Heart of the Matter

So much has been written about obesity and the “obesity epidemic” recently that the subject has become a bit tired. The simple indulgence of ordering an ice cream cone in the summertime can be embarrassing if you ask for a single dip. The young teenager over the counter often shows a face of disbelief if you are not willing to take the other two scoops that you paid for and deserve.

The epidemic nature of obesity has been reinforced by the observations that it is communicable. Investigators at the Framingham Heart Study, Dr. Nicholas Christakis and James Fowler, Ph.D., suggest that to prevent obesity, we should choose our friends carefully, even if they are halfway across the country (N. Engl. J. Med. 2007;357:370–9). My mother told me a long time ago that I should be careful about the friends I go around with, but she wasn't exactly talking about their eating habits.

The authors of this intriguing study indicate that we should stay away from fat friends, and if we insist on maintaining these friendships, we should be aware of how much we eat. From their observations it appears that our attainment of obesity is related to our social networks that supersede family or other environmental experiences.

They also indicate that the spread of obesity through these networks occurs in a quantifiable pattern. The presence of obesity in a mutual friend increases the development of obesity in an individual by 171%. However, if the friendship was not a mutual one (e.g., a one-way friendship), then the obesity of the other member of the friendship did not affect the individual at risk. It appears that the depth of the one-way friendship determined the degree to which an individual was infected and affected by the obesity “virus.”

Of course, there are other ways to become obese. We go through our daily activities unaware of a number of signals sent out by marketers that also have an effect on how often and how much we eat.

Recent research has examined several aspects of market-driven inducements to overeat. One way this occurs is by labeling. Brian Wansink, Ph.D., of the applied economics and marketing department at Cornell University, New York, and his colleagues suggest that “low-fat” labeling actually increases food intake “by increasing perception of the appropriate serving size and decreasing consumptions of guilt” (J.Mark.Res. 2006;43:605–17).

Dr. Wansink and colleagues observed that when subjects were offered the same granola and M&M's labeled “regular” and “low-fat,” subjects ate more of the “low-fat” foods than the “regular” food, presuming that the “low-fat” label gave them the license to eat more. In addition, the authors observed that “serving-size (e.g., 'Contains 2 servings') reduces overeating only among guilt-prone normal weight consumers but not among overweight consumers.”

The shape of the vessel in which food is offered also can affect its intake. Tall glasses are perceived to have smaller quantities of fluid than short, fat glass even though they contain the same amount of fluid. Therefore, an individual will drink more of the former than the latter.

When individuals were offered a free bottle of the same red wine labeled either California vintage or North Dakota vintage, those who were served the California vintage tended to not only drink more, but eat more, and linger over dinner longer, presuming that the wine was much better and the dinner should be savored longer and in larger quantities (“Mindless Eating, Why We Eat More Than We Think” New York: Bantam Books, 2006).

All of these messages may affect our choice and amount of food eaten when we sit down for dinner. Everything from the depth and mutuality of social contacts, to the shape of the glass that we drink from, to the labeling of food can affect our eating habits.

Perhaps the best advice to guard against obesity comes from Orson Welles, the ultimate example of morbid obesity, who was quoted as saying, “My doctor told me to stop having intimate dinners for four. Unless there are three other people.” Not so subtle advice like this could do a lot to reduce the avoirdupois of Americans.

So much has been written about obesity and the “obesity epidemic” recently that the subject has become a bit tired. The simple indulgence of ordering an ice cream cone in the summertime can be embarrassing if you ask for a single dip. The young teenager over the counter often shows a face of disbelief if you are not willing to take the other two scoops that you paid for and deserve.

The epidemic nature of obesity has been reinforced by the observations that it is communicable. Investigators at the Framingham Heart Study, Dr. Nicholas Christakis and James Fowler, Ph.D., suggest that to prevent obesity, we should choose our friends carefully, even if they are halfway across the country (N. Engl. J. Med. 2007;357:370–9). My mother told me a long time ago that I should be careful about the friends I go around with, but she wasn't exactly talking about their eating habits.

The authors of this intriguing study indicate that we should stay away from fat friends, and if we insist on maintaining these friendships, we should be aware of how much we eat. From their observations it appears that our attainment of obesity is related to our social networks that supersede family or other environmental experiences.

They also indicate that the spread of obesity through these networks occurs in a quantifiable pattern. The presence of obesity in a mutual friend increases the development of obesity in an individual by 171%. However, if the friendship was not a mutual one (e.g., a one-way friendship), then the obesity of the other member of the friendship did not affect the individual at risk. It appears that the depth of the one-way friendship determined the degree to which an individual was infected and affected by the obesity “virus.”

Of course, there are other ways to become obese. We go through our daily activities unaware of a number of signals sent out by marketers that also have an effect on how often and how much we eat.

Recent research has examined several aspects of market-driven inducements to overeat. One way this occurs is by labeling. Brian Wansink, Ph.D., of the applied economics and marketing department at Cornell University, New York, and his colleagues suggest that “low-fat” labeling actually increases food intake “by increasing perception of the appropriate serving size and decreasing consumptions of guilt” (J.Mark.Res. 2006;43:605–17).

Dr. Wansink and colleagues observed that when subjects were offered the same granola and M&M's labeled “regular” and “low-fat,” subjects ate more of the “low-fat” foods than the “regular” food, presuming that the “low-fat” label gave them the license to eat more. In addition, the authors observed that “serving-size (e.g., 'Contains 2 servings') reduces overeating only among guilt-prone normal weight consumers but not among overweight consumers.”

The shape of the vessel in which food is offered also can affect its intake. Tall glasses are perceived to have smaller quantities of fluid than short, fat glass even though they contain the same amount of fluid. Therefore, an individual will drink more of the former than the latter.

When individuals were offered a free bottle of the same red wine labeled either California vintage or North Dakota vintage, those who were served the California vintage tended to not only drink more, but eat more, and linger over dinner longer, presuming that the wine was much better and the dinner should be savored longer and in larger quantities (“Mindless Eating, Why We Eat More Than We Think” New York: Bantam Books, 2006).

All of these messages may affect our choice and amount of food eaten when we sit down for dinner. Everything from the depth and mutuality of social contacts, to the shape of the glass that we drink from, to the labeling of food can affect our eating habits.

Perhaps the best advice to guard against obesity comes from Orson Welles, the ultimate example of morbid obesity, who was quoted as saying, “My doctor told me to stop having intimate dinners for four. Unless there are three other people.” Not so subtle advice like this could do a lot to reduce the avoirdupois of Americans.

So much has been written about obesity and the “obesity epidemic” recently that the subject has become a bit tired. The simple indulgence of ordering an ice cream cone in the summertime can be embarrassing if you ask for a single dip. The young teenager over the counter often shows a face of disbelief if you are not willing to take the other two scoops that you paid for and deserve.

The epidemic nature of obesity has been reinforced by the observations that it is communicable. Investigators at the Framingham Heart Study, Dr. Nicholas Christakis and James Fowler, Ph.D., suggest that to prevent obesity, we should choose our friends carefully, even if they are halfway across the country (N. Engl. J. Med. 2007;357:370–9). My mother told me a long time ago that I should be careful about the friends I go around with, but she wasn't exactly talking about their eating habits.

The authors of this intriguing study indicate that we should stay away from fat friends, and if we insist on maintaining these friendships, we should be aware of how much we eat. From their observations it appears that our attainment of obesity is related to our social networks that supersede family or other environmental experiences.

They also indicate that the spread of obesity through these networks occurs in a quantifiable pattern. The presence of obesity in a mutual friend increases the development of obesity in an individual by 171%. However, if the friendship was not a mutual one (e.g., a one-way friendship), then the obesity of the other member of the friendship did not affect the individual at risk. It appears that the depth of the one-way friendship determined the degree to which an individual was infected and affected by the obesity “virus.”

Of course, there are other ways to become obese. We go through our daily activities unaware of a number of signals sent out by marketers that also have an effect on how often and how much we eat.

Recent research has examined several aspects of market-driven inducements to overeat. One way this occurs is by labeling. Brian Wansink, Ph.D., of the applied economics and marketing department at Cornell University, New York, and his colleagues suggest that “low-fat” labeling actually increases food intake “by increasing perception of the appropriate serving size and decreasing consumptions of guilt” (J.Mark.Res. 2006;43:605–17).

Dr. Wansink and colleagues observed that when subjects were offered the same granola and M&M's labeled “regular” and “low-fat,” subjects ate more of the “low-fat” foods than the “regular” food, presuming that the “low-fat” label gave them the license to eat more. In addition, the authors observed that “serving-size (e.g., 'Contains 2 servings') reduces overeating only among guilt-prone normal weight consumers but not among overweight consumers.”

The shape of the vessel in which food is offered also can affect its intake. Tall glasses are perceived to have smaller quantities of fluid than short, fat glass even though they contain the same amount of fluid. Therefore, an individual will drink more of the former than the latter.

When individuals were offered a free bottle of the same red wine labeled either California vintage or North Dakota vintage, those who were served the California vintage tended to not only drink more, but eat more, and linger over dinner longer, presuming that the wine was much better and the dinner should be savored longer and in larger quantities (“Mindless Eating, Why We Eat More Than We Think” New York: Bantam Books, 2006).

All of these messages may affect our choice and amount of food eaten when we sit down for dinner. Everything from the depth and mutuality of social contacts, to the shape of the glass that we drink from, to the labeling of food can affect our eating habits.

Perhaps the best advice to guard against obesity comes from Orson Welles, the ultimate example of morbid obesity, who was quoted as saying, “My doctor told me to stop having intimate dinners for four. Unless there are three other people.” Not so subtle advice like this could do a lot to reduce the avoirdupois of Americans.

Two comments in the President's Page of the Aug. 7 issue of the Journal of the American College of Cardiology raise some concern about the future course of the ACC.

We all understand the problems of keeping each of the cardiac specialties under the “big tent” of cardiology, and we applaud the efforts of the college to prevent the balkanization of our discipline. The advances in interventional cardiology, imaging, molecular biology, treating heart failure, and arrhythmia therapy, to name just a few, make it even more difficult for practicing cardiologists to obtain and retain familiarity with the therapeutic options available to our patients. The college, through its journal and meetings, has been a platform upon which new therapeutic concepts can be presented and older ones challenged. Peer review, which has been the hallmark of the determination of what and when this information is offered for reporting and examination, has been a well-worn, if not occasionally flawed, process.

The President's Page outlines the extensive attempts made by the college to accommodate the needs of the interventional community for representations to the public and to the medical community (J. Am. Coll. Cardiol. 2007;50:558–9). In spite of these efforts, it appears that a few restless members of the interventional community have been critical of ACC leadership for the way new and controversial data have been released at national meetings and to the press.

