Heart of the Matter

Readmissions after hospital discharge for acute myocardial infarction, heart failure, and pneumonia have now become major targets for proposed Medicare savings as part of the current budget tightening in Washington. Hospitals in the past have viewed readmissions either with disdain and disinterest or as a "cash cow."

Readmissions have been good business, as long as Medicare reimbursed hospitals for individual admissions no matter how long or short or how frequent. Readmissions are estimated to cost $17 billion annually. As Medicare costs continue to increase, the control of readmissions appears to be a good target for saving some money. As a result, Medicare levied a maximum reduction of 1% on payments last year on 307 of the nation’s hospitals that were deemed to have too many readmissions (New York Times, Nov. 26, 2012).

Readmissions for AMI and heart failure are among the most frequent hospital admissions and readmissions. Readmissions in cardiology have been an important outcome measure in clinical trials for the last half century. As mortality rates decreased over the years, rehospitalization became more important as clinicians realized its importance in the composite outcome measure of cost and benefit of new therapies. Two of the potential causes of readmission have been early discharge and the lack of postdischarge medical support. The urgency for early discharge for both heart failure and AMI has been driven largely by the misplaced emphasis on shorter hospital stays.

A recent international trial examined readmission rates as an outcome measure in patients who were treated with a percutaneous coronary intervention after an ST-elevation MI. According to that study, the readmission rate in the United States is almost twice that of European centers. Much of this increase was related to a shorter hospital stay in the United States that was half that of the European centers: 8 vs. 3 days (JAMA 2012;307:66-74).

In the last few years there has actually been a speed contest in some cardiology quarters to see how quickly patients can be discharged after a STEMI. As a result, a "drive through" mentality for percutaneous coronary intervention and AMI treatment has developed. Some of this has been generated by hospital administration, but with full participation by cardiologists. There appears to be little or no benefit to the short stay other than on the hospital bottom line. It now appears that, in the future, the financial benefit of this expedited care will be challenged.

Heart failure admissions suffer from similar expedited care. The duration of a hospital stay for heart failure decreased from 8.8 to 6.3 days between 1996 and 2006. Similar international disparity exists as observed with AMI. The rate of readmission in 30 days after discharge is estimated to be roughly 20%. The occurrence of readmission within 30 days is not just an abstract statistic and an inconvenience to patients but is associated with a mortality in the same period of 6.4%, which exceeded inpatient mortality (JAMA 2010;303;2141-7).

Many patients admitted with fluid overload leave the hospital on the same medication that they were taking prior to admission and at the same weight as at admission. Some of this is the result of undertreatment with diuretics, driven by misconceptions about serum creatinine levels, but in many situations patients may not even be weighed. Heart failure patients are often elderly who have significant concomitant disease and require careful in-hospital modification of heart failure therapy. Many of these elderly patients also require the institution of medical and social support prior to discharge.

Inner-city and referral hospitals indicate that they are being unfairly penalized by the nature of the demographic and severity of their patient mix. Some of this pushback is warranted. The "one size fits all" approach by Medicare may well require some modification in view of the variation in both the medical and social complexity. Some form of staging of severity and the need for outpatient nurse support needs to be considered.

Hospitals, nevertheless, are scrambling to respond to the Medicare threat and have begun to apply resources and innovation to solve this pressing issue. Cardiologists themselves also can have an important impact on the problem. We all need to slow down and spend some time dealing with the long-term solutions to short-term problems like acute heart failure and AMI.

Dr. Goldstein writes the column, "Heart of the Matter," which appears regularly in Cardiology News, a Frontline Medical Communications publication. He is professor of medicine at Wayne State University and division head emeritus of cardiovascular medicine at Henry Ford Hospital, both in Detroit. He is on data safety monitoring committees for the National Institutes of Health and several pharmaceutical companies.

Readmissions after hospital discharge for acute myocardial infarction, heart failure, and pneumonia have now become major targets for proposed Medicare savings as part of the current budget tightening in Washington. Hospitals in the past have viewed readmissions either with disdain and disinterest or as a "cash cow."

Readmissions have been good business, as long as Medicare reimbursed hospitals for individual admissions no matter how long or short or how frequent. Readmissions are estimated to cost $17 billion annually. As Medicare costs continue to increase, the control of readmissions appears to be a good target for saving some money. As a result, Medicare levied a maximum reduction of 1% on payments last year on 307 of the nation’s hospitals that were deemed to have too many readmissions (New York Times, Nov. 26, 2012).

Readmissions for AMI and heart failure are among the most frequent hospital admissions and readmissions. Readmissions in cardiology have been an important outcome measure in clinical trials for the last half century. As mortality rates decreased over the years, rehospitalization became more important as clinicians realized its importance in the composite outcome measure of cost and benefit of new therapies. Two of the potential causes of readmission have been early discharge and the lack of postdischarge medical support. The urgency for early discharge for both heart failure and AMI has been driven largely by the misplaced emphasis on shorter hospital stays.

A recent international trial examined readmission rates as an outcome measure in patients who were treated with a percutaneous coronary intervention after an ST-elevation MI. According to that study, the readmission rate in the United States is almost twice that of European centers. Much of this increase was related to a shorter hospital stay in the United States that was half that of the European centers: 8 vs. 3 days (JAMA 2012;307:66-74).

In the last few years there has actually been a speed contest in some cardiology quarters to see how quickly patients can be discharged after a STEMI. As a result, a "drive through" mentality for percutaneous coronary intervention and AMI treatment has developed. Some of this has been generated by hospital administration, but with full participation by cardiologists. There appears to be little or no benefit to the short stay other than on the hospital bottom line. It now appears that, in the future, the financial benefit of this expedited care will be challenged.

Heart failure admissions suffer from similar expedited care. The duration of a hospital stay for heart failure decreased from 8.8 to 6.3 days between 1996 and 2006. Similar international disparity exists as observed with AMI. The rate of readmission in 30 days after discharge is estimated to be roughly 20%. The occurrence of readmission within 30 days is not just an abstract statistic and an inconvenience to patients but is associated with a mortality in the same period of 6.4%, which exceeded inpatient mortality (JAMA 2010;303;2141-7).

