicals. Alternatively, coenzyme Q10 may boost the production of the prostaglandin prostacyclin (PGI₂) a potent vasodilator and inhibitor of platelet aggregation, or it may enhance the sensitivity of arterial smooth muscle to PGI₂, or both.^1,22

In patients taking statins

Hydroxymethylglutaryl coenzyme A reductase inhibitors (statins), first-line agents for lowering cholesterol levels to prevent cardiovascular disease, are some of the most commonly prescribed medications.^23,24 However, statin therapy carries a risk of myopathy, which can range from muscle aches to rhabdomyolysis. ^23,24

In a clinical advisory,²⁵ the American College of Cardiology, the American Heart Association, and the National Heart, Lung, and Blood Institute recommend that patients on statin therapy who experience muscle soreness, tenderness, or pain with serum creatine kinase levels 3 to 10 times the upper limit of normal should have their creatine kinase level checked weekly. If the level is 3 to 10 times the upper limit of normal, statin therapy may be continued, but if it exceeds 10 times the upper limit, then statins and other potential offending agents (eg, niacin, fibrate) need to be discontinued.

Statins inhibit the synthesis of cholesterol by reducing the production of mevalonate, a precursor of both cholesterol and coenzyme Q10. Since both cholesterol and coenzyme Q10 are produced by the same pathway, it is not surprising that statins have been reported to reduce serum and muscle coenzyme Q10 levels.^9–14 However, one study did not report a significant reduction of coenzyme Q10 levels in muscle tissue in patients treated with simvastatin 20 mg for 6 months.²⁶

Nonetheless, researchers have hypothesized that a reduction in coenzyme Q10 levels in muscle tissue causes mitochondrial dysfunction, which could increase the risk of statininduced myopathy,^13–17 and some believe that treatment with coenzyme Q10 may reduce myalgic symptoms and allow patients to remain on statin therapy.^13,24

Researchers have investigated the potential of coenzyme Q10 supplementation to reduce or prevent statin-induced myopathy.^15–17 (More on this below.)

Interestingly, a randomized, placebo-controlled trial²⁷ found that 6 months of daily therapy with simvastatin (Zocor) 20 mg or pravastatin (Pravachol) 40 mg lowered systolic and diastolic blood pressure significantly in patients with no documented history of cardiovascular disease or diabetes. A possible mechanism of statin-induced blood pressure reduction is the up-regulation of endothelial nitric oxide synthetase, a potent vasodilator. Coenzyme Q10 levels were not assessed during this study. Whether coenzyme Q10 supplementation used to treat statin-induced myalgia enhances or inhibits the antihypertensive effects of statins is not yet known.

EVIDENCE OF EFFECTIVENESS IN HYPERTENSION

Rosenfeldt et al²⁸ performed a meta-analysis and found that some trials documented statistically significant reductions in diastolic or systolic blood pressure or both, while others reported negligible effects.^3,29 In one small trial,³⁰ blood pressures actually went up in patients taking coenzyme Q10. Coenzyme Q10 dosages and length of therapy varied from study to study in the meta-analysis. Only minor adverse effects such as gastrointestinal upset and headache were reported.

Yamagami et al³ randomly assigned 20 patients with hypertension and a low coenzyme Q10 level to receive 100 mg of coenzyme Q10 or placebo daily for 12 weeks. Patients continued their usual antihypertensive regimen during the study period. Blood pressures, coenzyme Q10 levels, and antihypertensive drugs used were comparable between the study groups.

After 12 weeks of therapy, the mean coenzyme Q10 level in the active-treatment group had more than doubled, from 0.704 to 1.597 μg/mL. This group also experienced a statistically significant drop in systolic blood pressure, from 167 mm Hg at baseline to 148 mm Hg at 12 weeks. In the placebo group, the systolic blood pressure was 168 mm Hg at baseline and 164 mm Hg at 12 weeks; the change was not statistically significant. Diastolic pressure was not significantly lower at 12 weeks than at baseline in either group.

The authors concluded that coenzyme Q10 supplementation brought a mild reduction in high blood pressure in patients who had low coenzyme Q10 serum levels.

Digiesi et al³¹ randomized 18 patients with essential hypertension to receive either coenzyme Q10 100 mg or placebo daily for 10 weeks. All antihypertensive therapy was discontinued at baseline. After the first 10 weeks, patients went through a 2-week washout period and then were switched to the opposite therapy for an additional 10 weeks. Mean baseline blood pressure values were 167 mm Hg systolic and 103 mm Hg diastolic.

Those taking the supplement had a statistically significant decrease in systolic and diastolic pressures (P < .001). The antihypertensive effect was noted in the 3rd or 4th week of active treatment and persisted for the duration of therapy. The effects dissipated 7 to 10 days after coenzyme Q10 was stopped.

Langsjoen et al⁵ evaluated the effects of adding coenzyme Q10 to the antihypertensive drug regimen of 109 patients who had a primary diagnosis of essential hypertension in a prospective observational study. Patients with hypertension as a secondary diagnosis and other cardiovascular diseases were excluded. Variable doses of coenzyme Q10 were given, adjusted according to clinical response and to achieve serum levels greater than 2.0 μg/mL. The average dose was 225 mg/day; the mean serum level attained was 3.02 μg/mL.

Over several months, patients taking the supplement had a reduction in mean systolic pressure from 159 mm Hg at baseline to 147 mm Hg (P < .001), and a reduction in mean diastolic pressure from 94 to 85 mm Hg (P < .001). Thirty-seven percent of patients were able to discontinue one antihypertensive drug, 11% discontinued two drugs, and 4% were able to stop taking three drugs. However, 46% remained on the same antihypertensive regimen, and 3% needed an additional drug.

Singh et al⁶ randomized 64 patients who had coronary artery disease and who had been on antihypertensive drugs for more than 1 year to receive either B-complex vitamins or coenzyme Q10 (hydrosoluble Q-Gel) 60 mg orally once daily for 8 weeks. Five patients were not available for follow-up; therefore, only 59 patients were evaluated. Fifty-five (93%) of the 59 patients were taking only one antihypertensive drug. Initial antihypertensive drug use was similar between study groups and was continued throughout the trial.

After 8 weeks of therapy, the coenzyme Q10 group had significantly lower systolic and diastolic blood pressure than the placebo group (P < .05 for both). There was also a statistically significant decrease in the dosage of antihypertensive drugs in the coenzyme Q10 group but not in the placebo group (P < .05), reflecting coenzyme Q10’s additive antihypertensive effect.

Burke et al⁷ randomized 41 men and 35 women with isolated systolic hypertension (systolic pressure 150–170 mm Hg, diastolic pressure < 90 mm Hg) to receive a twice-daily dose of 60 mg of emulsified coenzyme Q10 (hydrosoluble Q-Gel) with 150 IU of vitamin E or placebo containing vitamin E alone for 12 weeks. The study also included 5 men and 4 women with normal blood pressure, all of whom received coenzyme Q10. A total of 80 patients completed treatment. The primary goal of the study was to determine the efficacy of coenzyme Q10 in the treatment of isolated systolic hypertension in patients without comorbid conditions. Blood pressures were monitored twice a week during the trial, by the same nurse.

After 12 weeks of treatment, the mean reduction in systolic pressure in hypertensive patients on coenzyme Q10 was 17.8 ± 7.3 mm Hg. There were no significant changes in diastolic pressure in any study group with treatment. Patients with isolated systolic hypertension who were taking coenzyme Q10 had a statistically significant reduction in systolic pressure compared with baseline and placebo (P < .01 for both). Approximately 55% of patients on coenzyme Q10 achieved a reduction in systolic pressure of 4 mm Hg or greater, while 45% did not respond to therapy. The mean plasma coenzyme Q10 level of the treatment group increased from 0.47 ± 0.19 μg/mL to 2.69 ± 0.54 μg/mL after 12 weeks; however, the study did not have the statistical power to demonstrate a relationship between coenzyme Q10 levels and changes in blood pressure. Twenty-seven (34%) of the 80 patients were taking a statin while on coenzyme Q10 therapy.

STUDIES IN STATIN-INDUCED MYOPATHY

Thibault et al³² and Kim et al³³ reported that patients taking lovastatin (Mevacor) at dosages as high as 35 mg/kg/day to inhibit tumor growth achieved symptomatic relief of statin-induced musculoskeletal toxicity after coenzyme Q10 supplementation.

Caso et al¹⁵ performed a small pilot study in 32 patients to determine if coenzyme Q10 supplementation would improve myalgic symptoms in patients treated with statins. In this double-blind, randomized trial, patients received either coenzyme Q10 100 mg/day or vitamin E 400 IU/day for 30 days. The extent of muscle pain and its interference with daily activities were determined before and after therapy using the Brief Pain Inventory Questionnaire. The statins were atorvastatin (Lipitor) 10 mg or 20 mg, lovastatin 40 mg, pravastatin 40 mg, and simvastatin 10, 20, 40, and 80 mg. Five patients in the coenzyme Q10 group and four patients in the vitamin E group were taking nonsteroidal anti-inflammatory drugs before and during the trial. The intensity of muscle pain and its interference with daily activities were similar between study groups before the start of therapy.

After 30 days of treatment with coenzyme Q10, the pain intensity had decreased significantly from baseline (P < .001). In contrast, no change in pain intensity from baseline was noted in patients receiving vitamin E. The Pain Severity Score was significantly different between study groups, favoring the coenzyme Q10 group (P < .001). Sixteen of 18 patients on coenzyme Q10 reported a reduction in pain, while only 3 of 14 patients on vitamin E reported a similar response. Also, the interference of pain with daily activities significantly improved with coenzyme Q10 (P < .02), whereas vitamin E did not have a significant impact on this.

Young et al¹⁷ randomized 44 patients with prior statin-induced myalgia to receive increasing doses of simvastatin (10–40 mg/day) in combination with either coenzyme Q10 (Q-Gel) 200 mg/day or placebo. The primary goal was to determine if coenzyme Q10 supplementation would help improve statin tolerance in patients with a history of statininduced myalgia. Plasma coenzyme Q10 and lipid levels were measured at baseline and at the end of the study. The intensity of myalgia was assessed with a visual analogue scale.

At 12 weeks, the coenzyme Q10 plasma level was significantly higher in the treatment group than in the placebo group (P < .001). However, no differences were noted between groups in the number of patients who tolerated the 40-mg/day simvastatin dose (P = .34) or in the number of patients who remained on any simvastatin dose (P = .47). Additionally, myalgia scores did not differ between groups (P = .63). The authors acknowledged that there were only small increases in the myalgia pain scores reported in either group. Therefore, patients in the treatment group may not have experienced sufficiently severe muscle pain to have benefited from coenzyme Q10 supplementation.