They have been particularly concerned about the manner in which the COURAGE (Clinical Outcomes Utilizing Revascularization and Aggressive Drug Evaluation) trial and the data on late thrombosis risk with drug-eluting stents were presented. The President's Page referred to the “public confusion generated by the results of the COURAGE” trial and outlined the extensive attempts made by the college to accommodate the needs of the interventional community for representation to the public and to the medical community. However, the media circus that occurred as a result of the premature release of the COURAGE outcomes at an industry sponsored symposium should be separated from the results of the COURAGE trial.

The message—that percutaneous coronary intervention does not decrease death or myocardial infarction rates when added to optimal medical therapy in patients with stable coronary artery disease—was clear. Learning more about the benefits and risks of implanting drug-eluting stents in stable patients who seem to do quite well with optimal medical therapy is a critical issue. The result has been a rapid decrease in the use of PCI (percutaneous coronary intervention) by both the interventionalists and clinical cardiologists.

The statement by the authors that “we are concerned about the most significant risk to the profession and our patients, which is health care reform,” is particularly puzzling. It is clear that the college must walk a thin line between its physician advocacy and its quality initiatives. However, many of us see health care reform as an opportunity to effect better care for our patients and a more equitable distribution of our health care resources. The ACC in fact has been well ahead of other specialties in the effort to establish guidelines, which have been specifically directed to this goal.

The membership has acted on the premise that in order to provide an informed and science-based approach to the use of health resources and in order to avoid either over- or under-treatment, guidelines are necessary. Every physician is well aware of the wide variation and often inappropriate use of resources in cardiology. Although we may modify their use in an individual patient, we all fall back on those guidelines to provide a frame of reference for care. Health care reform, if done correctly, can be an instrument to provide an informed homogeneity of care to our patients; it should not be viewed as a risk but as an opportunity to participate in changes that are long overdue.

It is hard to see how the ACC can be a productive participant in the future form of health care if we are driven by a concern about protecting our risks.

Two comments in the President's Page of the Aug. 7 issue of the Journal of the American College of Cardiology raise some concern about the future course of the ACC.

We all understand the problems of keeping each of the cardiac specialties under the “big tent” of cardiology, and we applaud the efforts of the college to prevent the balkanization of our discipline. The advances in interventional cardiology, imaging, molecular biology, treating heart failure, and arrhythmia therapy, to name just a few, make it even more difficult for practicing cardiologists to obtain and retain familiarity with the therapeutic options available to our patients. The college, through its journal and meetings, has been a platform upon which new therapeutic concepts can be presented and older ones challenged. Peer review, which has been the hallmark of the determination of what and when this information is offered for reporting and examination, has been a well-worn, if not occasionally flawed, process.

The President's Page outlines the extensive attempts made by the college to accommodate the needs of the interventional community for representations to the public and to the medical community (J. Am. Coll. Cardiol. 2007;50:558–9). In spite of these efforts, it appears that a few restless members of the interventional community have been critical of ACC leadership for the way new and controversial data have been released at national meetings and to the press.

They have been particularly concerned about the manner in which the COURAGE (Clinical Outcomes Utilizing Revascularization and Aggressive Drug Evaluation) trial and the data on late thrombosis risk with drug-eluting stents were presented. The President's Page referred to the “public confusion generated by the results of the COURAGE” trial and outlined the extensive attempts made by the college to accommodate the needs of the interventional community for representation to the public and to the medical community. However, the media circus that occurred as a result of the premature release of the COURAGE outcomes at an industry sponsored symposium should be separated from the results of the COURAGE trial.

The message—that percutaneous coronary intervention does not decrease death or myocardial infarction rates when added to optimal medical therapy in patients with stable coronary artery disease—was clear. Learning more about the benefits and risks of implanting drug-eluting stents in stable patients who seem to do quite well with optimal medical therapy is a critical issue. The result has been a rapid decrease in the use of PCI (percutaneous coronary intervention) by both the interventionalists and clinical cardiologists.

The statement by the authors that “we are concerned about the most significant risk to the profession and our patients, which is health care reform,” is particularly puzzling. It is clear that the college must walk a thin line between its physician advocacy and its quality initiatives. However, many of us see health care reform as an opportunity to effect better care for our patients and a more equitable distribution of our health care resources. The ACC in fact has been well ahead of other specialties in the effort to establish guidelines, which have been specifically directed to this goal.

The membership has acted on the premise that in order to provide an informed and science-based approach to the use of health resources and in order to avoid either over- or under-treatment, guidelines are necessary. Every physician is well aware of the wide variation and often inappropriate use of resources in cardiology. Although we may modify their use in an individual patient, we all fall back on those guidelines to provide a frame of reference for care. Health care reform, if done correctly, can be an instrument to provide an informed homogeneity of care to our patients; it should not be viewed as a risk but as an opportunity to participate in changes that are long overdue.

It is hard to see how the ACC can be a productive participant in the future form of health care if we are driven by a concern about protecting our risks.

Two comments in the President's Page of the Aug. 7 issue of the Journal of the American College of Cardiology raise some concern about the future course of the ACC.

We all understand the problems of keeping each of the cardiac specialties under the “big tent” of cardiology, and we applaud the efforts of the college to prevent the balkanization of our discipline. The advances in interventional cardiology, imaging, molecular biology, treating heart failure, and arrhythmia therapy, to name just a few, make it even more difficult for practicing cardiologists to obtain and retain familiarity with the therapeutic options available to our patients. The college, through its journal and meetings, has been a platform upon which new therapeutic concepts can be presented and older ones challenged. Peer review, which has been the hallmark of the determination of what and when this information is offered for reporting and examination, has been a well-worn, if not occasionally flawed, process.

The President's Page outlines the extensive attempts made by the college to accommodate the needs of the interventional community for representations to the public and to the medical community (J. Am. Coll. Cardiol. 2007;50:558–9). In spite of these efforts, it appears that a few restless members of the interventional community have been critical of ACC leadership for the way new and controversial data have been released at national meetings and to the press.

They have been particularly concerned about the manner in which the COURAGE (Clinical Outcomes Utilizing Revascularization and Aggressive Drug Evaluation) trial and the data on late thrombosis risk with drug-eluting stents were presented. The President's Page referred to the “public confusion generated by the results of the COURAGE” trial and outlined the extensive attempts made by the college to accommodate the needs of the interventional community for representation to the public and to the medical community. However, the media circus that occurred as a result of the premature release of the COURAGE outcomes at an industry sponsored symposium should be separated from the results of the COURAGE trial.

The message—that percutaneous coronary intervention does not decrease death or myocardial infarction rates when added to optimal medical therapy in patients with stable coronary artery disease—was clear. Learning more about the benefits and risks of implanting drug-eluting stents in stable patients who seem to do quite well with optimal medical therapy is a critical issue. The result has been a rapid decrease in the use of PCI (percutaneous coronary intervention) by both the interventionalists and clinical cardiologists.

The statement by the authors that “we are concerned about the most significant risk to the profession and our patients, which is health care reform,” is particularly puzzling. It is clear that the college must walk a thin line between its physician advocacy and its quality initiatives. However, many of us see health care reform as an opportunity to effect better care for our patients and a more equitable distribution of our health care resources. The ACC in fact has been well ahead of other specialties in the effort to establish guidelines, which have been specifically directed to this goal.

The membership has acted on the premise that in order to provide an informed and science-based approach to the use of health resources and in order to avoid either over- or under-treatment, guidelines are necessary. Every physician is well aware of the wide variation and often inappropriate use of resources in cardiology. Although we may modify their use in an individual patient, we all fall back on those guidelines to provide a frame of reference for care. Health care reform, if done correctly, can be an instrument to provide an informed homogeneity of care to our patients; it should not be viewed as a risk but as an opportunity to participate in changes that are long overdue.

It is hard to see how the ACC can be a productive participant in the future form of health care if we are driven by a concern about protecting our risks.

A recent analysis indicates that the medical profession in general—and cardiology in particular—has received a lot of free meals and trips under the heading of professional education. The analysis reports that cardiologists have more of these “perks” than does any other group surveyed, including primary care doctors, anesthesiologists, and general surgeons (N. Engl. J. Med. 2007;356:1742–50). The implication of the survey suggests that cardiologists' therapeutic decisions are heavily influenced by industry. That's probably not too far from the truth. But the real issue is, Who is out there to educate the cardiologists about the newest drug or device if industry does not do it?

The pharmaceutical industry, by default, now provides almost 75% of all postgraduate education. The rapidity of the development of new drugs and devices that has occurred in the last decade has been overwhelming and has necessitated a close relationship between the developer and the practitioner. Any delay in application of the new device or drug by cardiologists is viewed as incompetence or ignorance.

It was not long ago—30 years—when β-blockers were introduced for the treatment of acute MI. Information based on clinical trials of more than 6,000 patients showed that the mortality of acute MI could be reduced by 45% if all patients received that class of drug. In spite of these data, almost 15 years after their publication fewer than 25% of patients were receiving β-blockers at the time of hospital discharge.

The National Institutes of Health at that time was not interested in carrying the message, even though one of the three major trials, the Beta Blocker Heart Attack Trial, was sponsored by the National Heart, Lung, and Blood Institute. Some concerned cardiologists approached the only drug company that sold a patented β-blocker at that time to help raise awareness of the importance of β-blocker therapy within the cardiology community. A number of symposia and dinner programs were organized to encourage the use of any β-blocker, some of which were generic, for the treatment of acute MI. We were modestly effective in increasing the usage to just under 50%. Yes, we were paid to give the talks and doctors did get a lot of free meals, but the message ultimately got out.

β-Blockers have been incorporated as standard therapy, but getting there was not easy. And it took over a quarter of a century to do it. Similar comments can be made about ACE inhibitors in heart failure: The ultimate introduction into clinical practice took almost a decade after the drugs were shown to be effective. In contrast, spironolactone was shown effective in heart failure in a trial sponsored by a pharmaceutical company. But because the drug was already off patent, the company felt that it had no responsibility to teach doctors how to use it, resulting in a significant increase in morbidity and mortality when spironolactone was used at the wrong dose and in the wrong patients.

Last year, a group sponsored by the American Board of Internal Medicine Foundation and the Institute on Medicine as a Profession called for academic medical centers to take the lead in eliminating potential conflicts of interest with drug companies by stopping “common practices” that included accepting funds for travel to CME meetings and serving on speakers' bureaus (JAMA 2006;295:429–33). If implemented, that will turn the clock back to the period in which the introduction of new drugs and devices proceeded at a glacial pace. It would be largely free of pharmaceutical support, relying heavily on a medical education system that currently provides little access or support for postgraduate education.