Many patients admitted with fluid overload leave the hospital on the same medication that they were taking prior to admission and at the same weight as at admission. Some of this is the result of undertreatment with diuretics, driven by misconceptions about serum creatinine levels, but in many situations patients may not even be weighed. Heart failure patients are often elderly who have significant concomitant disease and require careful in-hospital modification of heart failure therapy. Many of these elderly patients also require the institution of medical and social support prior to discharge.

Inner-city and referral hospitals indicate that they are being unfairly penalized by the nature of the demographic and severity of their patient mix. Some of this pushback is warranted. The "one size fits all" approach by Medicare may well require some modification in view of the variation in both the medical and social complexity. Some form of staging of severity and the need for outpatient nurse support needs to be considered.

Hospitals, nevertheless, are scrambling to respond to the Medicare threat and have begun to apply resources and innovation to solve this pressing issue. Cardiologists themselves also can have an important impact on the problem. We all need to slow down and spend some time dealing with the long-term solutions to short-term problems like acute heart failure and AMI.

Dr. Goldstein writes the column, "Heart of the Matter," which appears regularly in Cardiology News, a Frontline Medical Communications publication. He is professor of medicine at Wayne State University and division head emeritus of cardiovascular medicine at Henry Ford Hospital, both in Detroit. He is on data safety monitoring committees for the National Institutes of Health and several pharmaceutical companies.

Readmissions after hospital discharge for acute myocardial infarction, heart failure, and pneumonia have now become major targets for proposed Medicare savings as part of the current budget tightening in Washington. Hospitals in the past have viewed readmissions either with disdain and disinterest or as a "cash cow."

Readmissions have been good business, as long as Medicare reimbursed hospitals for individual admissions no matter how long or short or how frequent. Readmissions are estimated to cost $17 billion annually. As Medicare costs continue to increase, the control of readmissions appears to be a good target for saving some money. As a result, Medicare levied a maximum reduction of 1% on payments last year on 307 of the nation’s hospitals that were deemed to have too many readmissions (New York Times, Nov. 26, 2012).

Readmissions for AMI and heart failure are among the most frequent hospital admissions and readmissions. Readmissions in cardiology have been an important outcome measure in clinical trials for the last half century. As mortality rates decreased over the years, rehospitalization became more important as clinicians realized its importance in the composite outcome measure of cost and benefit of new therapies. Two of the potential causes of readmission have been early discharge and the lack of postdischarge medical support. The urgency for early discharge for both heart failure and AMI has been driven largely by the misplaced emphasis on shorter hospital stays.

A recent international trial examined readmission rates as an outcome measure in patients who were treated with a percutaneous coronary intervention after an ST-elevation MI. According to that study, the readmission rate in the United States is almost twice that of European centers. Much of this increase was related to a shorter hospital stay in the United States that was half that of the European centers: 8 vs. 3 days (JAMA 2012;307:66-74).

In the last few years there has actually been a speed contest in some cardiology quarters to see how quickly patients can be discharged after a STEMI. As a result, a "drive through" mentality for percutaneous coronary intervention and AMI treatment has developed. Some of this has been generated by hospital administration, but with full participation by cardiologists. There appears to be little or no benefit to the short stay other than on the hospital bottom line. It now appears that, in the future, the financial benefit of this expedited care will be challenged.

Heart failure admissions suffer from similar expedited care. The duration of a hospital stay for heart failure decreased from 8.8 to 6.3 days between 1996 and 2006. Similar international disparity exists as observed with AMI. The rate of readmission in 30 days after discharge is estimated to be roughly 20%. The occurrence of readmission within 30 days is not just an abstract statistic and an inconvenience to patients but is associated with a mortality in the same period of 6.4%, which exceeded inpatient mortality (JAMA 2010;303;2141-7).

Many patients admitted with fluid overload leave the hospital on the same medication that they were taking prior to admission and at the same weight as at admission. Some of this is the result of undertreatment with diuretics, driven by misconceptions about serum creatinine levels, but in many situations patients may not even be weighed. Heart failure patients are often elderly who have significant concomitant disease and require careful in-hospital modification of heart failure therapy. Many of these elderly patients also require the institution of medical and social support prior to discharge.

Inner-city and referral hospitals indicate that they are being unfairly penalized by the nature of the demographic and severity of their patient mix. Some of this pushback is warranted. The "one size fits all" approach by Medicare may well require some modification in view of the variation in both the medical and social complexity. Some form of staging of severity and the need for outpatient nurse support needs to be considered.

Hospitals, nevertheless, are scrambling to respond to the Medicare threat and have begun to apply resources and innovation to solve this pressing issue. Cardiologists themselves also can have an important impact on the problem. We all need to slow down and spend some time dealing with the long-term solutions to short-term problems like acute heart failure and AMI.

Dr. Goldstein writes the column, "Heart of the Matter," which appears regularly in Cardiology News, a Frontline Medical Communications publication. He is professor of medicine at Wayne State University and division head emeritus of cardiovascular medicine at Henry Ford Hospital, both in Detroit. He is on data safety monitoring committees for the National Institutes of Health and several pharmaceutical companies.

From the time that propranolol significantly lowered mortality after an acute myocardial infarction in the Beta-Blocker Heart Attack Trial in 1981, it took nearly 20 years for beta-blocker therapy to take hold as standard practice in AMI patients. Now, results of a recent trial may cause many to question the established therapy.

The Nov. 6, 1981, issue of JAMA announced that the National Heart, Lung, and Blood Institute had "taken the unusual step of curtailing" the Beta-Blocker Heart Attack Trial (BHAT) on the basis of findings that treatment of patients with the beta-adrenergic blocking agent, propranolol, resulted in a 26% decrease in all-cause mortality and a 23% decrease in sudden death (JAMA 1982;247:1707-14).