IS COENZYME Q10 SAFE?

Studies have indicated that these supplements are well tolerated, with relatively few adverse effects or potential drug interactions.^1,2,34

The FDA does not routinely assess the purity or quality of over-the-counter coenzyme Q10 products.³⁵ However, the United States Pharmacopeia (USP) does test dietary supplements to make sure that they are not mislabeled and that they do not contain contaminants. ³⁶

A USP-verified dietary supplement should:

• Contain the exact ingredients listed on the label in the listed potency and amounts
• Not include harmful levels of certain contaminants such as lead, mercury, pesticides, or bacteria
• Appropriately disintegrate and release its contents into the body within a specified period of time
• Be produced using the FDA’s current Good Manufacturing Practices.³⁶

Side effects, contraindications, warnings

Coenzyme Q10 is a relatively safe dietary supplement. It is contraindicated in patients who are allergic to it or to any of its components.² Most clinical trials have not reported significant adverse effects that necessitated stopping therapy.³⁴ However, gastrointestinal effects such as abdominal discomfort, nausea, vomiting, diarrhea, and anorexia have occurred.^1,2,34 Allergic rash and headache have also been reported.^1,2,34 In addition, coenzyme Q10’s antiplatelet effect may increase the risk of bleeding. ^37,38 It undergoes biotransformation in the liver and is eliminated primarily via the biliary tract,³⁹ so it can accumulate in patients with hepatic impairment or biliary obstruction.

Interactions with drugs

Coenzyme Q10’s effects on platelet function may increase the risk of bleeding in patients taking antiplatelet drugs such as aspirin or clopidogrel (Plavix).^37,38 On the other hand, since it acts like vitamin K, it may counteract the anticoagulant effects of warfarin (Coumadin). ^1,2,40

Coenzyme Q10 may have an additive antihypertensive effect when given with antihypertensive drugs.⁴¹

Coenzyme Q10 may improve beta-cell function and enhance insulin sensitivity, which may reduce insulin requirements for diabetic patients.^42,43

SLOWLY ABSORBED

Coenzyme Q10 is absorbed slowly from the gastrointestinal tract, possibly because it has a high molecular weight and is not very watersoluble. ³⁹

One pharmacokinetic study found that after a single 100-mg oral dose of coenzyme Q10, the mean peak plasma levels of about 1 μg/mL occurred between 5 and 10 hours (mean 6.5 hours).⁴⁴ Coenzyme Q10 100 mg given orally three times daily produced a mean steadystate plasma level of 5.4 μg/mL; about 90% of this steady-state concentration was achieved after 4 days.³⁹

Some formulations have significantly better oral bioavailability and therefore produce higher plasma levels. Soft-gel capsules, especially those with vegetable oil or vitamin E, may have better absorption.⁴³

A pharmacokinetic study showed that the area under the curve of the plasma coenzyme Q10 concentration was more than twice as high with Q-Gel soft-gel capsules, a completely solubilized formulation, than with softgel capsules with an oil suspension, powderfilled hard-shell capsules, or regular tablets.⁴⁵ Another study reported that colloidal-Q10, a formulation contained in VESIsorb (a novel drug delivery system sold as CoQsource) had greater bioavailability than solubilized and oil-based preparations.⁴⁶ Commercially available solubilized preparations containing ubiquinol, a metabolized form of coenzyme Q10, have been shown to produce higher serum levels than solubilized products.⁴⁷

Of note: unless the manufacturer claims that its product is water-soluble, the USP does not evaluate its dissolution rate.⁴⁸ Therefore, USP-verified coenzyme Q10 products that are not water-soluble may have lower bioavailability than their solubilized counterparts.

Dry dosage forms of coenzyme Q10 (eg, tablets, capsules) may be more readily absorbed if taken with a fatty meal.⁴³

SLOWLY ELIMINATED

Taken orally, coenzyme Q10 has a low clearance rate, with an elimination half-life of about 34 hours.³⁹

After absorption, exogenous coenzyme Q10 is taken up by chylomicrons that transport it to the liver, where it is incorporated into verylow-density lipoproteins. It is then distributed to various organs, including the adrenal glands, spleen, kidneys, lungs, and heart. Coenzyme Q10 is eliminated primarily via the biliary tract. About 60% of an oral dose is eliminated in the feces during chronic oral administration.³⁹

TWICE-DAILY DOSING

A typical daily dose of coenzyme Q10 for treating hypertension is 120 to 200 mg, usually given orally in two divided doses.¹ For statininduced myopathy, 100 to 200 mg orally daily has been used.¹

Coenzyme Q10 is given in divided doses to enhance its absorption and to minimize gastrointestinal effects.^1,43 Taking it with a fatty meal may also increase its absorption.⁴³

Since solubilized forms of coenzyme Q10 and ubiquinol have significantly greater bioavailability than nonsolubilized forms, the therapeutic dose of these formulations may be lower.⁴⁷

MONITORING DURING TREATMENT

Without supplementation, the mean serum level of endogenous coenzyme Q10 has been reported to be 0.99 ± 0.30 mg/L (range 0.55– 1.87).¹⁸ Serum levels above 2 μg/mL have been associated with significant reductions in blood pressure.^5,7,28

The possible effects of coenzyme Q10 on blood pressure, blood glucose levels, serum creatine kinase levels, and myopathic symptoms should be kept in mind when monitoring patients who have hypertension,⁴¹ diabetes,^41,42 or statin-induced myalgia.^15,17 Coenzyme Q10’s possible potentiating effects on antiplatelet drugs and its inhibitory effect on warfarin should be kept in mind as well.

COST VARIES

Coenzyme Q10 is available in different dosage forms (eg, regular and rapid-release softgel capsules, regular and chewable tablets, chewable wafers, and liquid) from a variety of manufacturers. Products come in different strengths, typically ranging from 30 to 400 mg. USP-verified formulations are listed at www.usp.org/USPVerified/dietarySupplements/under “Verified Supplements.” Only USP-verified products that claim to be water-soluble meet USP dissolution requirements.

The cost varies, depending on the vendor. In general, dosage forms with greater bioavailability, such as Q-Gel and ubiquinol supplements, are more expensive. For example, a regimen of 60 mg twice daily of regular-release coenzyme Q capsules may cost approximately $20 per month, compared with $60 per month for the same supply of Q-Gel Ultra capsules. However, in some cases, supplements that produce higher serum levels may be more cost-effective.

CURRENT ROLE IN THERAPY

As an antihypertensive adjunct

Several small clinical trials have shown that coenzyme Q10 supplementation can lower blood pressure. The supplements were reported to be safe and well tolerated. Moreover, some patients with essential hypertension who were taking coenzyme Q10 were able to discontinue one or more antihypertensive drugs. A significant reduction in blood pressure with use of coenzyme Q10 would be expected to reduce the adverse consequences of hypertension in the same manner as conventional antihypertensive agents.

However, no large, double-blind, randomized study has evaluated the impact of coenzyme Q10 when taken with other antihypertensive drugs (eg, angiotensin-converting enzyme inhibitors, beta-blockers, diuretics) on specific clinical end points such as the incidence of stroke or death from a major cardiac event. Furthermore, its effects on cardiac function, exercise tolerance, and quality of life have not been determined.

The bottom line. In some cases, it seems reasonable to recommend this product as an adjunct to conventional antihypertensive therapy. Larger, well-designed clinical trials of coenzyme Q10’s antihypertensive effects on specific clinical end points such as the risk of stroke or myocardial infarction are needed to define its true therapeutic value.

As a treatment for statin-induced myalgia

Clinical evidence supporting coenzyme Q10’s use in the treatment of statin-induced myopathy is limited. Whether coenzyme Q10 is depleted from muscle tissue during statin therapy has not been confirmed. Supplementation helped reduce the severity of musculoskeletal effects of megadoses of lovastatin. However, clinical trials of coenzyme Q10 in the treatment of myalgia associated with antilipidemic statin doses did not consistently report significant improvement. Nevertheless, coenzyme Q10 has been shown to be relatively safe, with few adverse effects.

The bottom line. In some cases, coenzyme Q could be considered as a possible treatment for statin-induced myalgia, pending large-scale studies to determine if it is truly effective for this purpose.

Coenzyme Q10 supplements have been purported to be effective for treating a variety of disorders,^1,2 in particular hypertension and statin-induced myalgia.

Several studies^3–7 found that coenzyme Q10 supplementation significantly lowered blood pressure in hypertensive patients. Moreover, some trials have demonstrated that statin therapy reduces serum or muscle levels of coenzyme Q10,^8–14 prompting investigations to determine whether coenzyme Q10 deficiency is related to statin-induced muscle pain.^15–17

In this review, we discuss the efficacy and safety of coenzyme Q10 supplementation in patients with hypertension and those taking statins, and some of the caveats about using supplements that are not approved by the US Food and Drug Administration (FDA), as well as the bioavailability and quality of available formulations.

WHAT IS COENZYME Q10?

Coenzyme Q10, also known as coenzyme Q, ubidecarenone, and ubiquinone, is found in all human cells, with the highest concentrations in the heart, liver, kidney, and pancreas.^1,2 It is a potent antioxidant, a membrane stabilizer, and an integral cofactor in the mitochondrial respiratory chain, helping to generate adenosine triphosphate, the major cellular energy source.^1,2,18 It may also regulate genes associated with cell metabolism.¹⁹

RATIONALE FOR SUPPLEMENTATION

Coenzyme Q10 supplementation has been used, recommended, or studied in heart failure, hypertension, parkinsonism, mitochondrial encephalomyopathies, and other ailments.