A number of for-profit companies have emerged to provide postgraduate education in part supported by merged pharmaceutical funds. At the same time, the Internet has become an accessible source of medical information. None of these, however, takes the place of the personal interaction between a clinical scientist involved with the R&D of new medical science and a listening audience.

Without question, we'd all feel better if we did not have industry editing our presentation slides and telling us what to say. It is an unhealthy environment in which to educate physicians. But the academic medical centers need to step up to the plate and provide that support. So far there they have not even reached the batting circle.

A recent analysis indicates that the medical profession in general—and cardiology in particular—has received a lot of free meals and trips under the heading of professional education. The analysis reports that cardiologists have more of these “perks” than does any other group surveyed, including primary care doctors, anesthesiologists, and general surgeons (N. Engl. J. Med. 2007;356:1742–50). The implication of the survey suggests that cardiologists' therapeutic decisions are heavily influenced by industry. That's probably not too far from the truth. But the real issue is, Who is out there to educate the cardiologists about the newest drug or device if industry does not do it?

The pharmaceutical industry, by default, now provides almost 75% of all postgraduate education. The rapidity of the development of new drugs and devices that has occurred in the last decade has been overwhelming and has necessitated a close relationship between the developer and the practitioner. Any delay in application of the new device or drug by cardiologists is viewed as incompetence or ignorance.

It was not long ago—30 years—when β-blockers were introduced for the treatment of acute MI. Information based on clinical trials of more than 6,000 patients showed that the mortality of acute MI could be reduced by 45% if all patients received that class of drug. In spite of these data, almost 15 years after their publication fewer than 25% of patients were receiving β-blockers at the time of hospital discharge.

The National Institutes of Health at that time was not interested in carrying the message, even though one of the three major trials, the Beta Blocker Heart Attack Trial, was sponsored by the National Heart, Lung, and Blood Institute. Some concerned cardiologists approached the only drug company that sold a patented β-blocker at that time to help raise awareness of the importance of β-blocker therapy within the cardiology community. A number of symposia and dinner programs were organized to encourage the use of any β-blocker, some of which were generic, for the treatment of acute MI. We were modestly effective in increasing the usage to just under 50%. Yes, we were paid to give the talks and doctors did get a lot of free meals, but the message ultimately got out.

β-Blockers have been incorporated as standard therapy, but getting there was not easy. And it took over a quarter of a century to do it. Similar comments can be made about ACE inhibitors in heart failure: The ultimate introduction into clinical practice took almost a decade after the drugs were shown to be effective. In contrast, spironolactone was shown effective in heart failure in a trial sponsored by a pharmaceutical company. But because the drug was already off patent, the company felt that it had no responsibility to teach doctors how to use it, resulting in a significant increase in morbidity and mortality when spironolactone was used at the wrong dose and in the wrong patients.

Last year, a group sponsored by the American Board of Internal Medicine Foundation and the Institute on Medicine as a Profession called for academic medical centers to take the lead in eliminating potential conflicts of interest with drug companies by stopping “common practices” that included accepting funds for travel to CME meetings and serving on speakers' bureaus (JAMA 2006;295:429–33). If implemented, that will turn the clock back to the period in which the introduction of new drugs and devices proceeded at a glacial pace. It would be largely free of pharmaceutical support, relying heavily on a medical education system that currently provides little access or support for postgraduate education.

A number of for-profit companies have emerged to provide postgraduate education in part supported by merged pharmaceutical funds. At the same time, the Internet has become an accessible source of medical information. None of these, however, takes the place of the personal interaction between a clinical scientist involved with the R&D of new medical science and a listening audience.

Without question, we'd all feel better if we did not have industry editing our presentation slides and telling us what to say. It is an unhealthy environment in which to educate physicians. But the academic medical centers need to step up to the plate and provide that support. So far there they have not even reached the batting circle.

A recent analysis indicates that the medical profession in general—and cardiology in particular—has received a lot of free meals and trips under the heading of professional education. The analysis reports that cardiologists have more of these “perks” than does any other group surveyed, including primary care doctors, anesthesiologists, and general surgeons (N. Engl. J. Med. 2007;356:1742–50). The implication of the survey suggests that cardiologists' therapeutic decisions are heavily influenced by industry. That's probably not too far from the truth. But the real issue is, Who is out there to educate the cardiologists about the newest drug or device if industry does not do it?

The pharmaceutical industry, by default, now provides almost 75% of all postgraduate education. The rapidity of the development of new drugs and devices that has occurred in the last decade has been overwhelming and has necessitated a close relationship between the developer and the practitioner. Any delay in application of the new device or drug by cardiologists is viewed as incompetence or ignorance.

It was not long ago—30 years—when β-blockers were introduced for the treatment of acute MI. Information based on clinical trials of more than 6,000 patients showed that the mortality of acute MI could be reduced by 45% if all patients received that class of drug. In spite of these data, almost 15 years after their publication fewer than 25% of patients were receiving β-blockers at the time of hospital discharge.

The National Institutes of Health at that time was not interested in carrying the message, even though one of the three major trials, the Beta Blocker Heart Attack Trial, was sponsored by the National Heart, Lung, and Blood Institute. Some concerned cardiologists approached the only drug company that sold a patented β-blocker at that time to help raise awareness of the importance of β-blocker therapy within the cardiology community. A number of symposia and dinner programs were organized to encourage the use of any β-blocker, some of which were generic, for the treatment of acute MI. We were modestly effective in increasing the usage to just under 50%. Yes, we were paid to give the talks and doctors did get a lot of free meals, but the message ultimately got out.

β-Blockers have been incorporated as standard therapy, but getting there was not easy. And it took over a quarter of a century to do it. Similar comments can be made about ACE inhibitors in heart failure: The ultimate introduction into clinical practice took almost a decade after the drugs were shown to be effective. In contrast, spironolactone was shown effective in heart failure in a trial sponsored by a pharmaceutical company. But because the drug was already off patent, the company felt that it had no responsibility to teach doctors how to use it, resulting in a significant increase in morbidity and mortality when spironolactone was used at the wrong dose and in the wrong patients.

Last year, a group sponsored by the American Board of Internal Medicine Foundation and the Institute on Medicine as a Profession called for academic medical centers to take the lead in eliminating potential conflicts of interest with drug companies by stopping “common practices” that included accepting funds for travel to CME meetings and serving on speakers' bureaus (JAMA 2006;295:429–33). If implemented, that will turn the clock back to the period in which the introduction of new drugs and devices proceeded at a glacial pace. It would be largely free of pharmaceutical support, relying heavily on a medical education system that currently provides little access or support for postgraduate education.

A number of for-profit companies have emerged to provide postgraduate education in part supported by merged pharmaceutical funds. At the same time, the Internet has become an accessible source of medical information. None of these, however, takes the place of the personal interaction between a clinical scientist involved with the R&D of new medical science and a listening audience.

Without question, we'd all feel better if we did not have industry editing our presentation slides and telling us what to say. It is an unhealthy environment in which to educate physicians. But the academic medical centers need to step up to the plate and provide that support. So far there they have not even reached the batting circle.

As the smoke settles over the firestorm created by the recent rosiglitazone revelations, many questions remain and much can be learned from the public discourse in both the medical and lay press. So what can be said about how the story evolved and ultimately reached a nonconclusion?

Rosiglitazone (Avandia, GlaxoSmithKline), a thiazolidinedione (TZD) was approved by the Food and Drug Administration for use in 1999 as an effective agent for lowering blood sugar. A modest amount of clinical data indicates that lowering blood sugar can have a beneficial effect on the microvascular changes associated with diabetes mellitus. Lowering blood sugar became a surrogate end point in the judgment of the FDA for a presumed clinical benefit in diabetes.

Some information existed to suggest that although rosiglitazone did indeed lower blood sugar, it might have some adverse effects on coronary heart disease. In fact, in September 2006, the European Medicines Agency had placed a warning label on rosiglitazone about the risk of cardiac ischemic events. In the United States, the FDA was in the process of reevaluating its judgment on this issue when along came the recent meta-analysis published by Dr. Steven Nissen and Kathy Walski (N. Engl. J. Med. 2007;356:2457-71).

One had to be impressed with the speed at which the authors, editorial writers, and the New England Journal of Medicine achieved major national and international headline exposure from a meta-analysis based on the meager and disparate data created from widely variable event classification.

The fact that a trial aimed at elucidating the potential mortality/morbidity effects of the drug was already underway in Europe and Australia was particularly unfortunate. The Rosiglitazone Evaluated for Cardiac Outcomes and Regulation of Glycemia in Diabetes (RECORD) trial was about halfway through its 6-year follow-up when the uproar occurred. RECORD randomized 4,447 patients to rosiglitazone or placebo in addition to standard oral diabetic agents. Even though its design was flawed by its unblinded nature, it surely might have provided some information relative to the risks of rosiglitazone. With the release of its interim 3-year follow-up data (N. Engl. J. Med. 2007, 357[doi: 10.1056/NEJMoa073394

All of this played out in an atmosphere in which the FDA has been recently taking its hits. The direction the FDA was taking regarding rosiglitazone is not entirely clear. Records suggest that it was under consideration and that one FDA reviewer was chastised for proposing restriction of its use. The slow and possibly flawed response by the FDA can hardly be countenanced. More importantly, the practice of the FDA to accept surrogate data in cardiovascular disease evaluation is a continuing problem. The FDA's approval of a drug based solely on its ability to lower blood sugar, without consideration of major cardiovascular safety and efficacy, is unacceptable.

Whether all of this could have been achieved without all the brouhaha is not certain. It is clear that the authors of the New England Journal paper were in discussion with members of Congress long before its publication. Whether there were discussions with the FDA is not clear. It does suggest that there was an attempt to “get to” the FDA or at least influence its policies. The possible contamination of science by politics is disturbing. Politics needs to be confined to the editorial pages, not in the meat of a scientific manuscript and its publication.

The ultimate decision forced by Congress on GSK and Takeda, the maker of the similar drug pioglitazone, could well have been achieved if cooler heads had been in charge. In addition we might still hold our scientific journals in high regard.

As the smoke settles over the firestorm created by the recent rosiglitazone revelations, many questions remain and much can be learned from the public discourse in both the medical and lay press. So what can be said about how the story evolved and ultimately reached a nonconclusion?

Rosiglitazone (Avandia, GlaxoSmithKline), a thiazolidinedione (TZD) was approved by the Food and Drug Administration for use in 1999 as an effective agent for lowering blood sugar. A modest amount of clinical data indicates that lowering blood sugar can have a beneficial effect on the microvascular changes associated with diabetes mellitus. Lowering blood sugar became a surrogate end point in the judgment of the FDA for a presumed clinical benefit in diabetes.