The study included 3,837 patients treated within 5-21 days of an acute myocardial infarction (AMI) and randomized to either propranolol 160-240 mg/day or placebo. Two-thirds of the patients had a ST-elevation MI; the remaining patients had symptoms compatible with an AMI with electrocardiographic changes accompanied by an increase in serum enzymatic elevations (serum glutamic oxaloacetic transaminase or creatine phosphokinase). This followed the report of similar results in Europe with the beta-blocker timolol in a similar group of patients. Since those early reports of randomized clinical trials, based on a subgroup analysis of BHAT, confirmed the benefit of beta-blocker therapy for both ischemic and nonischemic systolic heart failure. As steering committee chair of BHAT, I was excited about the result of our study and anticipated that beta-blocker therapy would rapidly become part of the treatment of AMI.

This was not to be. It took almost 20 years before beta-blocker therapy was incorporated into the standard treatment of AMI patients. In the interval, thousands of patients who could have benefited with this therapy died. As late as 1998, fewer than 50% of AMI patients without contraindication to therapy received that class of drug.

Why did it take so long? At the time of the BHAT results, many of the leading academic cardiologists were enamored with the use of calcium entry blocking agents for AMI, for which there were little data but a lot of encouragement by pharmaceutical companies. When propranolol went off patent and became available as a generic, there was little industrial support to publicize its benefit. Furthermore, there was little interest at the National Heart, Lung, and Blood Institute to educate physicians about the importance of BHAT. In 1996, beta-blocker therapy post-AMI was established as a quality standard by the National Committee for Quality Assurance (NCQA). At about the same time, it was incorporated in the American College of Cardiology guidelines. Not until 2000, 19 years after the initial report of beta-blocker therapy, did its usage reach 90% at discharge. A recent study from the NCQA indicated that 6 months after discharge only 71% of patients were taking the medication.

In the intervening 2 decades, the definition of an AMI has dramatically changed as a result of more sensitive, if less specific, enzyme measurements. In 1981, most of the patients in BHAT had a STEMI, whereas contemporary clinical trials include less than one-third STEMI patients. Therapy certainly has changed: first with the use of thrombolytic therapy and subsequently with the wide use of interventional angioplasty technology, particularly in the STEMI population. Aspirin, statins, and ACE inhibitors have also been added to the therapeutic mix.

Now, an observational study of almost 7,000 patients with a history of an AMI collected in 2004 and followed for 43 months, suggests that beta-blocker therapy is no longer necessary. Using a composite end point including cardiovascular death, nonfatal MI, or stroke, patients receiving propranolol had an event rate of 16.9%, compared with 18.6% not taking beta-blocker (hazard ratio, .90; P less than .14) (JAMA 2012;308:1340-9). It should be noted, however, that 74% of the patients in the study had a history of hypertension, 44% angina, and 22% heart failure, all clinical problems for which beta-blockers have been proven to be effective.

The most recent American College of Cardiology/American Heart Association guidelines suggest that beta-blocker therapy "is greatest (benefit) among patients with recent myocardial infarction [of up to 3 years prior] and/or left ventricular systolic dysfunction [left ventricular ejection fraction of 40% or less]. For those patient without these class I indication, [beta]-blocker therapy is optional (class IIa or IIb) (Circulation 2011;124:2458-73). I suppose that if you can find an AMI patient without hypertension, angina, or heart failure, discontinuing beta-blocker therapy could be justified. Until that rare patient appears in my office, I plan to maintain beta-blockers in my post-AMI patients.

Dr. Goldstein, medical editor of Cardiology News, is a professor of medicine at Wayne State University and division head emeritus of cardiovascular medicine at Henry Ford Hospital, both in Detroit. He is on data safety monitoring committees for the National Institutes of Health and several pharmaceutical companies.

This column, "Heart of the Matter," appears regularly in Cardiology News.

From the time that propranolol significantly lowered mortality after an acute myocardial infarction in the Beta-Blocker Heart Attack Trial in 1981, it took nearly 20 years for beta-blocker therapy to take hold as standard practice in AMI patients. Now, results of a recent trial may cause many to question the established therapy.

The Nov. 6, 1981, issue of JAMA announced that the National Heart, Lung, and Blood Institute had "taken the unusual step of curtailing" the Beta-Blocker Heart Attack Trial (BHAT) on the basis of findings that treatment of patients with the beta-adrenergic blocking agent, propranolol, resulted in a 26% decrease in all-cause mortality and a 23% decrease in sudden death (JAMA 1982;247:1707-14).

The study included 3,837 patients treated within 5-21 days of an acute myocardial infarction (AMI) and randomized to either propranolol 160-240 mg/day or placebo. Two-thirds of the patients had a ST-elevation MI; the remaining patients had symptoms compatible with an AMI with electrocardiographic changes accompanied by an increase in serum enzymatic elevations (serum glutamic oxaloacetic transaminase or creatine phosphokinase). This followed the report of similar results in Europe with the beta-blocker timolol in a similar group of patients. Since those early reports of randomized clinical trials, based on a subgroup analysis of BHAT, confirmed the benefit of beta-blocker therapy for both ischemic and nonischemic systolic heart failure. As steering committee chair of BHAT, I was excited about the result of our study and anticipated that beta-blocker therapy would rapidly become part of the treatment of AMI.

This was not to be. It took almost 20 years before beta-blocker therapy was incorporated into the standard treatment of AMI patients. In the interval, thousands of patients who could have benefited with this therapy died. As late as 1998, fewer than 50% of AMI patients without contraindication to therapy received that class of drug.

Why did it take so long? At the time of the BHAT results, many of the leading academic cardiologists were enamored with the use of calcium entry blocking agents for AMI, for which there were little data but a lot of encouragement by pharmaceutical companies. When propranolol went off patent and became available as a generic, there was little industrial support to publicize its benefit. Furthermore, there was little interest at the National Heart, Lung, and Blood Institute to educate physicians about the importance of BHAT. In 1996, beta-blocker therapy post-AMI was established as a quality standard by the National Committee for Quality Assurance (NCQA). At about the same time, it was incorporated in the American College of Cardiology guidelines. Not until 2000, 19 years after the initial report of beta-blocker therapy, did its usage reach 90% at discharge. A recent study from the NCQA indicated that 6 months after discharge only 71% of patients were taking the medication.