In hypertension

Depending on the class, various antihypertensive drugs can have adverse effects such as depression, cough, and cardiac and renal dysfunction. ^20,21 Furthermore, many patients need to take more than one drug to control their blood pressure, increasing their risk of side effects. Some researchers believe coenzyme Q10 supplementation may reduce the need to take multiple antihypertensive drugs.⁵

Coenzyme Q10 appears to lower blood pressure. The exact mechanism is not known, but one theory is that it reduces peripheral resistance by preserving nitric oxide.²¹ Nitric oxide relaxes peripheral arteries, lowering blood pressure. In some forms of hypertension, superoxide radicals that inactivate nitric oxide are overproduced; coenzyme Q10, with its antioxidant effects, may prevent the inactivation of nitric oxide by these free radicals. Alternatively, coenzyme Q10 may boost the production of the prostaglandin prostacyclin (PGI₂) a potent vasodilator and inhibitor of platelet aggregation, or it may enhance the sensitivity of arterial smooth muscle to PGI₂, or both.^1,22

In patients taking statins

Hydroxymethylglutaryl coenzyme A reductase inhibitors (statins), first-line agents for lowering cholesterol levels to prevent cardiovascular disease, are some of the most commonly prescribed medications.^23,24 However, statin therapy carries a risk of myopathy, which can range from muscle aches to rhabdomyolysis. ^23,24

In a clinical advisory,²⁵ the American College of Cardiology, the American Heart Association, and the National Heart, Lung, and Blood Institute recommend that patients on statin therapy who experience muscle soreness, tenderness, or pain with serum creatine kinase levels 3 to 10 times the upper limit of normal should have their creatine kinase level checked weekly. If the level is 3 to 10 times the upper limit of normal, statin therapy may be continued, but if it exceeds 10 times the upper limit, then statins and other potential offending agents (eg, niacin, fibrate) need to be discontinued.

Statins inhibit the synthesis of cholesterol by reducing the production of mevalonate, a precursor of both cholesterol and coenzyme Q10. Since both cholesterol and coenzyme Q10 are produced by the same pathway, it is not surprising that statins have been reported to reduce serum and muscle coenzyme Q10 levels.^9–14 However, one study did not report a significant reduction of coenzyme Q10 levels in muscle tissue in patients treated with simvastatin 20 mg for 6 months.²⁶

Nonetheless, researchers have hypothesized that a reduction in coenzyme Q10 levels in muscle tissue causes mitochondrial dysfunction, which could increase the risk of statininduced myopathy,^13–17 and some believe that treatment with coenzyme Q10 may reduce myalgic symptoms and allow patients to remain on statin therapy.^13,24

Researchers have investigated the potential of coenzyme Q10 supplementation to reduce or prevent statin-induced myopathy.^15–17 (More on this below.)

Interestingly, a randomized, placebo-controlled trial²⁷ found that 6 months of daily therapy with simvastatin (Zocor) 20 mg or pravastatin (Pravachol) 40 mg lowered systolic and diastolic blood pressure significantly in patients with no documented history of cardiovascular disease or diabetes. A possible mechanism of statin-induced blood pressure reduction is the up-regulation of endothelial nitric oxide synthetase, a potent vasodilator. Coenzyme Q10 levels were not assessed during this study. Whether coenzyme Q10 supplementation used to treat statin-induced myalgia enhances or inhibits the antihypertensive effects of statins is not yet known.

EVIDENCE OF EFFECTIVENESS IN HYPERTENSION

Rosenfeldt et al²⁸ performed a meta-analysis and found that some trials documented statistically significant reductions in diastolic or systolic blood pressure or both, while others reported negligible effects.^3,29 In one small trial,³⁰ blood pressures actually went up in patients taking coenzyme Q10. Coenzyme Q10 dosages and length of therapy varied from study to study in the meta-analysis. Only minor adverse effects such as gastrointestinal upset and headache were reported.

Yamagami et al³ randomly assigned 20 patients with hypertension and a low coenzyme Q10 level to receive 100 mg of coenzyme Q10 or placebo daily for 12 weeks. Patients continued their usual antihypertensive regimen during the study period. Blood pressures, coenzyme Q10 levels, and antihypertensive drugs used were comparable between the study groups.

After 12 weeks of therapy, the mean coenzyme Q10 level in the active-treatment group had more than doubled, from 0.704 to 1.597 μg/mL. This group also experienced a statistically significant drop in systolic blood pressure, from 167 mm Hg at baseline to 148 mm Hg at 12 weeks. In the placebo group, the systolic blood pressure was 168 mm Hg at baseline and 164 mm Hg at 12 weeks; the change was not statistically significant. Diastolic pressure was not significantly lower at 12 weeks than at baseline in either group.

The authors concluded that coenzyme Q10 supplementation brought a mild reduction in high blood pressure in patients who had low coenzyme Q10 serum levels.

Digiesi et al³¹ randomized 18 patients with essential hypertension to receive either coenzyme Q10 100 mg or placebo daily for 10 weeks. All antihypertensive therapy was discontinued at baseline. After the first 10 weeks, patients went through a 2-week washout period and then were switched to the opposite therapy for an additional 10 weeks. Mean baseline blood pressure values were 167 mm Hg systolic and 103 mm Hg diastolic.

Those taking the supplement had a statistically significant decrease in systolic and diastolic pressures (P < .001). The antihypertensive effect was noted in the 3rd or 4th week of active treatment and persisted for the duration of therapy. The effects dissipated 7 to 10 days after coenzyme Q10 was stopped.

Langsjoen et al⁵ evaluated the effects of adding coenzyme Q10 to the antihypertensive drug regimen of 109 patients who had a primary diagnosis of essential hypertension in a prospective observational study. Patients with hypertension as a secondary diagnosis and other cardiovascular diseases were excluded. Variable doses of coenzyme Q10 were given, adjusted according to clinical response and to achieve serum levels greater than 2.0 μg/mL. The average dose was 225 mg/day; the mean serum level attained was 3.02 μg/mL.

Over several months, patients taking the supplement had a reduction in mean systolic pressure from 159 mm Hg at baseline to 147 mm Hg (P < .001), and a reduction in mean diastolic pressure from 94 to 85 mm Hg (P < .001). Thirty-seven percent of patients were able to discontinue one antihypertensive drug, 11% discontinued two drugs, and 4% were able to stop taking three drugs. However, 46% remained on the same antihypertensive regimen, and 3% needed an additional drug.

Singh et al⁶ randomized 64 patients who had coronary artery disease and who had been on antihypertensive drugs for more than 1 year to receive either B-complex vitamins or coenzyme Q10 (hydrosoluble Q-Gel) 60 mg orally once daily for 8 weeks. Five patients were not available for follow-up; therefore, only 59 patients were evaluated. Fifty-five (93%) of the 59 patients were taking only one antihypertensive drug. Initial antihypertensive drug use was similar between study groups and was continued throughout the trial.

After 8 weeks of therapy, the coenzyme Q10 group had significantly lower systolic and diastolic blood pressure than the placebo group (P < .05 for both). There was also a statistically significant decrease in the dosage of antihypertensive drugs in the coenzyme Q10 group but not in the placebo group (P < .05), reflecting coenzyme Q10’s additive antihypertensive effect.

Burke et al⁷ randomized 41 men and 35 women with isolated systolic hypertension (systolic pressure 150–170 mm Hg, diastolic pressure < 90 mm Hg) to receive a twice-daily dose of 60 mg of emulsified coenzyme Q10 (hydrosoluble Q-Gel) with 150 IU of vitamin E or placebo containing vitamin E alone for 12 weeks. The study also included 5 men and 4 women with normal blood pressure, all of whom received coenzyme Q10. A total of 80 patients completed treatment. The primary goal of the study was to determine the efficacy of coenzyme Q10 in the treatment of isolated systolic hypertension in patients without comorbid conditions. Blood pressures were monitored twice a week during the trial, by the same nurse.

After 12 weeks of treatment, the mean reduction in systolic pressure in hypertensive patients on coenzyme Q10 was 17.8 ± 7.3 mm Hg. There were no significant changes in diastolic pressure in any study group with treatment. Patients with isolated systolic hypertension who were taking coenzyme Q10 had a statistically significant reduction in systolic pressure compared with baseline and placebo (P < .01 for both). Approximately 55% of patients on coenzyme Q10 achieved a reduction in systolic pressure of 4 mm Hg or greater, while 45% did not respond to therapy. The mean plasma coenzyme Q10 level of the treatment group increased from 0.47 ± 0.19 μg/mL to 2.69 ± 0.54 μg/mL after 12 weeks; however, the study did not have the statistical power to demonstrate a relationship between coenzyme Q10 levels and changes in blood pressure. Twenty-seven (34%) of the 80 patients were taking a statin while on coenzyme Q10 therapy.

STUDIES IN STATIN-INDUCED MYOPATHY

Thibault et al³² and Kim et al³³ reported that patients taking lovastatin (Mevacor) at dosages as high as 35 mg/kg/day to inhibit tumor growth achieved symptomatic relief of statin-induced musculoskeletal toxicity after coenzyme Q10 supplementation.

Caso et al¹⁵ performed a small pilot study in 32 patients to determine if coenzyme Q10 supplementation would improve myalgic symptoms in patients treated with statins. In this double-blind, randomized trial, patients received either coenzyme Q10 100 mg/day or vitamin E 400 IU/day for 30 days. The extent of muscle pain and its interference with daily activities were determined before and after therapy using the Brief Pain Inventory Questionnaire. The statins were atorvastatin (Lipitor) 10 mg or 20 mg, lovastatin 40 mg, pravastatin 40 mg, and simvastatin 10, 20, 40, and 80 mg. Five patients in the coenzyme Q10 group and four patients in the vitamin E group were taking nonsteroidal anti-inflammatory drugs before and during the trial. The intensity of muscle pain and its interference with daily activities were similar between study groups before the start of therapy.

After 30 days of treatment with coenzyme Q10, the pain intensity had decreased significantly from baseline (P < .001). In contrast, no change in pain intensity from baseline was noted in patients receiving vitamin E. The Pain Severity Score was significantly different between study groups, favoring the coenzyme Q10 group (P < .001). Sixteen of 18 patients on coenzyme Q10 reported a reduction in pain, while only 3 of 14 patients on vitamin E reported a similar response. Also, the interference of pain with daily activities significantly improved with coenzyme Q10 (P < .02), whereas vitamin E did not have a significant impact on this.

Young et al¹⁷ randomized 44 patients with prior statin-induced myalgia to receive increasing doses of simvastatin (10–40 mg/day) in combination with either coenzyme Q10 (Q-Gel) 200 mg/day or placebo. The primary goal was to determine if coenzyme Q10 supplementation would help improve statin tolerance in patients with a history of statininduced myalgia. Plasma coenzyme Q10 and lipid levels were measured at baseline and at the end of the study. The intensity of myalgia was assessed with a visual analogue scale.

At 12 weeks, the coenzyme Q10 plasma level was significantly higher in the treatment group than in the placebo group (P < .001). However, no differences were noted between groups in the number of patients who tolerated the 40-mg/day simvastatin dose (P = .34) or in the number of patients who remained on any simvastatin dose (P = .47). Additionally, myalgia scores did not differ between groups (P = .63). The authors acknowledged that there were only small increases in the myalgia pain scores reported in either group. Therefore, patients in the treatment group may not have experienced sufficiently severe muscle pain to have benefited from coenzyme Q10 supplementation.