Some information existed to suggest that although rosiglitazone did indeed lower blood sugar, it might have some adverse effects on coronary heart disease. In fact, in September 2006, the European Medicines Agency had placed a warning label on rosiglitazone about the risk of cardiac ischemic events. In the United States, the FDA was in the process of reevaluating its judgment on this issue when along came the recent meta-analysis published by Dr. Steven Nissen and Kathy Walski (N. Engl. J. Med. 2007;356:2457-71).

One had to be impressed with the speed at which the authors, editorial writers, and the New England Journal of Medicine achieved major national and international headline exposure from a meta-analysis based on the meager and disparate data created from widely variable event classification.

The fact that a trial aimed at elucidating the potential mortality/morbidity effects of the drug was already underway in Europe and Australia was particularly unfortunate. The Rosiglitazone Evaluated for Cardiac Outcomes and Regulation of Glycemia in Diabetes (RECORD) trial was about halfway through its 6-year follow-up when the uproar occurred. RECORD randomized 4,447 patients to rosiglitazone or placebo in addition to standard oral diabetic agents. Even though its design was flawed by its unblinded nature, it surely might have provided some information relative to the risks of rosiglitazone. With the release of its interim 3-year follow-up data (N. Engl. J. Med. 2007, 357[doi: 10.1056/NEJMoa073394

All of this played out in an atmosphere in which the FDA has been recently taking its hits. The direction the FDA was taking regarding rosiglitazone is not entirely clear. Records suggest that it was under consideration and that one FDA reviewer was chastised for proposing restriction of its use. The slow and possibly flawed response by the FDA can hardly be countenanced. More importantly, the practice of the FDA to accept surrogate data in cardiovascular disease evaluation is a continuing problem. The FDA's approval of a drug based solely on its ability to lower blood sugar, without consideration of major cardiovascular safety and efficacy, is unacceptable.

Whether all of this could have been achieved without all the brouhaha is not certain. It is clear that the authors of the New England Journal paper were in discussion with members of Congress long before its publication. Whether there were discussions with the FDA is not clear. It does suggest that there was an attempt to “get to” the FDA or at least influence its policies. The possible contamination of science by politics is disturbing. Politics needs to be confined to the editorial pages, not in the meat of a scientific manuscript and its publication.

The ultimate decision forced by Congress on GSK and Takeda, the maker of the similar drug pioglitazone, could well have been achieved if cooler heads had been in charge. In addition we might still hold our scientific journals in high regard.

As the smoke settles over the firestorm created by the recent rosiglitazone revelations, many questions remain and much can be learned from the public discourse in both the medical and lay press. So what can be said about how the story evolved and ultimately reached a nonconclusion?

Rosiglitazone (Avandia, GlaxoSmithKline), a thiazolidinedione (TZD) was approved by the Food and Drug Administration for use in 1999 as an effective agent for lowering blood sugar. A modest amount of clinical data indicates that lowering blood sugar can have a beneficial effect on the microvascular changes associated with diabetes mellitus. Lowering blood sugar became a surrogate end point in the judgment of the FDA for a presumed clinical benefit in diabetes.

Some information existed to suggest that although rosiglitazone did indeed lower blood sugar, it might have some adverse effects on coronary heart disease. In fact, in September 2006, the European Medicines Agency had placed a warning label on rosiglitazone about the risk of cardiac ischemic events. In the United States, the FDA was in the process of reevaluating its judgment on this issue when along came the recent meta-analysis published by Dr. Steven Nissen and Kathy Walski (N. Engl. J. Med. 2007;356:2457-71).

One had to be impressed with the speed at which the authors, editorial writers, and the New England Journal of Medicine achieved major national and international headline exposure from a meta-analysis based on the meager and disparate data created from widely variable event classification.

The fact that a trial aimed at elucidating the potential mortality/morbidity effects of the drug was already underway in Europe and Australia was particularly unfortunate. The Rosiglitazone Evaluated for Cardiac Outcomes and Regulation of Glycemia in Diabetes (RECORD) trial was about halfway through its 6-year follow-up when the uproar occurred. RECORD randomized 4,447 patients to rosiglitazone or placebo in addition to standard oral diabetic agents. Even though its design was flawed by its unblinded nature, it surely might have provided some information relative to the risks of rosiglitazone. With the release of its interim 3-year follow-up data (N. Engl. J. Med. 2007, 357[doi: 10.1056/NEJMoa073394

All of this played out in an atmosphere in which the FDA has been recently taking its hits. The direction the FDA was taking regarding rosiglitazone is not entirely clear. Records suggest that it was under consideration and that one FDA reviewer was chastised for proposing restriction of its use. The slow and possibly flawed response by the FDA can hardly be countenanced. More importantly, the practice of the FDA to accept surrogate data in cardiovascular disease evaluation is a continuing problem. The FDA's approval of a drug based solely on its ability to lower blood sugar, without consideration of major cardiovascular safety and efficacy, is unacceptable.

Whether all of this could have been achieved without all the brouhaha is not certain. It is clear that the authors of the New England Journal paper were in discussion with members of Congress long before its publication. Whether there were discussions with the FDA is not clear. It does suggest that there was an attempt to “get to” the FDA or at least influence its policies. The possible contamination of science by politics is disturbing. Politics needs to be confined to the editorial pages, not in the meat of a scientific manuscript and its publication.

The ultimate decision forced by Congress on GSK and Takeda, the maker of the similar drug pioglitazone, could well have been achieved if cooler heads had been in charge. In addition we might still hold our scientific journals in high regard.

The translation of clinical trial results to the bedside has always been a complex and often uncertain exercise. The specific patient who precisely fits the evidence-based data is usually the exception to the rule.

Randomized clinical trials by their nature are focused on specific disease states with the exclusion of other concurrent medical problems. They include populations that often have little resemblance to the patients that you and I see in the clinic or hospital free of any comorbidity. The entry restrictions are crafted to identify patients who are most likely to benefit from the drug or device under study and to ensure their safety during its progress. Although not exclusive to the younger patient, the trials tend to recruit younger patients with little comorbidity.

The demographic restrictions on the design and management of clinical trials make it even more difficult to apply their results to guidelines and quality standards. Unfortunately, we have few data which reflect on either the safety or efficacy when “proven” therapy is applied to the general and particularly the Medicare patient.

The Medicare population is considerably older than patients entered into randomized clinical trials, with a greater mortality and morbidity burden of comorbid disease. However, they now represent the majority of patients admitted to the hospital with acute myocardial infarction. A recent publication using data collected over 9 years from 1992–1993 to 2000–2001 from the Medicare database sheds light on important trends that occurred in that population from that period (Circulation 2006;114:2806–14).

During that time, the Medicare MI patients increased in age from 75.7 years to 78.3 years and a quarter of those patients were over 85. The incidence of ST-segment elevation MI decreased from 37.4% to 23.5%. Because of the increased incidence of concomitant morbidity such as diabetes, chronic renal disease, and pulmonary disease, only about a third of patients surviving their MIs were “ideal patients” to whom guidelines or quality standards could be applied. During the study period the days in the hospital decreased from 10.1 days to 6.9 days. Although mortality adjusted for comorbidity had decreased during that period, the 1-year crude mortality increased from 27.6% to 31.0%.

It is clear from these observations that much of the clinical trial research that influences “evidence-based” medicine does not fully describe the reality of the world we function in. The science of clinical trials, highly refined in the last 50 years, has provided an immense amount of information about medical therapeutics. Yet it provides only a snapshot in time in a clinical environment that is changing rapidly around us. This is particularly true when studying degenerative diseases such as cardiovascular disease, which is influenced by a rapidly aging population. This study emphasizes the striking difficulty associated with the application of MI guidelines and standards to the Medicare population that has to a large degree been essentially excluded from contemporary clinical research studies. It is clear that a more dynamic access to the Medicare database could provide important insight into the risks and benefits of cardiac therapy. The sooner we have that information, the sooner we can be more effective at applying appropriate therapy to the real world and our aging patients.

The translation of clinical trial results to the bedside has always been a complex and often uncertain exercise. The specific patient who precisely fits the evidence-based data is usually the exception to the rule.

Randomized clinical trials by their nature are focused on specific disease states with the exclusion of other concurrent medical problems. They include populations that often have little resemblance to the patients that you and I see in the clinic or hospital free of any comorbidity. The entry restrictions are crafted to identify patients who are most likely to benefit from the drug or device under study and to ensure their safety during its progress. Although not exclusive to the younger patient, the trials tend to recruit younger patients with little comorbidity.

The demographic restrictions on the design and management of clinical trials make it even more difficult to apply their results to guidelines and quality standards. Unfortunately, we have few data which reflect on either the safety or efficacy when “proven” therapy is applied to the general and particularly the Medicare patient.

The Medicare population is considerably older than patients entered into randomized clinical trials, with a greater mortality and morbidity burden of comorbid disease. However, they now represent the majority of patients admitted to the hospital with acute myocardial infarction. A recent publication using data collected over 9 years from 1992–1993 to 2000–2001 from the Medicare database sheds light on important trends that occurred in that population from that period (Circulation 2006;114:2806–14).

During that time, the Medicare MI patients increased in age from 75.7 years to 78.3 years and a quarter of those patients were over 85. The incidence of ST-segment elevation MI decreased from 37.4% to 23.5%. Because of the increased incidence of concomitant morbidity such as diabetes, chronic renal disease, and pulmonary disease, only about a third of patients surviving their MIs were “ideal patients” to whom guidelines or quality standards could be applied. During the study period the days in the hospital decreased from 10.1 days to 6.9 days. Although mortality adjusted for comorbidity had decreased during that period, the 1-year crude mortality increased from 27.6% to 31.0%.

It is clear from these observations that much of the clinical trial research that influences “evidence-based” medicine does not fully describe the reality of the world we function in. The science of clinical trials, highly refined in the last 50 years, has provided an immense amount of information about medical therapeutics. Yet it provides only a snapshot in time in a clinical environment that is changing rapidly around us. This is particularly true when studying degenerative diseases such as cardiovascular disease, which is influenced by a rapidly aging population. This study emphasizes the striking difficulty associated with the application of MI guidelines and standards to the Medicare population that has to a large degree been essentially excluded from contemporary clinical research studies. It is clear that a more dynamic access to the Medicare database could provide important insight into the risks and benefits of cardiac therapy. The sooner we have that information, the sooner we can be more effective at applying appropriate therapy to the real world and our aging patients.

The translation of clinical trial results to the bedside has always been a complex and often uncertain exercise. The specific patient who precisely fits the evidence-based data is usually the exception to the rule.