In the intervening 2 decades, the definition of an AMI has dramatically changed as a result of more sensitive, if less specific, enzyme measurements. In 1981, most of the patients in BHAT had a STEMI, whereas contemporary clinical trials include less than one-third STEMI patients. Therapy certainly has changed: first with the use of thrombolytic therapy and subsequently with the wide use of interventional angioplasty technology, particularly in the STEMI population. Aspirin, statins, and ACE inhibitors have also been added to the therapeutic mix.

Now, an observational study of almost 7,000 patients with a history of an AMI collected in 2004 and followed for 43 months, suggests that beta-blocker therapy is no longer necessary. Using a composite end point including cardiovascular death, nonfatal MI, or stroke, patients receiving propranolol had an event rate of 16.9%, compared with 18.6% not taking beta-blocker (hazard ratio, .90; P less than .14) (JAMA 2012;308:1340-9). It should be noted, however, that 74% of the patients in the study had a history of hypertension, 44% angina, and 22% heart failure, all clinical problems for which beta-blockers have been proven to be effective.

The most recent American College of Cardiology/American Heart Association guidelines suggest that beta-blocker therapy "is greatest (benefit) among patients with recent myocardial infarction [of up to 3 years prior] and/or left ventricular systolic dysfunction [left ventricular ejection fraction of 40% or less]. For those patient without these class I indication, [beta]-blocker therapy is optional (class IIa or IIb) (Circulation 2011;124:2458-73). I suppose that if you can find an AMI patient without hypertension, angina, or heart failure, discontinuing beta-blocker therapy could be justified. Until that rare patient appears in my office, I plan to maintain beta-blockers in my post-AMI patients.

Dr. Goldstein, medical editor of Cardiology News, is a professor of medicine at Wayne State University and division head emeritus of cardiovascular medicine at Henry Ford Hospital, both in Detroit. He is on data safety monitoring committees for the National Institutes of Health and several pharmaceutical companies.

This column, "Heart of the Matter," appears regularly in Cardiology News.

From the time that propranolol significantly lowered mortality after an acute myocardial infarction in the Beta-Blocker Heart Attack Trial in 1981, it took nearly 20 years for beta-blocker therapy to take hold as standard practice in AMI patients. Now, results of a recent trial may cause many to question the established therapy.

The Nov. 6, 1981, issue of JAMA announced that the National Heart, Lung, and Blood Institute had "taken the unusual step of curtailing" the Beta-Blocker Heart Attack Trial (BHAT) on the basis of findings that treatment of patients with the beta-adrenergic blocking agent, propranolol, resulted in a 26% decrease in all-cause mortality and a 23% decrease in sudden death (JAMA 1982;247:1707-14).

The study included 3,837 patients treated within 5-21 days of an acute myocardial infarction (AMI) and randomized to either propranolol 160-240 mg/day or placebo. Two-thirds of the patients had a ST-elevation MI; the remaining patients had symptoms compatible with an AMI with electrocardiographic changes accompanied by an increase in serum enzymatic elevations (serum glutamic oxaloacetic transaminase or creatine phosphokinase). This followed the report of similar results in Europe with the beta-blocker timolol in a similar group of patients. Since those early reports of randomized clinical trials, based on a subgroup analysis of BHAT, confirmed the benefit of beta-blocker therapy for both ischemic and nonischemic systolic heart failure. As steering committee chair of BHAT, I was excited about the result of our study and anticipated that beta-blocker therapy would rapidly become part of the treatment of AMI.

This was not to be. It took almost 20 years before beta-blocker therapy was incorporated into the standard treatment of AMI patients. In the interval, thousands of patients who could have benefited with this therapy died. As late as 1998, fewer than 50% of AMI patients without contraindication to therapy received that class of drug.

Why did it take so long? At the time of the BHAT results, many of the leading academic cardiologists were enamored with the use of calcium entry blocking agents for AMI, for which there were little data but a lot of encouragement by pharmaceutical companies. When propranolol went off patent and became available as a generic, there was little industrial support to publicize its benefit. Furthermore, there was little interest at the National Heart, Lung, and Blood Institute to educate physicians about the importance of BHAT. In 1996, beta-blocker therapy post-AMI was established as a quality standard by the National Committee for Quality Assurance (NCQA). At about the same time, it was incorporated in the American College of Cardiology guidelines. Not until 2000, 19 years after the initial report of beta-blocker therapy, did its usage reach 90% at discharge. A recent study from the NCQA indicated that 6 months after discharge only 71% of patients were taking the medication.

In the intervening 2 decades, the definition of an AMI has dramatically changed as a result of more sensitive, if less specific, enzyme measurements. In 1981, most of the patients in BHAT had a STEMI, whereas contemporary clinical trials include less than one-third STEMI patients. Therapy certainly has changed: first with the use of thrombolytic therapy and subsequently with the wide use of interventional angioplasty technology, particularly in the STEMI population. Aspirin, statins, and ACE inhibitors have also been added to the therapeutic mix.

Now, an observational study of almost 7,000 patients with a history of an AMI collected in 2004 and followed for 43 months, suggests that beta-blocker therapy is no longer necessary. Using a composite end point including cardiovascular death, nonfatal MI, or stroke, patients receiving propranolol had an event rate of 16.9%, compared with 18.6% not taking beta-blocker (hazard ratio, .90; P less than .14) (JAMA 2012;308:1340-9). It should be noted, however, that 74% of the patients in the study had a history of hypertension, 44% angina, and 22% heart failure, all clinical problems for which beta-blockers have been proven to be effective.

The most recent American College of Cardiology/American Heart Association guidelines suggest that beta-blocker therapy "is greatest (benefit) among patients with recent myocardial infarction [of up to 3 years prior] and/or left ventricular systolic dysfunction [left ventricular ejection fraction of 40% or less]. For those patient without these class I indication, [beta]-blocker therapy is optional (class IIa or IIb) (Circulation 2011;124:2458-73). I suppose that if you can find an AMI patient without hypertension, angina, or heart failure, discontinuing beta-blocker therapy could be justified. Until that rare patient appears in my office, I plan to maintain beta-blockers in my post-AMI patients.