IS COENZYME Q10 SAFE?

Studies have indicated that these supplements are well tolerated, with relatively few adverse effects or potential drug interactions.^1,2,34

The FDA does not routinely assess the purity or quality of over-the-counter coenzyme Q10 products.³⁵ However, the United States Pharmacopeia (USP) does test dietary supplements to make sure that they are not mislabeled and that they do not contain contaminants. ³⁶

A USP-verified dietary supplement should:

• Contain the exact ingredients listed on the label in the listed potency and amounts
• Not include harmful levels of certain contaminants such as lead, mercury, pesticides, or bacteria
• Appropriately disintegrate and release its contents into the body within a specified period of time
• Be produced using the FDA’s current Good Manufacturing Practices.³⁶

Side effects, contraindications, warnings

Coenzyme Q10 is a relatively safe dietary supplement. It is contraindicated in patients who are allergic to it or to any of its components.² Most clinical trials have not reported significant adverse effects that necessitated stopping therapy.³⁴ However, gastrointestinal effects such as abdominal discomfort, nausea, vomiting, diarrhea, and anorexia have occurred.^1,2,34 Allergic rash and headache have also been reported.^1,2,34 In addition, coenzyme Q10’s antiplatelet effect may increase the risk of bleeding. ^37,38 It undergoes biotransformation in the liver and is eliminated primarily via the biliary tract,³⁹ so it can accumulate in patients with hepatic impairment or biliary obstruction.

Interactions with drugs

Coenzyme Q10’s effects on platelet function may increase the risk of bleeding in patients taking antiplatelet drugs such as aspirin or clopidogrel (Plavix).^37,38 On the other hand, since it acts like vitamin K, it may counteract the anticoagulant effects of warfarin (Coumadin). ^1,2,40

Coenzyme Q10 may have an additive antihypertensive effect when given with antihypertensive drugs.⁴¹

Coenzyme Q10 may improve beta-cell function and enhance insulin sensitivity, which may reduce insulin requirements for diabetic patients.^42,43

SLOWLY ABSORBED

Coenzyme Q10 is absorbed slowly from the gastrointestinal tract, possibly because it has a high molecular weight and is not very watersoluble. ³⁹

One pharmacokinetic study found that after a single 100-mg oral dose of coenzyme Q10, the mean peak plasma levels of about 1 μg/mL occurred between 5 and 10 hours (mean 6.5 hours).⁴⁴ Coenzyme Q10 100 mg given orally three times daily produced a mean steadystate plasma level of 5.4 μg/mL; about 90% of this steady-state concentration was achieved after 4 days.³⁹

Some formulations have significantly better oral bioavailability and therefore produce higher plasma levels. Soft-gel capsules, especially those with vegetable oil or vitamin E, may have better absorption.⁴³

A pharmacokinetic study showed that the area under the curve of the plasma coenzyme Q10 concentration was more than twice as high with Q-Gel soft-gel capsules, a completely solubilized formulation, than with softgel capsules with an oil suspension, powderfilled hard-shell capsules, or regular tablets.⁴⁵ Another study reported that colloidal-Q10, a formulation contained in VESIsorb (a novel drug delivery system sold as CoQsource) had greater bioavailability than solubilized and oil-based preparations.⁴⁶ Commercially available solubilized preparations containing ubiquinol, a metabolized form of coenzyme Q10, have been shown to produce higher serum levels than solubilized products.⁴⁷

Of note: unless the manufacturer claims that its product is water-soluble, the USP does not evaluate its dissolution rate.⁴⁸ Therefore, USP-verified coenzyme Q10 products that are not water-soluble may have lower bioavailability than their solubilized counterparts.

Dry dosage forms of coenzyme Q10 (eg, tablets, capsules) may be more readily absorbed if taken with a fatty meal.⁴³

SLOWLY ELIMINATED

Taken orally, coenzyme Q10 has a low clearance rate, with an elimination half-life of about 34 hours.³⁹

After absorption, exogenous coenzyme Q10 is taken up by chylomicrons that transport it to the liver, where it is incorporated into verylow-density lipoproteins. It is then distributed to various organs, including the adrenal glands, spleen, kidneys, lungs, and heart. Coenzyme Q10 is eliminated primarily via the biliary tract. About 60% of an oral dose is eliminated in the feces during chronic oral administration.³⁹

TWICE-DAILY DOSING

A typical daily dose of coenzyme Q10 for treating hypertension is 120 to 200 mg, usually given orally in two divided doses.¹ For statininduced myopathy, 100 to 200 mg orally daily has been used.¹

Coenzyme Q10 is given in divided doses to enhance its absorption and to minimize gastrointestinal effects.^1,43 Taking it with a fatty meal may also increase its absorption.⁴³

Since solubilized forms of coenzyme Q10 and ubiquinol have significantly greater bioavailability than nonsolubilized forms, the therapeutic dose of these formulations may be lower.⁴⁷

MONITORING DURING TREATMENT

Without supplementation, the mean serum level of endogenous coenzyme Q10 has been reported to be 0.99 ± 0.30 mg/L (range 0.55– 1.87).¹⁸ Serum levels above 2 μg/mL have been associated with significant reductions in blood pressure.^5,7,28

The possible effects of coenzyme Q10 on blood pressure, blood glucose levels, serum creatine kinase levels, and myopathic symptoms should be kept in mind when monitoring patients who have hypertension,⁴¹ diabetes,^41,42 or statin-induced myalgia.^15,17 Coenzyme Q10’s possible potentiating effects on antiplatelet drugs and its inhibitory effect on warfarin should be kept in mind as well.

COST VARIES

Coenzyme Q10 is available in different dosage forms (eg, regular and rapid-release softgel capsules, regular and chewable tablets, chewable wafers, and liquid) from a variety of manufacturers. Products come in different strengths, typically ranging from 30 to 400 mg. USP-verified formulations are listed at www.usp.org/USPVerified/dietarySupplements/under “Verified Supplements.” Only USP-verified products that claim to be water-soluble meet USP dissolution requirements.

The cost varies, depending on the vendor. In general, dosage forms with greater bioavailability, such as Q-Gel and ubiquinol supplements, are more expensive. For example, a regimen of 60 mg twice daily of regular-release coenzyme Q capsules may cost approximately $20 per month, compared with $60 per month for the same supply of Q-Gel Ultra capsules. However, in some cases, supplements that produce higher serum levels may be more cost-effective.

CURRENT ROLE IN THERAPY

As an antihypertensive adjunct

Several small clinical trials have shown that coenzyme Q10 supplementation can lower blood pressure. The supplements were reported to be safe and well tolerated. Moreover, some patients with essential hypertension who were taking coenzyme Q10 were able to discontinue one or more antihypertensive drugs. A significant reduction in blood pressure with use of coenzyme Q10 would be expected to reduce the adverse consequences of hypertension in the same manner as conventional antihypertensive agents.

However, no large, double-blind, randomized study has evaluated the impact of coenzyme Q10 when taken with other antihypertensive drugs (eg, angiotensin-converting enzyme inhibitors, beta-blockers, diuretics) on specific clinical end points such as the incidence of stroke or death from a major cardiac event. Furthermore, its effects on cardiac function, exercise tolerance, and quality of life have not been determined.

The bottom line. In some cases, it seems reasonable to recommend this product as an adjunct to conventional antihypertensive therapy. Larger, well-designed clinical trials of coenzyme Q10’s antihypertensive effects on specific clinical end points such as the risk of stroke or myocardial infarction are needed to define its true therapeutic value.

As a treatment for statin-induced myalgia

Clinical evidence supporting coenzyme Q10’s use in the treatment of statin-induced myopathy is limited. Whether coenzyme Q10 is depleted from muscle tissue during statin therapy has not been confirmed. Supplementation helped reduce the severity of musculoskeletal effects of megadoses of lovastatin. However, clinical trials of coenzyme Q10 in the treatment of myalgia associated with antilipidemic statin doses did not consistently report significant improvement. Nevertheless, coenzyme Q10 has been shown to be relatively safe, with few adverse effects.

The bottom line. In some cases, coenzyme Q could be considered as a possible treatment for statin-induced myalgia, pending large-scale studies to determine if it is truly effective for this purpose.

Coenzyme Q10 supplements have been purported to be effective for treating a variety of disorders,^1,2 in particular hypertension and statin-induced myalgia.

Several studies^3–7 found that coenzyme Q10 supplementation significantly lowered blood pressure in hypertensive patients. Moreover, some trials have demonstrated that statin therapy reduces serum or muscle levels of coenzyme Q10,^8–14 prompting investigations to determine whether coenzyme Q10 deficiency is related to statin-induced muscle pain.^15–17

In this review, we discuss the efficacy and safety of coenzyme Q10 supplementation in patients with hypertension and those taking statins, and some of the caveats about using supplements that are not approved by the US Food and Drug Administration (FDA), as well as the bioavailability and quality of available formulations.

WHAT IS COENZYME Q10?

Coenzyme Q10, also known as coenzyme Q, ubidecarenone, and ubiquinone, is found in all human cells, with the highest concentrations in the heart, liver, kidney, and pancreas.^1,2 It is a potent antioxidant, a membrane stabilizer, and an integral cofactor in the mitochondrial respiratory chain, helping to generate adenosine triphosphate, the major cellular energy source.^1,2,18 It may also regulate genes associated with cell metabolism.¹⁹

RATIONALE FOR SUPPLEMENTATION

Coenzyme Q10 supplementation has been used, recommended, or studied in heart failure, hypertension, parkinsonism, mitochondrial encephalomyopathies, and other ailments.

In hypertension

Depending on the class, various antihypertensive drugs can have adverse effects such as depression, cough, and cardiac and renal dysfunction. ^20,21 Furthermore, many patients need to take more than one drug to control their blood pressure, increasing their risk of side effects. Some researchers believe coenzyme Q10 supplementation may reduce the need to take multiple antihypertensive drugs.⁵

Coenzyme Q10 appears to lower blood pressure. The exact mechanism is not known, but one theory is that it reduces peripheral resistance by preserving nitric oxide.²¹ Nitric oxide relaxes peripheral arteries, lowering blood pressure. In some forms of hypertension, superoxide radicals that inactivate nitric oxide are overproduced; coenzyme Q10, with its antioxidant effects, may prevent the inactivation of nitric oxide by these free radicals. Alternatively, coenzyme Q10 may boost the production of the prostaglandin prostacyclin (PGI₂) a potent vasodilator and inhibitor of platelet aggregation, or it may enhance the sensitivity of arterial smooth muscle to PGI₂, or both.^1,22

In patients taking statins

Hydroxymethylglutaryl coenzyme A reductase inhibitors (statins), first-line agents for lowering cholesterol levels to prevent cardiovascular disease, are some of the most commonly prescribed medications.^23,24 However, statin therapy carries a risk of myopathy, which can range from muscle aches to rhabdomyolysis. ^23,24

In a clinical advisory,²⁵ the American College of Cardiology, the American Heart Association, and the National Heart, Lung, and Blood Institute recommend that patients on statin therapy who experience muscle soreness, tenderness, or pain with serum creatine kinase levels 3 to 10 times the upper limit of normal should have their creatine kinase level checked weekly. If the level is 3 to 10 times the upper limit of normal, statin therapy may be continued, but if it exceeds 10 times the upper limit, then statins and other potential offending agents (eg, niacin, fibrate) need to be discontinued.