Randomized clinical trials by their nature are focused on specific disease states with the exclusion of other concurrent medical problems. They include populations that often have little resemblance to the patients that you and I see in the clinic or hospital free of any comorbidity. The entry restrictions are crafted to identify patients who are most likely to benefit from the drug or device under study and to ensure their safety during its progress. Although not exclusive to the younger patient, the trials tend to recruit younger patients with little comorbidity.

The demographic restrictions on the design and management of clinical trials make it even more difficult to apply their results to guidelines and quality standards. Unfortunately, we have few data which reflect on either the safety or efficacy when “proven” therapy is applied to the general and particularly the Medicare patient.

The Medicare population is considerably older than patients entered into randomized clinical trials, with a greater mortality and morbidity burden of comorbid disease. However, they now represent the majority of patients admitted to the hospital with acute myocardial infarction. A recent publication using data collected over 9 years from 1992–1993 to 2000–2001 from the Medicare database sheds light on important trends that occurred in that population from that period (Circulation 2006;114:2806–14).

During that time, the Medicare MI patients increased in age from 75.7 years to 78.3 years and a quarter of those patients were over 85. The incidence of ST-segment elevation MI decreased from 37.4% to 23.5%. Because of the increased incidence of concomitant morbidity such as diabetes, chronic renal disease, and pulmonary disease, only about a third of patients surviving their MIs were “ideal patients” to whom guidelines or quality standards could be applied. During the study period the days in the hospital decreased from 10.1 days to 6.9 days. Although mortality adjusted for comorbidity had decreased during that period, the 1-year crude mortality increased from 27.6% to 31.0%.

It is clear from these observations that much of the clinical trial research that influences “evidence-based” medicine does not fully describe the reality of the world we function in. The science of clinical trials, highly refined in the last 50 years, has provided an immense amount of information about medical therapeutics. Yet it provides only a snapshot in time in a clinical environment that is changing rapidly around us. This is particularly true when studying degenerative diseases such as cardiovascular disease, which is influenced by a rapidly aging population. This study emphasizes the striking difficulty associated with the application of MI guidelines and standards to the Medicare population that has to a large degree been essentially excluded from contemporary clinical research studies. It is clear that a more dynamic access to the Medicare database could provide important insight into the risks and benefits of cardiac therapy. The sooner we have that information, the sooner we can be more effective at applying appropriate therapy to the real world and our aging patients.

Mr. Salvatore Armani is on my schedule today. I saw him about 4 weeks ago when he was referred because he was experiencing chest pressure climbing up a flight of stairs.

I had seen him almost 3 years ago when he was 65 and was referred to me for the treatment of his hypertension. In the interval, he had been followed by his internist until the development of his recent symptoms. His blood pressure was fairly well controlled on thiazide diuretics and a calcium entry blocker. His internist had started him on statin therapy.

Although it was clear that his symptoms represented angina, I ordered an exercise echocardiogram to define the ischemic region of his ventricle and to get a feeling about the severity of his symptoms. Last week, his stress echocardiogram came back indicating that he had significant ECG and echocardiographic evidence of ischemia in the posterolateral region of the ventricle occurring in the second phase of his stress test when his heart rate reached 120 and his blood pressure was 170/80. He had experienced some chest pressure at that time.

Before the report of the COURAGE (Clinical Outcomes Utilizing Revascularization and Aggressive Drug Evaluation) trial (CARDIOLOGY NEWS, April 2007, p. 1) I would have automatically referred him to my interventional colleagues for angiography and almost certain angioplasty. Today, I paused and reflected on the message of the trial.

It was information that was not new to me. I knew for some time that angioplasty and, for that matter, coronary artery bypass graft, had little or no impact on mortality or morbidity of coronary artery disease. The Coronary Artery Surgery Study (Circulation 1983;68:939–50) more than 20 years ago had clearly shown that, with the exception of those patients with left ventricular dysfunction, there was no mortality benefit achieved by bypass surgery. Even in those patients with left ventricular dysfunction, the benefits were uncertain.

More recently, a meta-analysis of percutaneous coronary intervention over the past 10 years (Circulation 2005;111:2906–12) showed that there was no mortality benefit, but a marginal benefit in angina could be achieved with angioplasty in an era devoid of statin therapy and when ?-blockade was less than optimal. This was information that was easily accessible to anyone reading the cardiology literature, and it was reinforced by American College of Cardiology/American Heart Association guidelines.

On numerous occasions, I had sat down with patients in an attempt to outline these facts, but my lecture routinely fell on deaf ears and my reluctance to arrange an angiogram was perceived by my patients. They thanked me for my advice and went “up the street” to get their angioplasty. I had even given the same lecture to my close friends. They figured that I had not kept up with what was going on in cardiology and drove off to have there angioplasties performed by more “forward looking” cardiologists. Frankly, I had been beaten down and I found it easier to go along with the crowd.

The results of COURAGE may bring in a new era in our understanding of the benefits and risks of percutaneous coronary intervention and how we should apply it in the treatment of coronary artery disease. Today, I have not only medical science behind me, but the Wall Street Journal, the New York Times, and even the Detroit Free Press. All of these papers and many more prided themselves in hyping up the miracles that could be achieved by stents and extolling the wonders performed by the cardiologists “up the street.” Now they were suddenly on my side. They printed in bold headlines that pills were as good as a stent.

I guess I'll try it out again on Sal.

Mr. Salvatore Armani is on my schedule today. I saw him about 4 weeks ago when he was referred because he was experiencing chest pressure climbing up a flight of stairs.

I had seen him almost 3 years ago when he was 65 and was referred to me for the treatment of his hypertension. In the interval, he had been followed by his internist until the development of his recent symptoms. His blood pressure was fairly well controlled on thiazide diuretics and a calcium entry blocker. His internist had started him on statin therapy.

Although it was clear that his symptoms represented angina, I ordered an exercise echocardiogram to define the ischemic region of his ventricle and to get a feeling about the severity of his symptoms. Last week, his stress echocardiogram came back indicating that he had significant ECG and echocardiographic evidence of ischemia in the posterolateral region of the ventricle occurring in the second phase of his stress test when his heart rate reached 120 and his blood pressure was 170/80. He had experienced some chest pressure at that time.

Before the report of the COURAGE (Clinical Outcomes Utilizing Revascularization and Aggressive Drug Evaluation) trial (CARDIOLOGY NEWS, April 2007, p. 1) I would have automatically referred him to my interventional colleagues for angiography and almost certain angioplasty. Today, I paused and reflected on the message of the trial.

It was information that was not new to me. I knew for some time that angioplasty and, for that matter, coronary artery bypass graft, had little or no impact on mortality or morbidity of coronary artery disease. The Coronary Artery Surgery Study (Circulation 1983;68:939–50) more than 20 years ago had clearly shown that, with the exception of those patients with left ventricular dysfunction, there was no mortality benefit achieved by bypass surgery. Even in those patients with left ventricular dysfunction, the benefits were uncertain.

More recently, a meta-analysis of percutaneous coronary intervention over the past 10 years (Circulation 2005;111:2906–12) showed that there was no mortality benefit, but a marginal benefit in angina could be achieved with angioplasty in an era devoid of statin therapy and when ?-blockade was less than optimal. This was information that was easily accessible to anyone reading the cardiology literature, and it was reinforced by American College of Cardiology/American Heart Association guidelines.

On numerous occasions, I had sat down with patients in an attempt to outline these facts, but my lecture routinely fell on deaf ears and my reluctance to arrange an angiogram was perceived by my patients. They thanked me for my advice and went “up the street” to get their angioplasty. I had even given the same lecture to my close friends. They figured that I had not kept up with what was going on in cardiology and drove off to have there angioplasties performed by more “forward looking” cardiologists. Frankly, I had been beaten down and I found it easier to go along with the crowd.

The results of COURAGE may bring in a new era in our understanding of the benefits and risks of percutaneous coronary intervention and how we should apply it in the treatment of coronary artery disease. Today, I have not only medical science behind me, but the Wall Street Journal, the New York Times, and even the Detroit Free Press. All of these papers and many more prided themselves in hyping up the miracles that could be achieved by stents and extolling the wonders performed by the cardiologists “up the street.” Now they were suddenly on my side. They printed in bold headlines that pills were as good as a stent.

I guess I'll try it out again on Sal.

Mr. Salvatore Armani is on my schedule today. I saw him about 4 weeks ago when he was referred because he was experiencing chest pressure climbing up a flight of stairs.

I had seen him almost 3 years ago when he was 65 and was referred to me for the treatment of his hypertension. In the interval, he had been followed by his internist until the development of his recent symptoms. His blood pressure was fairly well controlled on thiazide diuretics and a calcium entry blocker. His internist had started him on statin therapy.

Although it was clear that his symptoms represented angina, I ordered an exercise echocardiogram to define the ischemic region of his ventricle and to get a feeling about the severity of his symptoms. Last week, his stress echocardiogram came back indicating that he had significant ECG and echocardiographic evidence of ischemia in the posterolateral region of the ventricle occurring in the second phase of his stress test when his heart rate reached 120 and his blood pressure was 170/80. He had experienced some chest pressure at that time.

Before the report of the COURAGE (Clinical Outcomes Utilizing Revascularization and Aggressive Drug Evaluation) trial (CARDIOLOGY NEWS, April 2007, p. 1) I would have automatically referred him to my interventional colleagues for angiography and almost certain angioplasty. Today, I paused and reflected on the message of the trial.

It was information that was not new to me. I knew for some time that angioplasty and, for that matter, coronary artery bypass graft, had little or no impact on mortality or morbidity of coronary artery disease. The Coronary Artery Surgery Study (Circulation 1983;68:939–50) more than 20 years ago had clearly shown that, with the exception of those patients with left ventricular dysfunction, there was no mortality benefit achieved by bypass surgery. Even in those patients with left ventricular dysfunction, the benefits were uncertain.

More recently, a meta-analysis of percutaneous coronary intervention over the past 10 years (Circulation 2005;111:2906–12) showed that there was no mortality benefit, but a marginal benefit in angina could be achieved with angioplasty in an era devoid of statin therapy and when ?-blockade was less than optimal. This was information that was easily accessible to anyone reading the cardiology literature, and it was reinforced by American College of Cardiology/American Heart Association guidelines.

On numerous occasions, I had sat down with patients in an attempt to outline these facts, but my lecture routinely fell on deaf ears and my reluctance to arrange an angiogram was perceived by my patients. They thanked me for my advice and went “up the street” to get their angioplasty. I had even given the same lecture to my close friends. They figured that I had not kept up with what was going on in cardiology and drove off to have there angioplasties performed by more “forward looking” cardiologists. Frankly, I had been beaten down and I found it easier to go along with the crowd.