Dr. Goldstein, medical editor of Cardiology News, is a professor of medicine at Wayne State University and division head emeritus of cardiovascular medicine at Henry Ford Hospital, both in Detroit. He is on data safety monitoring committees for the National Institutes of Health and several pharmaceutical companies.

This column, "Heart of the Matter," appears regularly in Cardiology News.

The doctor’s office, at least my office, has changed over the last few decades with an increase in personnel added to make my life easier. Much of it has occurred as a response to the increased billing and authentication process that is required for reimbursement.

After all, when doctors were paid in cash or with a dozen eggs, there was little need for all the paperwork. Health insurance, both private and federal, has been the cause of much of this. At the same time, medical assistants, registered nurses, and a variety of ancillary staff have been added to make the patient’s visit smoother and to acquire the requisite information to satiate the vast network of communications that are generated with each office visit. All of these personnel are now an undisputable requirement for the function of today’s medical office.

In the process, the distance between the physician and the patient has increased. In many offices today, the patient may never see the doctor during the visit. To an increasing extent, the office contact with the patient is solely by an RN or physician assistant. In most cases, patients are satisfied with the service and are delighted not to spend a long time waiting to see the "doctor." Many of the visits are check-ups or annual or semiannual visits without any associated symptoms that can often be dealt with by a sympathetic and knowledgeable nurse. The patient is the winner to a great extent in this process by acquiring a sensitive ear and an expeditious visit. What is lost is the continued relationship of the patients and their physician. The biggest loss, I would suggest, is the doctor’s satisfaction of providing medical care that comes with every patient encounter, which keeps many of us energized to keep practicing medicine.

Now we have a new vision of how the primary care office of the future will function as a medical home (N. Engl. J. Med. 2012;367:891-3). In this vision, the physicians will be energized by a global payment system that will create an environment in which the doctor’s role is to pass real responsibility to their ancillary staff for which they would be held accountable. According to the authors, the physician’s office will be committed to promoting a healthy environment rather than merely treating disease. Why bother with the simple issue of treating sick patients when you can take on the entire environment of your community to prevent disease?

The authors go on to state that the physician would not waste time focusing on the "10% premature mortality that is influenced by medical treatment." In this work environment, the physician would be the team manager of a host of ancillary personnel, including medical assistants, RNs, social workers, nutritionists, and pharmacists, to name but a few. The physician would be energized by his or her role as a team leader. The physician, the authors explain, would see fewer patients and would not be caught running from room to room to see patients. Instead, he or she will become involved with care of the "community and understanding the upstream determinants of downstream sickness" and would spend there time in the community "advocating for the local farmer’s market to accept food stamps, organizing walking clubs for physical exercise, and lobbying ... to reduce emissions to improve air quality."

This, of course, is a far cry from the doctors who negotiated the care for their patient for a dozen eggs. It is clearly a role that is foreign to my generation. To some extent, though, patients may well gain in this futuristic environment. They will acquire an empathetic nurse who will be sensitive to their needs and who may be as good as a crotchety overworked doctor. All of the ancillary medical staff will gain a larger and more responsible role in the medical home. The physicians will morph into a new role that is more characteristic of an administrator and less as a practitioner. The doctors, however, will be the biggest losers as they disengage from the patient contact and care that is so crucial to the satisfaction of being a doctor.

Dr. Goldstein, medical editor of Cardiology News, is a professor of medicine at Wayne State University and division head emeritus of cardiovascular medicine at Henry Ford Hospital, both in Detroit. He is on data safety monitoring committees for the National Institutes of Health and several pharmaceutical companies.

The doctor’s office, at least my office, has changed over the last few decades with an increase in personnel added to make my life easier. Much of it has occurred as a response to the increased billing and authentication process that is required for reimbursement.

After all, when doctors were paid in cash or with a dozen eggs, there was little need for all the paperwork. Health insurance, both private and federal, has been the cause of much of this. At the same time, medical assistants, registered nurses, and a variety of ancillary staff have been added to make the patient’s visit smoother and to acquire the requisite information to satiate the vast network of communications that are generated with each office visit. All of these personnel are now an undisputable requirement for the function of today’s medical office.

In the process, the distance between the physician and the patient has increased. In many offices today, the patient may never see the doctor during the visit. To an increasing extent, the office contact with the patient is solely by an RN or physician assistant. In most cases, patients are satisfied with the service and are delighted not to spend a long time waiting to see the "doctor." Many of the visits are check-ups or annual or semiannual visits without any associated symptoms that can often be dealt with by a sympathetic and knowledgeable nurse. The patient is the winner to a great extent in this process by acquiring a sensitive ear and an expeditious visit. What is lost is the continued relationship of the patients and their physician. The biggest loss, I would suggest, is the doctor’s satisfaction of providing medical care that comes with every patient encounter, which keeps many of us energized to keep practicing medicine.

Now we have a new vision of how the primary care office of the future will function as a medical home (N. Engl. J. Med. 2012;367:891-3). In this vision, the physicians will be energized by a global payment system that will create an environment in which the doctor’s role is to pass real responsibility to their ancillary staff for which they would be held accountable. According to the authors, the physician’s office will be committed to promoting a healthy environment rather than merely treating disease. Why bother with the simple issue of treating sick patients when you can take on the entire environment of your community to prevent disease?

The authors go on to state that the physician would not waste time focusing on the "10% premature mortality that is influenced by medical treatment." In this work environment, the physician would be the team manager of a host of ancillary personnel, including medical assistants, RNs, social workers, nutritionists, and pharmacists, to name but a few. The physician would be energized by his or her role as a team leader. The physician, the authors explain, would see fewer patients and would not be caught running from room to room to see patients. Instead, he or she will become involved with care of the "community and understanding the upstream determinants of downstream sickness" and would spend there time in the community "advocating for the local farmer’s market to accept food stamps, organizing walking clubs for physical exercise, and lobbying ... to reduce emissions to improve air quality."