Statins inhibit the synthesis of cholesterol by reducing the production of mevalonate, a precursor of both cholesterol and coenzyme Q10. Since both cholesterol and coenzyme Q10 are produced by the same pathway, it is not surprising that statins have been reported to reduce serum and muscle coenzyme Q10 levels.^9–14 However, one study did not report a significant reduction of coenzyme Q10 levels in muscle tissue in patients treated with simvastatin 20 mg for 6 months.²⁶

Nonetheless, researchers have hypothesized that a reduction in coenzyme Q10 levels in muscle tissue causes mitochondrial dysfunction, which could increase the risk of statininduced myopathy,^13–17 and some believe that treatment with coenzyme Q10 may reduce myalgic symptoms and allow patients to remain on statin therapy.^13,24

Researchers have investigated the potential of coenzyme Q10 supplementation to reduce or prevent statin-induced myopathy.^15–17 (More on this below.)

Interestingly, a randomized, placebo-controlled trial²⁷ found that 6 months of daily therapy with simvastatin (Zocor) 20 mg or pravastatin (Pravachol) 40 mg lowered systolic and diastolic blood pressure significantly in patients with no documented history of cardiovascular disease or diabetes. A possible mechanism of statin-induced blood pressure reduction is the up-regulation of endothelial nitric oxide synthetase, a potent vasodilator. Coenzyme Q10 levels were not assessed during this study. Whether coenzyme Q10 supplementation used to treat statin-induced myalgia enhances or inhibits the antihypertensive effects of statins is not yet known.

EVIDENCE OF EFFECTIVENESS IN HYPERTENSION

Rosenfeldt et al²⁸ performed a meta-analysis and found that some trials documented statistically significant reductions in diastolic or systolic blood pressure or both, while others reported negligible effects.^3,29 In one small trial,³⁰ blood pressures actually went up in patients taking coenzyme Q10. Coenzyme Q10 dosages and length of therapy varied from study to study in the meta-analysis. Only minor adverse effects such as gastrointestinal upset and headache were reported.

Yamagami et al³ randomly assigned 20 patients with hypertension and a low coenzyme Q10 level to receive 100 mg of coenzyme Q10 or placebo daily for 12 weeks. Patients continued their usual antihypertensive regimen during the study period. Blood pressures, coenzyme Q10 levels, and antihypertensive drugs used were comparable between the study groups.

After 12 weeks of therapy, the mean coenzyme Q10 level in the active-treatment group had more than doubled, from 0.704 to 1.597 μg/mL. This group also experienced a statistically significant drop in systolic blood pressure, from 167 mm Hg at baseline to 148 mm Hg at 12 weeks. In the placebo group, the systolic blood pressure was 168 mm Hg at baseline and 164 mm Hg at 12 weeks; the change was not statistically significant. Diastolic pressure was not significantly lower at 12 weeks than at baseline in either group.

The authors concluded that coenzyme Q10 supplementation brought a mild reduction in high blood pressure in patients who had low coenzyme Q10 serum levels.

Digiesi et al³¹ randomized 18 patients with essential hypertension to receive either coenzyme Q10 100 mg or placebo daily for 10 weeks. All antihypertensive therapy was discontinued at baseline. After the first 10 weeks, patients went through a 2-week washout period and then were switched to the opposite therapy for an additional 10 weeks. Mean baseline blood pressure values were 167 mm Hg systolic and 103 mm Hg diastolic.

Those taking the supplement had a statistically significant decrease in systolic and diastolic pressures (P < .001). The antihypertensive effect was noted in the 3rd or 4th week of active treatment and persisted for the duration of therapy. The effects dissipated 7 to 10 days after coenzyme Q10 was stopped.

Langsjoen et al⁵ evaluated the effects of adding coenzyme Q10 to the antihypertensive drug regimen of 109 patients who had a primary diagnosis of essential hypertension in a prospective observational study. Patients with hypertension as a secondary diagnosis and other cardiovascular diseases were excluded. Variable doses of coenzyme Q10 were given, adjusted according to clinical response and to achieve serum levels greater than 2.0 μg/mL. The average dose was 225 mg/day; the mean serum level attained was 3.02 μg/mL.

Over several months, patients taking the supplement had a reduction in mean systolic pressure from 159 mm Hg at baseline to 147 mm Hg (P < .001), and a reduction in mean diastolic pressure from 94 to 85 mm Hg (P < .001). Thirty-seven percent of patients were able to discontinue one antihypertensive drug, 11% discontinued two drugs, and 4% were able to stop taking three drugs. However, 46% remained on the same antihypertensive regimen, and 3% needed an additional drug.

Singh et al⁶ randomized 64 patients who had coronary artery disease and who had been on antihypertensive drugs for more than 1 year to receive either B-complex vitamins or coenzyme Q10 (hydrosoluble Q-Gel) 60 mg orally once daily for 8 weeks. Five patients were not available for follow-up; therefore, only 59 patients were evaluated. Fifty-five (93%) of the 59 patients were taking only one antihypertensive drug. Initial antihypertensive drug use was similar between study groups and was continued throughout the trial.

After 8 weeks of therapy, the coenzyme Q10 group had significantly lower systolic and diastolic blood pressure than the placebo group (P < .05 for both). There was also a statistically significant decrease in the dosage of antihypertensive drugs in the coenzyme Q10 group but not in the placebo group (P < .05), reflecting coenzyme Q10’s additive antihypertensive effect.

Burke et al⁷ randomized 41 men and 35 women with isolated systolic hypertension (systolic pressure 150–170 mm Hg, diastolic pressure < 90 mm Hg) to receive a twice-daily dose of 60 mg of emulsified coenzyme Q10 (hydrosoluble Q-Gel) with 150 IU of vitamin E or placebo containing vitamin E alone for 12 weeks. The study also included 5 men and 4 women with normal blood pressure, all of whom received coenzyme Q10. A total of 80 patients completed treatment. The primary goal of the study was to determine the efficacy of coenzyme Q10 in the treatment of isolated systolic hypertension in patients without comorbid conditions. Blood pressures were monitored twice a week during the trial, by the same nurse.

After 12 weeks of treatment, the mean reduction in systolic pressure in hypertensive patients on coenzyme Q10 was 17.8 ± 7.3 mm Hg. There were no significant changes in diastolic pressure in any study group with treatment. Patients with isolated systolic hypertension who were taking coenzyme Q10 had a statistically significant reduction in systolic pressure compared with baseline and placebo (P < .01 for both). Approximately 55% of patients on coenzyme Q10 achieved a reduction in systolic pressure of 4 mm Hg or greater, while 45% did not respond to therapy. The mean plasma coenzyme Q10 level of the treatment group increased from 0.47 ± 0.19 μg/mL to 2.69 ± 0.54 μg/mL after 12 weeks; however, the study did not have the statistical power to demonstrate a relationship between coenzyme Q10 levels and changes in blood pressure. Twenty-seven (34%) of the 80 patients were taking a statin while on coenzyme Q10 therapy.

STUDIES IN STATIN-INDUCED MYOPATHY

Thibault et al³² and Kim et al³³ reported that patients taking lovastatin (Mevacor) at dosages as high as 35 mg/kg/day to inhibit tumor growth achieved symptomatic relief of statin-induced musculoskeletal toxicity after coenzyme Q10 supplementation.

Caso et al¹⁵ performed a small pilot study in 32 patients to determine if coenzyme Q10 supplementation would improve myalgic symptoms in patients treated with statins. In this double-blind, randomized trial, patients received either coenzyme Q10 100 mg/day or vitamin E 400 IU/day for 30 days. The extent of muscle pain and its interference with daily activities were determined before and after therapy using the Brief Pain Inventory Questionnaire. The statins were atorvastatin (Lipitor) 10 mg or 20 mg, lovastatin 40 mg, pravastatin 40 mg, and simvastatin 10, 20, 40, and 80 mg. Five patients in the coenzyme Q10 group and four patients in the vitamin E group were taking nonsteroidal anti-inflammatory drugs before and during the trial. The intensity of muscle pain and its interference with daily activities were similar between study groups before the start of therapy.

After 30 days of treatment with coenzyme Q10, the pain intensity had decreased significantly from baseline (P < .001). In contrast, no change in pain intensity from baseline was noted in patients receiving vitamin E. The Pain Severity Score was significantly different between study groups, favoring the coenzyme Q10 group (P < .001). Sixteen of 18 patients on coenzyme Q10 reported a reduction in pain, while only 3 of 14 patients on vitamin E reported a similar response. Also, the interference of pain with daily activities significantly improved with coenzyme Q10 (P < .02), whereas vitamin E did not have a significant impact on this.

Young et al¹⁷ randomized 44 patients with prior statin-induced myalgia to receive increasing doses of simvastatin (10–40 mg/day) in combination with either coenzyme Q10 (Q-Gel) 200 mg/day or placebo. The primary goal was to determine if coenzyme Q10 supplementation would help improve statin tolerance in patients with a history of statininduced myalgia. Plasma coenzyme Q10 and lipid levels were measured at baseline and at the end of the study. The intensity of myalgia was assessed with a visual analogue scale.

At 12 weeks, the coenzyme Q10 plasma level was significantly higher in the treatment group than in the placebo group (P < .001). However, no differences were noted between groups in the number of patients who tolerated the 40-mg/day simvastatin dose (P = .34) or in the number of patients who remained on any simvastatin dose (P = .47). Additionally, myalgia scores did not differ between groups (P = .63). The authors acknowledged that there were only small increases in the myalgia pain scores reported in either group. Therefore, patients in the treatment group may not have experienced sufficiently severe muscle pain to have benefited from coenzyme Q10 supplementation.

IS COENZYME Q10 SAFE?