The results of COURAGE may bring in a new era in our understanding of the benefits and risks of percutaneous coronary intervention and how we should apply it in the treatment of coronary artery disease. Today, I have not only medical science behind me, but the Wall Street Journal, the New York Times, and even the Detroit Free Press. All of these papers and many more prided themselves in hyping up the miracles that could be achieved by stents and extolling the wonders performed by the cardiologists “up the street.” Now they were suddenly on my side. They printed in bold headlines that pills were as good as a stent.

I guess I'll try it out again on Sal.

Achieving selection at a national or international program for the late-breaking clinical trials session is the “brass ring” for both the clinical trialist and sponsor, whether they are the pharmaceutical industry or the National Institutes of Health. A double brass ring is achieved if you can get simultaneous publication of your results in JAMA or, even better, in the New England Journal of Medicine.

This year at the American College of Cardiology meeting there were three separate late-breaking clinical trial (LBCT) sessions with 13 presentations and three sessions devoted to “smaller” LBCTs with 18 presentations. The mini-LBCT is a new addition to the program, as if the 13 LBCTs were not enough. In addition, the Innovations in Intervention Summit (I2) held five LBCT sessions with a total of 24 presentations. This seems to be a high water mark and may be a manifestation of either the plethora of clinical trials coming to fruition at this time or a lowering of scientific standards.

These are high-visibility sessions presented in auditoriums with audiences of up to 5,000, made up of doctors, nurses, a smattering of members of the press and, most importantly, representatives of the investment community. Measured against the more than 30 simultaneous sessions held at the mammoth Morial Convention Center in New Orleans with audiences averaging 100 or less, the magnetism of the LBCTs is obvious. At least 20% of the attendees at the annual meeting are breathlessly awaiting the next LBCT presentation.

The selection process for the program and its presentation, and, if you are lucky, a simultaneous publication, is tied up in a litany of embargo agreements meant to prevent any release of information prior to that magic moment of presentation. The precise penalty for breaking the embargo and the prerelease of data is not spelled out. Unlike other scientific presentations, no abstracts are printed in the program, so the audience is in the dark about both the design and the outcome of the trial. The reason for all this secrecy is not entirely clear, but more than likely it can be ascribed to marketing on the part of both the College and the journals.

Why good science should be cloaked in such mystery is not obvious. This year, the veil of secrecy was lifted from two presentations—on ranolazine and the investigational antioxidant succinobucol—that were preceded by reports by the drug makers of their failure to achieve the primary end points because of a potential impact on the stock price of the drug. Of course, not all of the trials present have positive outcomes. In fact, a positive outcome is somewhat of a rarity even though the science may be very important.

All of this hocus-pocus has absolutely nothing to do with science or with the dissemination of information other than restricting it. If anything, it suppresses and delays the process. It does result in inflating the impact of the LBCTs, no matter what their scientific and clinical importance, and it diminishes the value of the science of other presentations.

One way to deflate the hype is to publish in advance the abstracts of the LBCT, either in the program or as a supplement handed out at registration. This would provide the audience with some background to evaluate and understand the importance of the data when the magic moment of presentation occurs. Of course, the best way to deal with it is to remove all the restrictions associated with the presentation and publication of LBCTs, but, as one cardiology wonk put it, “It's all theater.”

Achieving selection at a national or international program for the late-breaking clinical trials session is the “brass ring” for both the clinical trialist and sponsor, whether they are the pharmaceutical industry or the National Institutes of Health. A double brass ring is achieved if you can get simultaneous publication of your results in JAMA or, even better, in the New England Journal of Medicine.

This year at the American College of Cardiology meeting there were three separate late-breaking clinical trial (LBCT) sessions with 13 presentations and three sessions devoted to “smaller” LBCTs with 18 presentations. The mini-LBCT is a new addition to the program, as if the 13 LBCTs were not enough. In addition, the Innovations in Intervention Summit (I2) held five LBCT sessions with a total of 24 presentations. This seems to be a high water mark and may be a manifestation of either the plethora of clinical trials coming to fruition at this time or a lowering of scientific standards.

These are high-visibility sessions presented in auditoriums with audiences of up to 5,000, made up of doctors, nurses, a smattering of members of the press and, most importantly, representatives of the investment community. Measured against the more than 30 simultaneous sessions held at the mammoth Morial Convention Center in New Orleans with audiences averaging 100 or less, the magnetism of the LBCTs is obvious. At least 20% of the attendees at the annual meeting are breathlessly awaiting the next LBCT presentation.

The selection process for the program and its presentation, and, if you are lucky, a simultaneous publication, is tied up in a litany of embargo agreements meant to prevent any release of information prior to that magic moment of presentation. The precise penalty for breaking the embargo and the prerelease of data is not spelled out. Unlike other scientific presentations, no abstracts are printed in the program, so the audience is in the dark about both the design and the outcome of the trial. The reason for all this secrecy is not entirely clear, but more than likely it can be ascribed to marketing on the part of both the College and the journals.

Why good science should be cloaked in such mystery is not obvious. This year, the veil of secrecy was lifted from two presentations—on ranolazine and the investigational antioxidant succinobucol—that were preceded by reports by the drug makers of their failure to achieve the primary end points because of a potential impact on the stock price of the drug. Of course, not all of the trials present have positive outcomes. In fact, a positive outcome is somewhat of a rarity even though the science may be very important.

All of this hocus-pocus has absolutely nothing to do with science or with the dissemination of information other than restricting it. If anything, it suppresses and delays the process. It does result in inflating the impact of the LBCTs, no matter what their scientific and clinical importance, and it diminishes the value of the science of other presentations.

One way to deflate the hype is to publish in advance the abstracts of the LBCT, either in the program or as a supplement handed out at registration. This would provide the audience with some background to evaluate and understand the importance of the data when the magic moment of presentation occurs. Of course, the best way to deal with it is to remove all the restrictions associated with the presentation and publication of LBCTs, but, as one cardiology wonk put it, “It's all theater.”

Achieving selection at a national or international program for the late-breaking clinical trials session is the “brass ring” for both the clinical trialist and sponsor, whether they are the pharmaceutical industry or the National Institutes of Health. A double brass ring is achieved if you can get simultaneous publication of your results in JAMA or, even better, in the New England Journal of Medicine.

This year at the American College of Cardiology meeting there were three separate late-breaking clinical trial (LBCT) sessions with 13 presentations and three sessions devoted to “smaller” LBCTs with 18 presentations. The mini-LBCT is a new addition to the program, as if the 13 LBCTs were not enough. In addition, the Innovations in Intervention Summit (I2) held five LBCT sessions with a total of 24 presentations. This seems to be a high water mark and may be a manifestation of either the plethora of clinical trials coming to fruition at this time or a lowering of scientific standards.

These are high-visibility sessions presented in auditoriums with audiences of up to 5,000, made up of doctors, nurses, a smattering of members of the press and, most importantly, representatives of the investment community. Measured against the more than 30 simultaneous sessions held at the mammoth Morial Convention Center in New Orleans with audiences averaging 100 or less, the magnetism of the LBCTs is obvious. At least 20% of the attendees at the annual meeting are breathlessly awaiting the next LBCT presentation.

The selection process for the program and its presentation, and, if you are lucky, a simultaneous publication, is tied up in a litany of embargo agreements meant to prevent any release of information prior to that magic moment of presentation. The precise penalty for breaking the embargo and the prerelease of data is not spelled out. Unlike other scientific presentations, no abstracts are printed in the program, so the audience is in the dark about both the design and the outcome of the trial. The reason for all this secrecy is not entirely clear, but more than likely it can be ascribed to marketing on the part of both the College and the journals.

Why good science should be cloaked in such mystery is not obvious. This year, the veil of secrecy was lifted from two presentations—on ranolazine and the investigational antioxidant succinobucol—that were preceded by reports by the drug makers of their failure to achieve the primary end points because of a potential impact on the stock price of the drug. Of course, not all of the trials present have positive outcomes. In fact, a positive outcome is somewhat of a rarity even though the science may be very important.

All of this hocus-pocus has absolutely nothing to do with science or with the dissemination of information other than restricting it. If anything, it suppresses and delays the process. It does result in inflating the impact of the LBCTs, no matter what their scientific and clinical importance, and it diminishes the value of the science of other presentations.

One way to deflate the hype is to publish in advance the abstracts of the LBCT, either in the program or as a supplement handed out at registration. This would provide the audience with some background to evaluate and understand the importance of the data when the magic moment of presentation occurs. Of course, the best way to deal with it is to remove all the restrictions associated with the presentation and publication of LBCTs, but, as one cardiology wonk put it, “It's all theater.”

The schism that has opened between the Society for Cardiovascular Angiography and Interventions and the guideline committee of the American Heart Association and American College of Cardiology in regard to stand-alone percutaneous coronary intervention is reminiscent of the advice given to teenagers about alcohol. It is clear that they shouldn't drink, but if they do, we should tell them how to do it safely. On the other hand, some would suggest that they should just say “No.”

The SCAI indicates that it is not “promoting” elective PCI without on-site surgical support. It is just providing “how-to” guidelines in case you are thinking about setting up a system to perform elective PCI in that setting. After all, PCI can be addicting. The fact that stand-alone PCI is being carried out in many communities in North America, not to mention most of the rest of the world, makes little difference to the AHA and ACC guideline committees. They are sticking to their previous statements that were supported by the SCAI, and just saying “No.”

Where is all of this coming from? It is hard to believe that with almost a million elective PCIs performed in the United States, there are patients going untreated because of a shortage of facilities or trained cardiologists. One could make a case that patients in remote areas of this country are not being well served if they need a PCI for the treatment of an acute MI, but thrombolysis is still a reasonable alternative with proven benefits.

There is a sense that although there is a concern about the patients in remote settings, much of the pressure for these changes is coming from urban areas. Many hospitals that are performing emergency primary PCI for acute MI in urban areas without on-site surgical backup use interventionalists who have elective PCI experience in other surgically supported laboratories. Expansion of elective PCI to these hospitals will not expand the availability of PCI to new populations, but will decrease the number of procedures performed at the established laboratories. If quality can be measured by quantity, these efforts will certainly not improve it. In addition, many of these established laboratories require a large volume of patients to train interventionalists.

Although it is quite possible that surgically supported interventional laboratories are in short supply in some places, such is not the case in the United States. In fact, there is an expansion of cardiosurgical programs, in part to support access to elective PCI. This is, of course, occurring largely as hospital marketing ventures in the paradoxical setting of a nationwide decrease in volume of coronary artery bypass surgeries. Cardiac surgery remains a profit center and often adds to the eminence of community hospitals.