This, of course, is a far cry from the doctors who negotiated the care for their patient for a dozen eggs. It is clearly a role that is foreign to my generation. To some extent, though, patients may well gain in this futuristic environment. They will acquire an empathetic nurse who will be sensitive to their needs and who may be as good as a crotchety overworked doctor. All of the ancillary medical staff will gain a larger and more responsible role in the medical home. The physicians will morph into a new role that is more characteristic of an administrator and less as a practitioner. The doctors, however, will be the biggest losers as they disengage from the patient contact and care that is so crucial to the satisfaction of being a doctor.

Dr. Goldstein, medical editor of Cardiology News, is a professor of medicine at Wayne State University and division head emeritus of cardiovascular medicine at Henry Ford Hospital, both in Detroit. He is on data safety monitoring committees for the National Institutes of Health and several pharmaceutical companies.

The doctor’s office, at least my office, has changed over the last few decades with an increase in personnel added to make my life easier. Much of it has occurred as a response to the increased billing and authentication process that is required for reimbursement.

After all, when doctors were paid in cash or with a dozen eggs, there was little need for all the paperwork. Health insurance, both private and federal, has been the cause of much of this. At the same time, medical assistants, registered nurses, and a variety of ancillary staff have been added to make the patient’s visit smoother and to acquire the requisite information to satiate the vast network of communications that are generated with each office visit. All of these personnel are now an undisputable requirement for the function of today’s medical office.

In the process, the distance between the physician and the patient has increased. In many offices today, the patient may never see the doctor during the visit. To an increasing extent, the office contact with the patient is solely by an RN or physician assistant. In most cases, patients are satisfied with the service and are delighted not to spend a long time waiting to see the "doctor." Many of the visits are check-ups or annual or semiannual visits without any associated symptoms that can often be dealt with by a sympathetic and knowledgeable nurse. The patient is the winner to a great extent in this process by acquiring a sensitive ear and an expeditious visit. What is lost is the continued relationship of the patients and their physician. The biggest loss, I would suggest, is the doctor’s satisfaction of providing medical care that comes with every patient encounter, which keeps many of us energized to keep practicing medicine.

Now we have a new vision of how the primary care office of the future will function as a medical home (N. Engl. J. Med. 2012;367:891-3). In this vision, the physicians will be energized by a global payment system that will create an environment in which the doctor’s role is to pass real responsibility to their ancillary staff for which they would be held accountable. According to the authors, the physician’s office will be committed to promoting a healthy environment rather than merely treating disease. Why bother with the simple issue of treating sick patients when you can take on the entire environment of your community to prevent disease?

The authors go on to state that the physician would not waste time focusing on the "10% premature mortality that is influenced by medical treatment." In this work environment, the physician would be the team manager of a host of ancillary personnel, including medical assistants, RNs, social workers, nutritionists, and pharmacists, to name but a few. The physician would be energized by his or her role as a team leader. The physician, the authors explain, would see fewer patients and would not be caught running from room to room to see patients. Instead, he or she will become involved with care of the "community and understanding the upstream determinants of downstream sickness" and would spend there time in the community "advocating for the local farmer’s market to accept food stamps, organizing walking clubs for physical exercise, and lobbying ... to reduce emissions to improve air quality."

This, of course, is a far cry from the doctors who negotiated the care for their patient for a dozen eggs. It is clearly a role that is foreign to my generation. To some extent, though, patients may well gain in this futuristic environment. They will acquire an empathetic nurse who will be sensitive to their needs and who may be as good as a crotchety overworked doctor. All of the ancillary medical staff will gain a larger and more responsible role in the medical home. The physicians will morph into a new role that is more characteristic of an administrator and less as a practitioner. The doctors, however, will be the biggest losers as they disengage from the patient contact and care that is so crucial to the satisfaction of being a doctor.

Dr. Goldstein, medical editor of Cardiology News, is a professor of medicine at Wayne State University and division head emeritus of cardiovascular medicine at Henry Ford Hospital, both in Detroit. He is on data safety monitoring committees for the National Institutes of Health and several pharmaceutical companies.

The advances in cardiac imaging that have taken place in the last few years have provided amazing visualization of cardiac function in health and disease. Imaging has also enabled us to target areas of the heart for medical and surgical intervention.

The images are so slick that we have been known to e-mail them to our patients to show them how clever we are. I am told that they have been used to liven up cocktail parties. In a larger sense, however, few new concepts have emerged as a result of these imaging advances that physiologists and anatomists have not already elegantly described in the past.

We have been obsessed with the possibility that imaging of the heart and the coronary vessels would unlock the mysteries of acute coronary events and provide predictive information of subsequent myocardial infarction. The advances in computed tomography – first with the exercise electrocardiogram (with and without radiographic imaging), followed by coronary angiography, and most recently with CT coronary angiography – are only the most recent attempts to identify the culprit in this long-running quest for the triggers of acute coronary events.

And yet, the answer eludes us. Even when we were able to image the atherosclerotic plaque itself, we found that new events occurred in seemingly normal vessels. So it is not surprising that the ROMICAT II (Rule Out Myocardial Infarction II) study – the most recent study evaluating emergency department patients with acute chest pain using CT angiography – failed to provide any new insight into the diagnosis and prediction of the acute coronary syndrome. Compared with standard evaluation, CT angiography failed to show any clinical benefit other than shortening the average stay in the ED by 7.6 hours (which is unquestionably a quality benefit if your emergency department is anything like mine).

ROMICAT II did show that coronary events were rare in this highly selected patient population who were aged 40-74 years, had no history of coronary artery disease or ischemic electrocardiographic abnormalities, and had normal troponin assays. In the succeeding 28 days following emergency evaluation, there were no acute coronary events detected, and there were only eight adverse cardiac events observed.

Because of the unlikely occurrence of coronary events, these patients can best be dealt with in a nonemergency setting. Both CT angiography and standard testing led to further tests during the 28-day follow-up, including exercise echocardiograms (with or without nuclear imaging) and coronary angiography in roughly three-fourths of the patients. Revascularization was performed in 10% of the population.