Studies have indicated that these supplements are well tolerated, with relatively few adverse effects or potential drug interactions.^1,2,34

The FDA does not routinely assess the purity or quality of over-the-counter coenzyme Q10 products.³⁵ However, the United States Pharmacopeia (USP) does test dietary supplements to make sure that they are not mislabeled and that they do not contain contaminants. ³⁶

A USP-verified dietary supplement should:

• Contain the exact ingredients listed on the label in the listed potency and amounts
• Not include harmful levels of certain contaminants such as lead, mercury, pesticides, or bacteria
• Appropriately disintegrate and release its contents into the body within a specified period of time
• Be produced using the FDA’s current Good Manufacturing Practices.³⁶

Side effects, contraindications, warnings

Coenzyme Q10 is a relatively safe dietary supplement. It is contraindicated in patients who are allergic to it or to any of its components.² Most clinical trials have not reported significant adverse effects that necessitated stopping therapy.³⁴ However, gastrointestinal effects such as abdominal discomfort, nausea, vomiting, diarrhea, and anorexia have occurred.^1,2,34 Allergic rash and headache have also been reported.^1,2,34 In addition, coenzyme Q10’s antiplatelet effect may increase the risk of bleeding. ^37,38 It undergoes biotransformation in the liver and is eliminated primarily via the biliary tract,³⁹ so it can accumulate in patients with hepatic impairment or biliary obstruction.

Interactions with drugs

Coenzyme Q10’s effects on platelet function may increase the risk of bleeding in patients taking antiplatelet drugs such as aspirin or clopidogrel (Plavix).^37,38 On the other hand, since it acts like vitamin K, it may counteract the anticoagulant effects of warfarin (Coumadin). ^1,2,40

Coenzyme Q10 may have an additive antihypertensive effect when given with antihypertensive drugs.⁴¹

Coenzyme Q10 may improve beta-cell function and enhance insulin sensitivity, which may reduce insulin requirements for diabetic patients.^42,43

SLOWLY ABSORBED

Coenzyme Q10 is absorbed slowly from the gastrointestinal tract, possibly because it has a high molecular weight and is not very watersoluble. ³⁹

One pharmacokinetic study found that after a single 100-mg oral dose of coenzyme Q10, the mean peak plasma levels of about 1 μg/mL occurred between 5 and 10 hours (mean 6.5 hours).⁴⁴ Coenzyme Q10 100 mg given orally three times daily produced a mean steadystate plasma level of 5.4 μg/mL; about 90% of this steady-state concentration was achieved after 4 days.³⁹

Some formulations have significantly better oral bioavailability and therefore produce higher plasma levels. Soft-gel capsules, especially those with vegetable oil or vitamin E, may have better absorption.⁴³

A pharmacokinetic study showed that the area under the curve of the plasma coenzyme Q10 concentration was more than twice as high with Q-Gel soft-gel capsules, a completely solubilized formulation, than with softgel capsules with an oil suspension, powderfilled hard-shell capsules, or regular tablets.⁴⁵ Another study reported that colloidal-Q10, a formulation contained in VESIsorb (a novel drug delivery system sold as CoQsource) had greater bioavailability than solubilized and oil-based preparations.⁴⁶ Commercially available solubilized preparations containing ubiquinol, a metabolized form of coenzyme Q10, have been shown to produce higher serum levels than solubilized products.⁴⁷

Of note: unless the manufacturer claims that its product is water-soluble, the USP does not evaluate its dissolution rate.⁴⁸ Therefore, USP-verified coenzyme Q10 products that are not water-soluble may have lower bioavailability than their solubilized counterparts.

Dry dosage forms of coenzyme Q10 (eg, tablets, capsules) may be more readily absorbed if taken with a fatty meal.⁴³

SLOWLY ELIMINATED

Taken orally, coenzyme Q10 has a low clearance rate, with an elimination half-life of about 34 hours.³⁹

After absorption, exogenous coenzyme Q10 is taken up by chylomicrons that transport it to the liver, where it is incorporated into verylow-density lipoproteins. It is then distributed to various organs, including the adrenal glands, spleen, kidneys, lungs, and heart. Coenzyme Q10 is eliminated primarily via the biliary tract. About 60% of an oral dose is eliminated in the feces during chronic oral administration.³⁹

TWICE-DAILY DOSING

A typical daily dose of coenzyme Q10 for treating hypertension is 120 to 200 mg, usually given orally in two divided doses.¹ For statininduced myopathy, 100 to 200 mg orally daily has been used.¹

Coenzyme Q10 is given in divided doses to enhance its absorption and to minimize gastrointestinal effects.^1,43 Taking it with a fatty meal may also increase its absorption.⁴³

Since solubilized forms of coenzyme Q10 and ubiquinol have significantly greater bioavailability than nonsolubilized forms, the therapeutic dose of these formulations may be lower.⁴⁷

MONITORING DURING TREATMENT

Without supplementation, the mean serum level of endogenous coenzyme Q10 has been reported to be 0.99 ± 0.30 mg/L (range 0.55– 1.87).¹⁸ Serum levels above 2 μg/mL have been associated with significant reductions in blood pressure.^5,7,28

The possible effects of coenzyme Q10 on blood pressure, blood glucose levels, serum creatine kinase levels, and myopathic symptoms should be kept in mind when monitoring patients who have hypertension,⁴¹ diabetes,^41,42 or statin-induced myalgia.^15,17 Coenzyme Q10’s possible potentiating effects on antiplatelet drugs and its inhibitory effect on warfarin should be kept in mind as well.

COST VARIES

Coenzyme Q10 is available in different dosage forms (eg, regular and rapid-release softgel capsules, regular and chewable tablets, chewable wafers, and liquid) from a variety of manufacturers. Products come in different strengths, typically ranging from 30 to 400 mg. USP-verified formulations are listed at www.usp.org/USPVerified/dietarySupplements/under “Verified Supplements.” Only USP-verified products that claim to be water-soluble meet USP dissolution requirements.

The cost varies, depending on the vendor. In general, dosage forms with greater bioavailability, such as Q-Gel and ubiquinol supplements, are more expensive. For example, a regimen of 60 mg twice daily of regular-release coenzyme Q capsules may cost approximately $20 per month, compared with $60 per month for the same supply of Q-Gel Ultra capsules. However, in some cases, supplements that produce higher serum levels may be more cost-effective.

CURRENT ROLE IN THERAPY

As an antihypertensive adjunct

Several small clinical trials have shown that coenzyme Q10 supplementation can lower blood pressure. The supplements were reported to be safe and well tolerated. Moreover, some patients with essential hypertension who were taking coenzyme Q10 were able to discontinue one or more antihypertensive drugs. A significant reduction in blood pressure with use of coenzyme Q10 would be expected to reduce the adverse consequences of hypertension in the same manner as conventional antihypertensive agents.

However, no large, double-blind, randomized study has evaluated the impact of coenzyme Q10 when taken with other antihypertensive drugs (eg, angiotensin-converting enzyme inhibitors, beta-blockers, diuretics) on specific clinical end points such as the incidence of stroke or death from a major cardiac event. Furthermore, its effects on cardiac function, exercise tolerance, and quality of life have not been determined.

The bottom line. In some cases, it seems reasonable to recommend this product as an adjunct to conventional antihypertensive therapy. Larger, well-designed clinical trials of coenzyme Q10’s antihypertensive effects on specific clinical end points such as the risk of stroke or myocardial infarction are needed to define its true therapeutic value.

As a treatment for statin-induced myalgia

Clinical evidence supporting coenzyme Q10’s use in the treatment of statin-induced myopathy is limited. Whether coenzyme Q10 is depleted from muscle tissue during statin therapy has not been confirmed. Supplementation helped reduce the severity of musculoskeletal effects of megadoses of lovastatin. However, clinical trials of coenzyme Q10 in the treatment of myalgia associated with antilipidemic statin doses did not consistently report significant improvement. Nevertheless, coenzyme Q10 has been shown to be relatively safe, with few adverse effects.

The bottom line. In some cases, coenzyme Q could be considered as a possible treatment for statin-induced myalgia, pending large-scale studies to determine if it is truly effective for this purpose.

In reply, based on his experience, Dr. Tom Abelson defends EMRs, predicting that their current weaknesses will be overcome as technology improves, and the faster we embrace this technologic advance, the faster fixes for initial limitations will be developed. We are, he says, just learning to swim.

The EMR is a tool, but a tool performs at the skill level of the user. The EMR is more powerful than the paper record it replaces, offering the promise of being searchable, interactive, and able to prompt us to perform in predefined ways, and also linking us at the point of care with reference materials. But the information contained in the EMR can be no better than what we enter. An EMR cannot supplant our need to think and act as physicians defending our patients’ best interests.

Our skill in using the EMR is evolving. Thus far, cut-and-paste and other electronic shortcuts are rampant and are a detriment to quality care, but these are examples of misuse and are not an intrinsic fault of the tool. These physician behaviors can be curtailed.

The EMR cannot be read like a book. Events, consultations, and nursing interventions do not readily unfold in chronologic order. Suggestions of consultants can be missed, and perhaps due to limited typing skills, clinical reasoning is not fully explained (was it always clearly explained on paper?). The notes, however, are legible.

We must not be enticed to let EMRs overly influence our billing practices. Rather, the EMR should be a tool to improve the accuracy of the record of the patient encounter.

The EMR can come between the doctor and patient, but it need not. We need to be a bit more attentive to the patient, push back intermittently from the keyboard, and make eye contact. We need to engage the patient with his or her EMR on screen—show some trended lab results or radiographic images and, when they leave, present them with a typed set of legible instructions and their drug list (noting that all this information, and more, can be available to the next physician that they see, by cyberlink or via fax).

For those of you adopting an EMR system, I suggest you make sure you get adequate, continued access to on-site support from your vendor. The tool must be trained to swim in your pool.

In reply, based on his experience, Dr. Tom Abelson defends EMRs, predicting that their current weaknesses will be overcome as technology improves, and the faster we embrace this technologic advance, the faster fixes for initial limitations will be developed. We are, he says, just learning to swim.

The EMR is a tool, but a tool performs at the skill level of the user. The EMR is more powerful than the paper record it replaces, offering the promise of being searchable, interactive, and able to prompt us to perform in predefined ways, and also linking us at the point of care with reference materials. But the information contained in the EMR can be no better than what we enter. An EMR cannot supplant our need to think and act as physicians defending our patients’ best interests.

Our skill in using the EMR is evolving. Thus far, cut-and-paste and other electronic shortcuts are rampant and are a detriment to quality care, but these are examples of misuse and are not an intrinsic fault of the tool. These physician behaviors can be curtailed.