It is clear that the SCAI statement represents a push to wider acceptance of stand-alone PCI throughout the country. The fact that complications and need for surgical intervention are rare in the centers now performing PCI has been used as an argument for its broader availability. Whether the same safety profile can be achieved when performed at smaller institutions with lower volumes remains to be seen.

The experience of transferring therapeutic interventions to the real world has not always been successful. In weighing the benefits of the expansion of PCI to this wider community, it may be that the appropriate response is just to say “No.”

The schism that has opened between the Society for Cardiovascular Angiography and Interventions and the guideline committee of the American Heart Association and American College of Cardiology in regard to stand-alone percutaneous coronary intervention is reminiscent of the advice given to teenagers about alcohol. It is clear that they shouldn't drink, but if they do, we should tell them how to do it safely. On the other hand, some would suggest that they should just say “No.”

The SCAI indicates that it is not “promoting” elective PCI without on-site surgical support. It is just providing “how-to” guidelines in case you are thinking about setting up a system to perform elective PCI in that setting. After all, PCI can be addicting. The fact that stand-alone PCI is being carried out in many communities in North America, not to mention most of the rest of the world, makes little difference to the AHA and ACC guideline committees. They are sticking to their previous statements that were supported by the SCAI, and just saying “No.”

Where is all of this coming from? It is hard to believe that with almost a million elective PCIs performed in the United States, there are patients going untreated because of a shortage of facilities or trained cardiologists. One could make a case that patients in remote areas of this country are not being well served if they need a PCI for the treatment of an acute MI, but thrombolysis is still a reasonable alternative with proven benefits.

There is a sense that although there is a concern about the patients in remote settings, much of the pressure for these changes is coming from urban areas. Many hospitals that are performing emergency primary PCI for acute MI in urban areas without on-site surgical backup use interventionalists who have elective PCI experience in other surgically supported laboratories. Expansion of elective PCI to these hospitals will not expand the availability of PCI to new populations, but will decrease the number of procedures performed at the established laboratories. If quality can be measured by quantity, these efforts will certainly not improve it. In addition, many of these established laboratories require a large volume of patients to train interventionalists.

Although it is quite possible that surgically supported interventional laboratories are in short supply in some places, such is not the case in the United States. In fact, there is an expansion of cardiosurgical programs, in part to support access to elective PCI. This is, of course, occurring largely as hospital marketing ventures in the paradoxical setting of a nationwide decrease in volume of coronary artery bypass surgeries. Cardiac surgery remains a profit center and often adds to the eminence of community hospitals.

It is clear that the SCAI statement represents a push to wider acceptance of stand-alone PCI throughout the country. The fact that complications and need for surgical intervention are rare in the centers now performing PCI has been used as an argument for its broader availability. Whether the same safety profile can be achieved when performed at smaller institutions with lower volumes remains to be seen.

The experience of transferring therapeutic interventions to the real world has not always been successful. In weighing the benefits of the expansion of PCI to this wider community, it may be that the appropriate response is just to say “No.”

The schism that has opened between the Society for Cardiovascular Angiography and Interventions and the guideline committee of the American Heart Association and American College of Cardiology in regard to stand-alone percutaneous coronary intervention is reminiscent of the advice given to teenagers about alcohol. It is clear that they shouldn't drink, but if they do, we should tell them how to do it safely. On the other hand, some would suggest that they should just say “No.”

The SCAI indicates that it is not “promoting” elective PCI without on-site surgical support. It is just providing “how-to” guidelines in case you are thinking about setting up a system to perform elective PCI in that setting. After all, PCI can be addicting. The fact that stand-alone PCI is being carried out in many communities in North America, not to mention most of the rest of the world, makes little difference to the AHA and ACC guideline committees. They are sticking to their previous statements that were supported by the SCAI, and just saying “No.”

Where is all of this coming from? It is hard to believe that with almost a million elective PCIs performed in the United States, there are patients going untreated because of a shortage of facilities or trained cardiologists. One could make a case that patients in remote areas of this country are not being well served if they need a PCI for the treatment of an acute MI, but thrombolysis is still a reasonable alternative with proven benefits.

There is a sense that although there is a concern about the patients in remote settings, much of the pressure for these changes is coming from urban areas. Many hospitals that are performing emergency primary PCI for acute MI in urban areas without on-site surgical backup use interventionalists who have elective PCI experience in other surgically supported laboratories. Expansion of elective PCI to these hospitals will not expand the availability of PCI to new populations, but will decrease the number of procedures performed at the established laboratories. If quality can be measured by quantity, these efforts will certainly not improve it. In addition, many of these established laboratories require a large volume of patients to train interventionalists.

Although it is quite possible that surgically supported interventional laboratories are in short supply in some places, such is not the case in the United States. In fact, there is an expansion of cardiosurgical programs, in part to support access to elective PCI. This is, of course, occurring largely as hospital marketing ventures in the paradoxical setting of a nationwide decrease in volume of coronary artery bypass surgeries. Cardiac surgery remains a profit center and often adds to the eminence of community hospitals.

It is clear that the SCAI statement represents a push to wider acceptance of stand-alone PCI throughout the country. The fact that complications and need for surgical intervention are rare in the centers now performing PCI has been used as an argument for its broader availability. Whether the same safety profile can be achieved when performed at smaller institutions with lower volumes remains to be seen.

The experience of transferring therapeutic interventions to the real world has not always been successful. In weighing the benefits of the expansion of PCI to this wider community, it may be that the appropriate response is just to say “No.”

The American College of Cardiology and the American College of Physicians have signed on to “pay for performance” whether we like it or not.

To prevent the scheduled 5% cut in physicians' fees under Medicare, our representatives agreed to a program that will pay physicians who volunteer to participate, an opportunity to win quality points to receive an additional 1.5% annually.

It is worth noting that the ACC and the ACP were 2 of only 4 out of 21 medical groups that supported the legislation. Notably, the American Medical Association chose to decline, having resisted this deal in part because of its reluctance to accept the concept of pay for performance.

Pay for performance will reward those physicians who adhere to quality standards, whatever they may be, and penalize those who do not. Most observers feel that this has nothing to do with quality and everything to do with the cost of care. Many are skeptical that it will achieve either objective.

The idea that doctors must be financially rewarded to provide quality medical care should be abhorrent to any practitioner. It suggests that doctors know what is best for the patient but will not provide that care unless they get a few more dollars in their pockets.

The Centers for Medicare and Medicaid Services and the Institute of Medicine have been the main enthusiasts for pay for performance. If they were serious about the quality of medical care, they might at least provide casual support for postgraduate education. Instead, postgraduate education remains the province of the pharmaceutical and device industries, which pay for at least 60% of these programs.

Long gone is the federal and academic support of postgraduate education. Instead, industry gets to set the educational agenda.

That agenda speaks to the increased use of new and expensive drugs and devices, which has a profound effect on increasing health care costs with marginal benefit to quality of care in a public health context.

Quality improvement has been the hallmark of the programs developed by the cardiology community and the ACC. In fact, improvements in the treatment and prevention of heart disease have comprised the major quality achievements of the past decade. They have been driven not by money, but by peer pressure and education. The quality standards that have been developed have gone a long way in decreasing hospital mortality.

The New York State coronary bypass surgery report-card system, instituted in 1989, has been the poster child of quality programs. The measurement and publication of mortality rates led to the establishment of benchmarks for performance and a significant decrease in bypass surgical mortality.

The establishment of quality standards for the treatment of myocardial infarction and heart failure has resulted in the incorporation of optimal standard therapy for discharge medication. At the same time, the establishment of optimal door-to-balloon time to angioplasty for ST-elevation myocardial infarctions remains under study but has already led to methodologies to achieve optimal time and improve infarct survival.

All of these initiatives have been led by the cardiology community and the ACC and were achieved by the profession without the onerous method of paying a doctor for better performance. The cardiology community has been at the forefront of quality initiatives, yet it was all scrapped when the ACC agreed to the Faustian deal of accepting pay for performance to prevent the 5% cut in physician pay. To do that, our representatives agreed to pay for quality rather than making it a professional duty.

So much for peer pressure and education to effect change. Now it's all in your paycheck.

The American College of Cardiology and the American College of Physicians have signed on to “pay for performance” whether we like it or not.

To prevent the scheduled 5% cut in physicians' fees under Medicare, our representatives agreed to a program that will pay physicians who volunteer to participate, an opportunity to win quality points to receive an additional 1.5% annually.

It is worth noting that the ACC and the ACP were 2 of only 4 out of 21 medical groups that supported the legislation. Notably, the American Medical Association chose to decline, having resisted this deal in part because of its reluctance to accept the concept of pay for performance.

Pay for performance will reward those physicians who adhere to quality standards, whatever they may be, and penalize those who do not. Most observers feel that this has nothing to do with quality and everything to do with the cost of care. Many are skeptical that it will achieve either objective.

The idea that doctors must be financially rewarded to provide quality medical care should be abhorrent to any practitioner. It suggests that doctors know what is best for the patient but will not provide that care unless they get a few more dollars in their pockets.

The Centers for Medicare and Medicaid Services and the Institute of Medicine have been the main enthusiasts for pay for performance. If they were serious about the quality of medical care, they might at least provide casual support for postgraduate education. Instead, postgraduate education remains the province of the pharmaceutical and device industries, which pay for at least 60% of these programs.

Long gone is the federal and academic support of postgraduate education. Instead, industry gets to set the educational agenda.

That agenda speaks to the increased use of new and expensive drugs and devices, which has a profound effect on increasing health care costs with marginal benefit to quality of care in a public health context.

Quality improvement has been the hallmark of the programs developed by the cardiology community and the ACC. In fact, improvements in the treatment and prevention of heart disease have comprised the major quality achievements of the past decade. They have been driven not by money, but by peer pressure and education. The quality standards that have been developed have gone a long way in decreasing hospital mortality.

The New York State coronary bypass surgery report-card system, instituted in 1989, has been the poster child of quality programs. The measurement and publication of mortality rates led to the establishment of benchmarks for performance and a significant decrease in bypass surgical mortality.

The establishment of quality standards for the treatment of myocardial infarction and heart failure has resulted in the incorporation of optimal standard therapy for discharge medication. At the same time, the establishment of optimal door-to-balloon time to angioplasty for ST-elevation myocardial infarctions remains under study but has already led to methodologies to achieve optimal time and improve infarct survival.

All of these initiatives have been led by the cardiology community and the ACC and were achieved by the profession without the onerous method of paying a doctor for better performance. The cardiology community has been at the forefront of quality initiatives, yet it was all scrapped when the ACC agreed to the Faustian deal of accepting pay for performance to prevent the 5% cut in physician pay. To do that, our representatives agreed to pay for quality rather than making it a professional duty.