So why are we even testing these patients and exposing them to all of the exigencies of ED and hospital admission? We are clearly not providing any service to them. At the same time, we are exposing them to increased radiation and the hazard of the testing procedures themselves. Some would say that the testing was driven by the risks of malpractice litigation. This study should provide some "cover" for that concern, which is undoubtedly real.

The continuing dependence on imaging technology to solve clinical problems has led to the numbing of our ability to perform cognitive processing of clinical data. Heart failure is no longer a clinical entity; it is an echocardiography image. The acute coronary syndrome is not a clinical syndrome, but rather an acquired image or blood test. Daily ward rounds have evolved into a hierarchical listing of the next imaging test to be performed on the patient in order to solve the clinical problem at hand. Consequently, the approach to the patient is no longer a quest to understand what is probable, but a search for the improbable.

A continuous barrage of publications in the medical and lay press has addressed the dollars wasted on imaging procedures, with seemingly little letup in the use of these technologies. Clearly, in the "zero-sum game" world of modern medicine, these costs will ultimately come out of physician’s income. Beyond that, we should realize that they add very little to the care of our patients and may actually add to their risks.

Dr. Goldstein, medical editor of Cardiology News, is a professor of medicine at Wayne State University and division head emeritus of cardiovascular medicine at Henry Ford Hospital, both in Detroit. He is on data safety monitoring committees for the National Institutes of Health and several pharmaceutical companies.

The advances in cardiac imaging that have taken place in the last few years have provided amazing visualization of cardiac function in health and disease. Imaging has also enabled us to target areas of the heart for medical and surgical intervention.

The images are so slick that we have been known to e-mail them to our patients to show them how clever we are. I am told that they have been used to liven up cocktail parties. In a larger sense, however, few new concepts have emerged as a result of these imaging advances that physiologists and anatomists have not already elegantly described in the past.

We have been obsessed with the possibility that imaging of the heart and the coronary vessels would unlock the mysteries of acute coronary events and provide predictive information of subsequent myocardial infarction. The advances in computed tomography – first with the exercise electrocardiogram (with and without radiographic imaging), followed by coronary angiography, and most recently with CT coronary angiography – are only the most recent attempts to identify the culprit in this long-running quest for the triggers of acute coronary events.

And yet, the answer eludes us. Even when we were able to image the atherosclerotic plaque itself, we found that new events occurred in seemingly normal vessels. So it is not surprising that the ROMICAT II (Rule Out Myocardial Infarction II) study – the most recent study evaluating emergency department patients with acute chest pain using CT angiography – failed to provide any new insight into the diagnosis and prediction of the acute coronary syndrome. Compared with standard evaluation, CT angiography failed to show any clinical benefit other than shortening the average stay in the ED by 7.6 hours (which is unquestionably a quality benefit if your emergency department is anything like mine).

ROMICAT II did show that coronary events were rare in this highly selected patient population who were aged 40-74 years, had no history of coronary artery disease or ischemic electrocardiographic abnormalities, and had normal troponin assays. In the succeeding 28 days following emergency evaluation, there were no acute coronary events detected, and there were only eight adverse cardiac events observed.

Because of the unlikely occurrence of coronary events, these patients can best be dealt with in a nonemergency setting. Both CT angiography and standard testing led to further tests during the 28-day follow-up, including exercise echocardiograms (with or without nuclear imaging) and coronary angiography in roughly three-fourths of the patients. Revascularization was performed in 10% of the population.

So why are we even testing these patients and exposing them to all of the exigencies of ED and hospital admission? We are clearly not providing any service to them. At the same time, we are exposing them to increased radiation and the hazard of the testing procedures themselves. Some would say that the testing was driven by the risks of malpractice litigation. This study should provide some "cover" for that concern, which is undoubtedly real.

The continuing dependence on imaging technology to solve clinical problems has led to the numbing of our ability to perform cognitive processing of clinical data. Heart failure is no longer a clinical entity; it is an echocardiography image. The acute coronary syndrome is not a clinical syndrome, but rather an acquired image or blood test. Daily ward rounds have evolved into a hierarchical listing of the next imaging test to be performed on the patient in order to solve the clinical problem at hand. Consequently, the approach to the patient is no longer a quest to understand what is probable, but a search for the improbable.

A continuous barrage of publications in the medical and lay press has addressed the dollars wasted on imaging procedures, with seemingly little letup in the use of these technologies. Clearly, in the "zero-sum game" world of modern medicine, these costs will ultimately come out of physician’s income. Beyond that, we should realize that they add very little to the care of our patients and may actually add to their risks.

Dr. Goldstein, medical editor of Cardiology News, is a professor of medicine at Wayne State University and division head emeritus of cardiovascular medicine at Henry Ford Hospital, both in Detroit. He is on data safety monitoring committees for the National Institutes of Health and several pharmaceutical companies.

The advances in cardiac imaging that have taken place in the last few years have provided amazing visualization of cardiac function in health and disease. Imaging has also enabled us to target areas of the heart for medical and surgical intervention.

The images are so slick that we have been known to e-mail them to our patients to show them how clever we are. I am told that they have been used to liven up cocktail parties. In a larger sense, however, few new concepts have emerged as a result of these imaging advances that physiologists and anatomists have not already elegantly described in the past.

We have been obsessed with the possibility that imaging of the heart and the coronary vessels would unlock the mysteries of acute coronary events and provide predictive information of subsequent myocardial infarction. The advances in computed tomography – first with the exercise electrocardiogram (with and without radiographic imaging), followed by coronary angiography, and most recently with CT coronary angiography – are only the most recent attempts to identify the culprit in this long-running quest for the triggers of acute coronary events.

And yet, the answer eludes us. Even when we were able to image the atherosclerotic plaque itself, we found that new events occurred in seemingly normal vessels. So it is not surprising that the ROMICAT II (Rule Out Myocardial Infarction II) study – the most recent study evaluating emergency department patients with acute chest pain using CT angiography – failed to provide any new insight into the diagnosis and prediction of the acute coronary syndrome. Compared with standard evaluation, CT angiography failed to show any clinical benefit other than shortening the average stay in the ED by 7.6 hours (which is unquestionably a quality benefit if your emergency department is anything like mine).