The EMR cannot be read like a book. Events, consultations, and nursing interventions do not readily unfold in chronologic order. Suggestions of consultants can be missed, and perhaps due to limited typing skills, clinical reasoning is not fully explained (was it always clearly explained on paper?). The notes, however, are legible.

We must not be enticed to let EMRs overly influence our billing practices. Rather, the EMR should be a tool to improve the accuracy of the record of the patient encounter.

The EMR can come between the doctor and patient, but it need not. We need to be a bit more attentive to the patient, push back intermittently from the keyboard, and make eye contact. We need to engage the patient with his or her EMR on screen—show some trended lab results or radiographic images and, when they leave, present them with a typed set of legible instructions and their drug list (noting that all this information, and more, can be available to the next physician that they see, by cyberlink or via fax).

For those of you adopting an EMR system, I suggest you make sure you get adequate, continued access to on-site support from your vendor. The tool must be trained to swim in your pool.

In reply, based on his experience, Dr. Tom Abelson defends EMRs, predicting that their current weaknesses will be overcome as technology improves, and the faster we embrace this technologic advance, the faster fixes for initial limitations will be developed. We are, he says, just learning to swim.

The EMR is a tool, but a tool performs at the skill level of the user. The EMR is more powerful than the paper record it replaces, offering the promise of being searchable, interactive, and able to prompt us to perform in predefined ways, and also linking us at the point of care with reference materials. But the information contained in the EMR can be no better than what we enter. An EMR cannot supplant our need to think and act as physicians defending our patients’ best interests.

Our skill in using the EMR is evolving. Thus far, cut-and-paste and other electronic shortcuts are rampant and are a detriment to quality care, but these are examples of misuse and are not an intrinsic fault of the tool. These physician behaviors can be curtailed.

The EMR cannot be read like a book. Events, consultations, and nursing interventions do not readily unfold in chronologic order. Suggestions of consultants can be missed, and perhaps due to limited typing skills, clinical reasoning is not fully explained (was it always clearly explained on paper?). The notes, however, are legible.

We must not be enticed to let EMRs overly influence our billing practices. Rather, the EMR should be a tool to improve the accuracy of the record of the patient encounter.

The EMR can come between the doctor and patient, but it need not. We need to be a bit more attentive to the patient, push back intermittently from the keyboard, and make eye contact. We need to engage the patient with his or her EMR on screen—show some trended lab results or radiographic images and, when they leave, present them with a typed set of legible instructions and their drug list (noting that all this information, and more, can be available to the next physician that they see, by cyberlink or via fax).

For those of you adopting an EMR system, I suggest you make sure you get adequate, continued access to on-site support from your vendor. The tool must be trained to swim in your pool.

While Dr. J. Timothy hanlon raises compelling issues about electronic medical records (EMRs),¹ I think that his goslow approach can lead to lost opportunities. The push toward implementing EMR systems does not amount to a dangerous dive into a shallow pool. Rather, we should be optimistic that we are just learning to swim.

For a contrasting view

Addressing these concerns during these early years of the EMR is constructive and necessary. But his commentary may leave physicians wondering what to do. Should the EMR be scrapped until it is fully developed outside the clinical realm? Is that goal even attainable? Are physicians who use EMR systems putting patient care and information security at risk? I believe there is a more positive way to look at each of the issues.

No new technology comes into the world 100% formed and vetted. The nature of progress is evolution based on experience, as unforeseen problems are corrected. Skepticism and vigilance are warranted, but so is optimism.

CONNECTIVITY WILL IMPROVE

Dr. Hanlon notes that many EMR systems are available and that, at this point, they do not communicate with one another. That is often true. But Google, Microsoft, and others are working on the issues of connectivity and “portability” of the EMR. It is reasonable to expect that eventually there will be winners and losers, just as when VHS won out over Beta in the early days of video recording. More efficient sharing of information will eventually be possible. It would be counterproductive to legislate a single EMR system nationwide before a number of EMRs can be fully tried and tested in the trenches of patient care.

In the meantime, it is no harder—in fact, it is easier than ever—for one physician to send information to another, either by printing it out and mailing or faxing it or by e-mailing it. Furthermore, that information is much more legible than the handwritten records we continue to receive from physicians who do not use EMRs.

Therefore, while one can criticize the current lack of complete intersystem communication, this is only a temporary limitation, and developing complete interconnectivity of EMR systems is a key goal.

STAYING VIGILANT ABOUT SECURITY

The security of EMRs has always been a concern. However, improvements in security have prevented a large-scale privacy breach since an incident in 2006 in which a laptop computer containing information on 26.5 million people was stolen from the home of a Veterans Administration employee.² For instance, Cleveland Clinic recently encrypted all of its laptop computers containing patient data, to protect patient information should a laptop be lost or stolen. This is only one of many security innovations that are being implemented. While we must remain highly vigilant and continue to improve security, we must remember that the paper chart is not immune to privacy breaches either, and when paper charts were stolen, the medical record was irretrievably lost and was not reproducible. This is not the case with the EMR.

QUALITY OF CARE IS PARAMOUNT

As Dr. Hanlon accurately notes, evidence that the EMR improves the quality of care is mixed so far. He is concerned that most of the studies showing improved outcomes came from “benchmark” institutions, and that the results may not be broadly applicable. Such pessimism is unwarranted, given that the EMR is in its relative infancy and the motivation to improve quality of care is paramount, especially in this era of health care reform. While benchmark institutions are in an ideal position to do the studies on quality, there is no reason to assume that the results will not be applicable to other institutions as well.

EDUCATION: AN AREA FOR INNOVATION

Dr. Hanlon notes that research on EMRs for medical education is in its infancy. But infants grow rapidly. While it may be true that students might have to learn to use different EMR systems at different institutions, these students have grown up with rapidly changing computer systems and can learn and adapt at a remarkable rate. Therefore, education is a wonderful area for innovation and research on the EMR. It is not a reason to fear the EMR or the present diversity of EMR systems.

ACCURACY CAN BE IMPROVED

Dr. Hanlon is correct that the problem of cutting and pasting of previous notes, potentially propagating an initial error (so-called high-risk copying³) is profound within the EMR. But I prefer to look at this as an area for innovation— such as nonerasable tags to identify copied material.

While errors in medication lists are possible, especially if practitioners use cut-and-paste methods and thus perpetuate a previous error, systems and workflows are being developed to overcome such problems. Some of these include special alerts when certain high-risk drugs are ordered, drop-down menus with drug dosing included, and links to databases that allow quick access to information on drug interactions.

And again, medication errors are not unique to the EMR. They also occur in paper charts as a result of photocopying, illegible handwriting, and transcription errors.

Compared with the paper chart, the EMR is more legible, and the ability to instantaneously transfer unchanged important and valid information potentially enhances the completeness and logic of a given note and provides the physician more time to spend evaluating (and looking at) the patient. So, rather than focusing on the negatives of the current problem of cutting and pasting, I prefer to focus on how to improve it. That is, how can we make the information in the EMR more accurate, catch errors, and then make the latest information easily accessible to users?

STAYING FOCUSED ON THE PATIENT, EVEN WITH A COMPUTER IN THE ROOM

A major complaint by patients and caregivers is that using an EMR makes the physician focus on a computer screen rather than looking at the patient. This concern is valid, but I think we can learn to stay focused on the patient, even with a computer in the examination room, and still take advantage of everything technology has to offer.

This issue will disappear in less than one generation. Young people are remarkably able to multitask while typing. They are able to talk with their patients while typing and to look them in the eyes. And typing letter by letter will become obsolete as soon as voice-recognition software and ways to edit its output accurately are perfected. Many of us at Cleveland Clinic use a combination of templates, typing, and voice-recognition dictation, and find this to be effective.

When we tell our grandchildren that we used to type each individual letter on a page, they will be as amazed as we are to hear that cars used to be started with an external crank.

DOCTOR-DOCTOR COMMUNICATION IS ENHANCED

I agree that template notes written by physicians who cannot type very well can lack the substance and color found in a well-reported medical history and examination. But voice-recognition transcription can help flesh out key parts of the history, differential diagnosis, and management plan. Further, the note can be produced on the spot, the patient can check the note for accuracy, and the conclusions can be shared instantaneously with all involved caregivers. Doctor-doctor communication is thus enhanced.

EVERY REASON TO MOVE FORWARD

Dr. Hanlon is also concerned about EMRs and the potential for “billing creep” and outright fraud. But fraud is as old as billing. What is required is continued vigilance and system controls, which actually might be more effective in an EMR system than in a paper billing system. Integrity will be neither enhanced nor diminished by digitization, unfortunately.

In summary, while Dr. Hanlon sees reason to slow down the move to EMRs, I see every reason to move forward. The problems he describes are part of the growing pains of any new technology. He is right that we cannot move blindly, ignoring the challenges of this technology. But slowing down will only delay its benefits.

While Dr. J. Timothy hanlon raises compelling issues about electronic medical records (EMRs),¹ I think that his goslow approach can lead to lost opportunities. The push toward implementing EMR systems does not amount to a dangerous dive into a shallow pool. Rather, we should be optimistic that we are just learning to swim.

For a contrasting view

Addressing these concerns during these early years of the EMR is constructive and necessary. But his commentary may leave physicians wondering what to do. Should the EMR be scrapped until it is fully developed outside the clinical realm? Is that goal even attainable? Are physicians who use EMR systems putting patient care and information security at risk? I believe there is a more positive way to look at each of the issues.

No new technology comes into the world 100% formed and vetted. The nature of progress is evolution based on experience, as unforeseen problems are corrected. Skepticism and vigilance are warranted, but so is optimism.

CONNECTIVITY WILL IMPROVE

Dr. Hanlon notes that many EMR systems are available and that, at this point, they do not communicate with one another. That is often true. But Google, Microsoft, and others are working on the issues of connectivity and “portability” of the EMR. It is reasonable to expect that eventually there will be winners and losers, just as when VHS won out over Beta in the early days of video recording. More efficient sharing of information will eventually be possible. It would be counterproductive to legislate a single EMR system nationwide before a number of EMRs can be fully tried and tested in the trenches of patient care.

In the meantime, it is no harder—in fact, it is easier than ever—for one physician to send information to another, either by printing it out and mailing or faxing it or by e-mailing it. Furthermore, that information is much more legible than the handwritten records we continue to receive from physicians who do not use EMRs.

Therefore, while one can criticize the current lack of complete intersystem communication, this is only a temporary limitation, and developing complete interconnectivity of EMR systems is a key goal.