So much for peer pressure and education to effect change. Now it's all in your paycheck.

The American College of Cardiology and the American College of Physicians have signed on to “pay for performance” whether we like it or not.

To prevent the scheduled 5% cut in physicians' fees under Medicare, our representatives agreed to a program that will pay physicians who volunteer to participate, an opportunity to win quality points to receive an additional 1.5% annually.

It is worth noting that the ACC and the ACP were 2 of only 4 out of 21 medical groups that supported the legislation. Notably, the American Medical Association chose to decline, having resisted this deal in part because of its reluctance to accept the concept of pay for performance.

Pay for performance will reward those physicians who adhere to quality standards, whatever they may be, and penalize those who do not. Most observers feel that this has nothing to do with quality and everything to do with the cost of care. Many are skeptical that it will achieve either objective.

The idea that doctors must be financially rewarded to provide quality medical care should be abhorrent to any practitioner. It suggests that doctors know what is best for the patient but will not provide that care unless they get a few more dollars in their pockets.

The Centers for Medicare and Medicaid Services and the Institute of Medicine have been the main enthusiasts for pay for performance. If they were serious about the quality of medical care, they might at least provide casual support for postgraduate education. Instead, postgraduate education remains the province of the pharmaceutical and device industries, which pay for at least 60% of these programs.

Long gone is the federal and academic support of postgraduate education. Instead, industry gets to set the educational agenda.

That agenda speaks to the increased use of new and expensive drugs and devices, which has a profound effect on increasing health care costs with marginal benefit to quality of care in a public health context.

Quality improvement has been the hallmark of the programs developed by the cardiology community and the ACC. In fact, improvements in the treatment and prevention of heart disease have comprised the major quality achievements of the past decade. They have been driven not by money, but by peer pressure and education. The quality standards that have been developed have gone a long way in decreasing hospital mortality.

The New York State coronary bypass surgery report-card system, instituted in 1989, has been the poster child of quality programs. The measurement and publication of mortality rates led to the establishment of benchmarks for performance and a significant decrease in bypass surgical mortality.

The establishment of quality standards for the treatment of myocardial infarction and heart failure has resulted in the incorporation of optimal standard therapy for discharge medication. At the same time, the establishment of optimal door-to-balloon time to angioplasty for ST-elevation myocardial infarctions remains under study but has already led to methodologies to achieve optimal time and improve infarct survival.

All of these initiatives have been led by the cardiology community and the ACC and were achieved by the profession without the onerous method of paying a doctor for better performance. The cardiology community has been at the forefront of quality initiatives, yet it was all scrapped when the ACC agreed to the Faustian deal of accepting pay for performance to prevent the 5% cut in physician pay. To do that, our representatives agreed to pay for quality rather than making it a professional duty.

So much for peer pressure and education to effect change. Now it's all in your paycheck.

Randomized clinical trials are built on the premise that if you know the answer you should not ask the question. With that framework, they are risky business.

The stock market has recently learned all about the downside of those risks. Nevertheless, the scientific community and industry have invested large amounts of time and energy in randomized clinical trials (RCTs) in an attempt to translate bench research to the patient's bedside. They also have required the patient's commitment to participate in these studies. RCTs have exposed the fallacies of many concepts but also have elucidated the benefits of a host of cardiovascular drugs. The success of clinical trials has resulted in the profound decrease in cardiovascular mortality that we have experienced in the last half-century.

It was not too long ago that RCTs provided the proof of the concept that lowering LDL cholesterol could result in improved survival in patients with coronary artery disease. As a result, statins have become established as one of the foundations of contemporary therapy for the treatment of atherosclerotic disease. Prior to statins, there was a variety of drugs that were studied in RCTs in an attempt to prevent coronary disease. The clinical success associated with the lowering of LDL was followed by the tantalizing potential of even greater benefit that might be attained by raising HDL. Supported with both epidemiologic and laboratory data, the pharmaceutical industry responded to the challenge by designing drugs that could specifically raise HDL.

Unfortunately, we still do not have data to support the concept that raising HDL is beneficial to humans. In the last few weeks we have learned, as a result of the ILLUMINATE trial, that our first, and probably not last, foray into the realm of raising HDL was associated with increased mortality in the patients receiving the active drug. We know little else about the trial to explain these findings, with the exception that the drug torcetrapib, a cholesteryl ester transfer protein (CETP) inhibitor, results in increases not only in HDL but also in systemic blood pressure. Whether the blood pressure response observed in the recent Pfizer trial is inherent in all molecules of this class or unique to torcetrapib remains for further investigation. There also is a suspicion that CETP inhibitors actually may increase cholesterol deposition in the atherosclerotic plaque. Niacin and exercise have been known to increase HDL, but there is little information to suggest that this is beneficial. The results from ILLUMINATE may cause some reflection on the purported benefit of raising HDL.

Other drugs are under investigation in regard to their possible beneficial effects on the progression of plaque formation. Antisense drugs directed at modifying apolipoprotein B and 5-lipoxygenase-activating proteins directed at down-regulation of leukotrienes are in the preliminary phase of clinical studies. In addition, preliminary data suggest that the administration of recombinant apo-A₁ Milano may have a significant effect on decreasing plaque size using intravascular ultrasound imaging.

It is clear that the universality of atherosclerosis speaks to the need for further investigation. The experience with torcetrapib is just one phase in our search for better therapy. It does send a message to the investment community that the buyer should beware: Science is a tricky business.

Randomized clinical trials are built on the premise that if you know the answer you should not ask the question. With that framework, they are risky business.

The stock market has recently learned all about the downside of those risks. Nevertheless, the scientific community and industry have invested large amounts of time and energy in randomized clinical trials (RCTs) in an attempt to translate bench research to the patient's bedside. They also have required the patient's commitment to participate in these studies. RCTs have exposed the fallacies of many concepts but also have elucidated the benefits of a host of cardiovascular drugs. The success of clinical trials has resulted in the profound decrease in cardiovascular mortality that we have experienced in the last half-century.

It was not too long ago that RCTs provided the proof of the concept that lowering LDL cholesterol could result in improved survival in patients with coronary artery disease. As a result, statins have become established as one of the foundations of contemporary therapy for the treatment of atherosclerotic disease. Prior to statins, there was a variety of drugs that were studied in RCTs in an attempt to prevent coronary disease. The clinical success associated with the lowering of LDL was followed by the tantalizing potential of even greater benefit that might be attained by raising HDL. Supported with both epidemiologic and laboratory data, the pharmaceutical industry responded to the challenge by designing drugs that could specifically raise HDL.

Unfortunately, we still do not have data to support the concept that raising HDL is beneficial to humans. In the last few weeks we have learned, as a result of the ILLUMINATE trial, that our first, and probably not last, foray into the realm of raising HDL was associated with increased mortality in the patients receiving the active drug. We know little else about the trial to explain these findings, with the exception that the drug torcetrapib, a cholesteryl ester transfer protein (CETP) inhibitor, results in increases not only in HDL but also in systemic blood pressure. Whether the blood pressure response observed in the recent Pfizer trial is inherent in all molecules of this class or unique to torcetrapib remains for further investigation. There also is a suspicion that CETP inhibitors actually may increase cholesterol deposition in the atherosclerotic plaque. Niacin and exercise have been known to increase HDL, but there is little information to suggest that this is beneficial. The results from ILLUMINATE may cause some reflection on the purported benefit of raising HDL.

Other drugs are under investigation in regard to their possible beneficial effects on the progression of plaque formation. Antisense drugs directed at modifying apolipoprotein B and 5-lipoxygenase-activating proteins directed at down-regulation of leukotrienes are in the preliminary phase of clinical studies. In addition, preliminary data suggest that the administration of recombinant apo-A₁ Milano may have a significant effect on decreasing plaque size using intravascular ultrasound imaging.

It is clear that the universality of atherosclerosis speaks to the need for further investigation. The experience with torcetrapib is just one phase in our search for better therapy. It does send a message to the investment community that the buyer should beware: Science is a tricky business.

Randomized clinical trials are built on the premise that if you know the answer you should not ask the question. With that framework, they are risky business.

The stock market has recently learned all about the downside of those risks. Nevertheless, the scientific community and industry have invested large amounts of time and energy in randomized clinical trials (RCTs) in an attempt to translate bench research to the patient's bedside. They also have required the patient's commitment to participate in these studies. RCTs have exposed the fallacies of many concepts but also have elucidated the benefits of a host of cardiovascular drugs. The success of clinical trials has resulted in the profound decrease in cardiovascular mortality that we have experienced in the last half-century.

It was not too long ago that RCTs provided the proof of the concept that lowering LDL cholesterol could result in improved survival in patients with coronary artery disease. As a result, statins have become established as one of the foundations of contemporary therapy for the treatment of atherosclerotic disease. Prior to statins, there was a variety of drugs that were studied in RCTs in an attempt to prevent coronary disease. The clinical success associated with the lowering of LDL was followed by the tantalizing potential of even greater benefit that might be attained by raising HDL. Supported with both epidemiologic and laboratory data, the pharmaceutical industry responded to the challenge by designing drugs that could specifically raise HDL.

Unfortunately, we still do not have data to support the concept that raising HDL is beneficial to humans. In the last few weeks we have learned, as a result of the ILLUMINATE trial, that our first, and probably not last, foray into the realm of raising HDL was associated with increased mortality in the patients receiving the active drug. We know little else about the trial to explain these findings, with the exception that the drug torcetrapib, a cholesteryl ester transfer protein (CETP) inhibitor, results in increases not only in HDL but also in systemic blood pressure. Whether the blood pressure response observed in the recent Pfizer trial is inherent in all molecules of this class or unique to torcetrapib remains for further investigation. There also is a suspicion that CETP inhibitors actually may increase cholesterol deposition in the atherosclerotic plaque. Niacin and exercise have been known to increase HDL, but there is little information to suggest that this is beneficial. The results from ILLUMINATE may cause some reflection on the purported benefit of raising HDL.

Other drugs are under investigation in regard to their possible beneficial effects on the progression of plaque formation. Antisense drugs directed at modifying apolipoprotein B and 5-lipoxygenase-activating proteins directed at down-regulation of leukotrienes are in the preliminary phase of clinical studies. In addition, preliminary data suggest that the administration of recombinant apo-A₁ Milano may have a significant effect on decreasing plaque size using intravascular ultrasound imaging.

It is clear that the universality of atherosclerosis speaks to the need for further investigation. The experience with torcetrapib is just one phase in our search for better therapy. It does send a message to the investment community that the buyer should beware: Science is a tricky business.