STAYING VIGILANT ABOUT SECURITY

The security of EMRs has always been a concern. However, improvements in security have prevented a large-scale privacy breach since an incident in 2006 in which a laptop computer containing information on 26.5 million people was stolen from the home of a Veterans Administration employee.² For instance, Cleveland Clinic recently encrypted all of its laptop computers containing patient data, to protect patient information should a laptop be lost or stolen. This is only one of many security innovations that are being implemented. While we must remain highly vigilant and continue to improve security, we must remember that the paper chart is not immune to privacy breaches either, and when paper charts were stolen, the medical record was irretrievably lost and was not reproducible. This is not the case with the EMR.

QUALITY OF CARE IS PARAMOUNT

As Dr. Hanlon accurately notes, evidence that the EMR improves the quality of care is mixed so far. He is concerned that most of the studies showing improved outcomes came from “benchmark” institutions, and that the results may not be broadly applicable. Such pessimism is unwarranted, given that the EMR is in its relative infancy and the motivation to improve quality of care is paramount, especially in this era of health care reform. While benchmark institutions are in an ideal position to do the studies on quality, there is no reason to assume that the results will not be applicable to other institutions as well.

EDUCATION: AN AREA FOR INNOVATION

Dr. Hanlon notes that research on EMRs for medical education is in its infancy. But infants grow rapidly. While it may be true that students might have to learn to use different EMR systems at different institutions, these students have grown up with rapidly changing computer systems and can learn and adapt at a remarkable rate. Therefore, education is a wonderful area for innovation and research on the EMR. It is not a reason to fear the EMR or the present diversity of EMR systems.

ACCURACY CAN BE IMPROVED

Dr. Hanlon is correct that the problem of cutting and pasting of previous notes, potentially propagating an initial error (so-called high-risk copying³) is profound within the EMR. But I prefer to look at this as an area for innovation— such as nonerasable tags to identify copied material.

While errors in medication lists are possible, especially if practitioners use cut-and-paste methods and thus perpetuate a previous error, systems and workflows are being developed to overcome such problems. Some of these include special alerts when certain high-risk drugs are ordered, drop-down menus with drug dosing included, and links to databases that allow quick access to information on drug interactions.

And again, medication errors are not unique to the EMR. They also occur in paper charts as a result of photocopying, illegible handwriting, and transcription errors.

Compared with the paper chart, the EMR is more legible, and the ability to instantaneously transfer unchanged important and valid information potentially enhances the completeness and logic of a given note and provides the physician more time to spend evaluating (and looking at) the patient. So, rather than focusing on the negatives of the current problem of cutting and pasting, I prefer to focus on how to improve it. That is, how can we make the information in the EMR more accurate, catch errors, and then make the latest information easily accessible to users?

STAYING FOCUSED ON THE PATIENT, EVEN WITH A COMPUTER IN THE ROOM

A major complaint by patients and caregivers is that using an EMR makes the physician focus on a computer screen rather than looking at the patient. This concern is valid, but I think we can learn to stay focused on the patient, even with a computer in the examination room, and still take advantage of everything technology has to offer.

This issue will disappear in less than one generation. Young people are remarkably able to multitask while typing. They are able to talk with their patients while typing and to look them in the eyes. And typing letter by letter will become obsolete as soon as voice-recognition software and ways to edit its output accurately are perfected. Many of us at Cleveland Clinic use a combination of templates, typing, and voice-recognition dictation, and find this to be effective.

When we tell our grandchildren that we used to type each individual letter on a page, they will be as amazed as we are to hear that cars used to be started with an external crank.

DOCTOR-DOCTOR COMMUNICATION IS ENHANCED

I agree that template notes written by physicians who cannot type very well can lack the substance and color found in a well-reported medical history and examination. But voice-recognition transcription can help flesh out key parts of the history, differential diagnosis, and management plan. Further, the note can be produced on the spot, the patient can check the note for accuracy, and the conclusions can be shared instantaneously with all involved caregivers. Doctor-doctor communication is thus enhanced.

EVERY REASON TO MOVE FORWARD

Dr. Hanlon is also concerned about EMRs and the potential for “billing creep” and outright fraud. But fraud is as old as billing. What is required is continued vigilance and system controls, which actually might be more effective in an EMR system than in a paper billing system. Integrity will be neither enhanced nor diminished by digitization, unfortunately.

In summary, while Dr. Hanlon sees reason to slow down the move to EMRs, I see every reason to move forward. The problems he describes are part of the growing pains of any new technology. He is right that we cannot move blindly, ignoring the challenges of this technology. But slowing down will only delay its benefits.

While Dr. J. Timothy hanlon raises compelling issues about electronic medical records (EMRs),¹ I think that his goslow approach can lead to lost opportunities. The push toward implementing EMR systems does not amount to a dangerous dive into a shallow pool. Rather, we should be optimistic that we are just learning to swim.

For a contrasting view

Addressing these concerns during these early years of the EMR is constructive and necessary. But his commentary may leave physicians wondering what to do. Should the EMR be scrapped until it is fully developed outside the clinical realm? Is that goal even attainable? Are physicians who use EMR systems putting patient care and information security at risk? I believe there is a more positive way to look at each of the issues.

No new technology comes into the world 100% formed and vetted. The nature of progress is evolution based on experience, as unforeseen problems are corrected. Skepticism and vigilance are warranted, but so is optimism.

CONNECTIVITY WILL IMPROVE

Dr. Hanlon notes that many EMR systems are available and that, at this point, they do not communicate with one another. That is often true. But Google, Microsoft, and others are working on the issues of connectivity and “portability” of the EMR. It is reasonable to expect that eventually there will be winners and losers, just as when VHS won out over Beta in the early days of video recording. More efficient sharing of information will eventually be possible. It would be counterproductive to legislate a single EMR system nationwide before a number of EMRs can be fully tried and tested in the trenches of patient care.

In the meantime, it is no harder—in fact, it is easier than ever—for one physician to send information to another, either by printing it out and mailing or faxing it or by e-mailing it. Furthermore, that information is much more legible than the handwritten records we continue to receive from physicians who do not use EMRs.

Therefore, while one can criticize the current lack of complete intersystem communication, this is only a temporary limitation, and developing complete interconnectivity of EMR systems is a key goal.

STAYING VIGILANT ABOUT SECURITY

The security of EMRs has always been a concern. However, improvements in security have prevented a large-scale privacy breach since an incident in 2006 in which a laptop computer containing information on 26.5 million people was stolen from the home of a Veterans Administration employee.² For instance, Cleveland Clinic recently encrypted all of its laptop computers containing patient data, to protect patient information should a laptop be lost or stolen. This is only one of many security innovations that are being implemented. While we must remain highly vigilant and continue to improve security, we must remember that the paper chart is not immune to privacy breaches either, and when paper charts were stolen, the medical record was irretrievably lost and was not reproducible. This is not the case with the EMR.

QUALITY OF CARE IS PARAMOUNT

As Dr. Hanlon accurately notes, evidence that the EMR improves the quality of care is mixed so far. He is concerned that most of the studies showing improved outcomes came from “benchmark” institutions, and that the results may not be broadly applicable. Such pessimism is unwarranted, given that the EMR is in its relative infancy and the motivation to improve quality of care is paramount, especially in this era of health care reform. While benchmark institutions are in an ideal position to do the studies on quality, there is no reason to assume that the results will not be applicable to other institutions as well.

EDUCATION: AN AREA FOR INNOVATION

Dr. Hanlon notes that research on EMRs for medical education is in its infancy. But infants grow rapidly. While it may be true that students might have to learn to use different EMR systems at different institutions, these students have grown up with rapidly changing computer systems and can learn and adapt at a remarkable rate. Therefore, education is a wonderful area for innovation and research on the EMR. It is not a reason to fear the EMR or the present diversity of EMR systems.

ACCURACY CAN BE IMPROVED

Dr. Hanlon is correct that the problem of cutting and pasting of previous notes, potentially propagating an initial error (so-called high-risk copying³) is profound within the EMR. But I prefer to look at this as an area for innovation— such as nonerasable tags to identify copied material.

While errors in medication lists are possible, especially if practitioners use cut-and-paste methods and thus perpetuate a previous error, systems and workflows are being developed to overcome such problems. Some of these include special alerts when certain high-risk drugs are ordered, drop-down menus with drug dosing included, and links to databases that allow quick access to information on drug interactions.

And again, medication errors are not unique to the EMR. They also occur in paper charts as a result of photocopying, illegible handwriting, and transcription errors.

Compared with the paper chart, the EMR is more legible, and the ability to instantaneously transfer unchanged important and valid information potentially enhances the completeness and logic of a given note and provides the physician more time to spend evaluating (and looking at) the patient. So, rather than focusing on the negatives of the current problem of cutting and pasting, I prefer to focus on how to improve it. That is, how can we make the information in the EMR more accurate, catch errors, and then make the latest information easily accessible to users?

STAYING FOCUSED ON THE PATIENT, EVEN WITH A COMPUTER IN THE ROOM

A major complaint by patients and caregivers is that using an EMR makes the physician focus on a computer screen rather than looking at the patient. This concern is valid, but I think we can learn to stay focused on the patient, even with a computer in the examination room, and still take advantage of everything technology has to offer.

This issue will disappear in less than one generation. Young people are remarkably able to multitask while typing. They are able to talk with their patients while typing and to look them in the eyes. And typing letter by letter will become obsolete as soon as voice-recognition software and ways to edit its output accurately are perfected. Many of us at Cleveland Clinic use a combination of templates, typing, and voice-recognition dictation, and find this to be effective.

When we tell our grandchildren that we used to type each individual letter on a page, they will be as amazed as we are to hear that cars used to be started with an external crank.

DOCTOR-DOCTOR COMMUNICATION IS ENHANCED

I agree that template notes written by physicians who cannot type very well can lack the substance and color found in a well-reported medical history and examination. But voice-recognition transcription can help flesh out key parts of the history, differential diagnosis, and management plan. Further, the note can be produced on the spot, the patient can check the note for accuracy, and the conclusions can be shared instantaneously with all involved caregivers. Doctor-doctor communication is thus enhanced.

EVERY REASON TO MOVE FORWARD

Dr. Hanlon is also concerned about EMRs and the potential for “billing creep” and outright fraud. But fraud is as old as billing. What is required is continued vigilance and system controls, which actually might be more effective in an EMR system than in a paper billing system. Integrity will be neither enhanced nor diminished by digitization, unfortunately.

In summary, while Dr. Hanlon sees reason to slow down the move to EMRs, I see every reason to move forward. The problems he describes are part of the growing pains of any new technology. He is right that we cannot move blindly, ignoring the challenges of this technology. But slowing down will only delay its benefits.