ROMICAT II did show that coronary events were rare in this highly selected patient population who were aged 40-74 years, had no history of coronary artery disease or ischemic electrocardiographic abnormalities, and had normal troponin assays. In the succeeding 28 days following emergency evaluation, there were no acute coronary events detected, and there were only eight adverse cardiac events observed.

Because of the unlikely occurrence of coronary events, these patients can best be dealt with in a nonemergency setting. Both CT angiography and standard testing led to further tests during the 28-day follow-up, including exercise echocardiograms (with or without nuclear imaging) and coronary angiography in roughly three-fourths of the patients. Revascularization was performed in 10% of the population.

So why are we even testing these patients and exposing them to all of the exigencies of ED and hospital admission? We are clearly not providing any service to them. At the same time, we are exposing them to increased radiation and the hazard of the testing procedures themselves. Some would say that the testing was driven by the risks of malpractice litigation. This study should provide some "cover" for that concern, which is undoubtedly real.

The continuing dependence on imaging technology to solve clinical problems has led to the numbing of our ability to perform cognitive processing of clinical data. Heart failure is no longer a clinical entity; it is an echocardiography image. The acute coronary syndrome is not a clinical syndrome, but rather an acquired image or blood test. Daily ward rounds have evolved into a hierarchical listing of the next imaging test to be performed on the patient in order to solve the clinical problem at hand. Consequently, the approach to the patient is no longer a quest to understand what is probable, but a search for the improbable.

A continuous barrage of publications in the medical and lay press has addressed the dollars wasted on imaging procedures, with seemingly little letup in the use of these technologies. Clearly, in the "zero-sum game" world of modern medicine, these costs will ultimately come out of physician’s income. Beyond that, we should realize that they add very little to the care of our patients and may actually add to their risks.

Dr. Goldstein, medical editor of Cardiology News, is a professor of medicine at Wayne State University and division head emeritus of cardiovascular medicine at Henry Ford Hospital, both in Detroit. He is on data safety monitoring committees for the National Institutes of Health and several pharmaceutical companies.

The permanent implantable cardiac heart pump was developed in the mid-20th century as an outgrowth of the success of heart-lung machines –which provided systemic support during cardiac arrest – required for valve replacement and later coronary bypass surgery.

The challenge to build a totally implantable heart has been the "holy grail" for almost half a century and occurred long before heart failure therapy was high on the agenda of cardiologists. It emerged as a result of the experimental perseverance and genius of Dr. Willem Kolff, who in 1957 was able to totally support dogs using an artificial heart device. Other surgeons, working in separate laboratories – including Dr. Adrian Kantrowitz, Dr. Denton Cooley, and Dr. Robert Jarvik – provided additional research support for the ultimate creation of the artificial heart. However, it wasn’t until 15 years later, in 1982, that Dr. Kolff captured the attention of the medical and lay press by supporting a Seattle dentist suffering from severe heart failure, Dr. Barney Clark, for 112 days with the heart that he and Dr. Jarvik had developed.

Since then, research on the totally implantable heart led to the approval in 2004 the SynCardia temporary Total Artificial Heart as a bridge to transplantation in patients with biventricular failure. In 2001, the first AbioCor totally implantable pump with an external power source was implanted. Initially approved by the FDA as a bridge to transplant for patients with biventricular failure, more recently it has been approved for patients with end stage heart failure as destination therapy.

As work went forward on the totally implantable heart, left ventricular assist devices (LVAD) were also being developed. The pharmacologic support of end stage left ventricular failure with vasodilators and inotropic agents has provided modest temporary benefit; but it has become obvious that we have reached a therapeutic wall with very few new medical options on the horizon. LVADs appeared to be our current best hope of providing additional short- and long-term support for the failing left ventricle.

Dr. E. Stanley Crawford and Dr. Domingo Liotta performed the first LVAD implant in 1966 in a patient who had cardiac arrest after surgery. Since then, there have been a variety of LVADs developed that were initially pulsatile, but now are more commonly continuous flow. Both types of devices are externally powered via drive lines and able to achieve flows up to 10 L/min and are interposed between a left ventricular apical conduit and an ascending aorta conduit. The initial LVADs were pulsatile devices based on the presumption that pulsatile flow was important for systemic perfusion and normal physiology. However, continuous-flow LVAD has proven to be quite compatible with normal organ function and perfusion, and shown better durability and lower mortality and morbidity compared to the pulsatile flow devices. (J. Am. Coll. Cardiol. 2011;57:1890-8).

In addition, as noted in "The Lead," LVADs have shown superiority over medical therapy in patients with advanced heart failure as destination therapy, and the 1-year mortality with continuous flow LVADs now approximates the experience with the 1-year mortality of patients receiving a heart transplant.

The expanded use of LVADs from creating a bridge for transplantation to destination therapy has opened an entirely new opportunity for the use of LVADs in the treatment of acute, but most importantly, chronic heart failure. The limitation of heart transplantation as a function of donor availability together with the limitation of medical therapy for heart failure patients has generated increased interest in LVADs for chronic therapy in patients with end-stage heart failure. The observation that in some patients, particularly those with reversible heart failure like myocarditis, the heart may actually recover during LVAD therapy and allow for its removal, provides a window into future clinical applications (N. Engl. J. Med. 2006:355;1873-84)

The potential for further miniaturization of these devices and the potential for total implantability also open new horizons for LVAD therapy. Total implantability hinges on the ability to apply technology of transcutaneous power source that is already available in a number of electronic implantable devices, including the total heart implant. The resolution of these technical issues will allow for further expansion of the clinical indications for LVAD therapy.

Dr. Goldstein, medical editor of Cardiology News, is a professor of medicine at Wayne State University and division head emeritus of cardiovascular medicine at Henry Ford Hospital, both in Detroit. He is on data safety monitoring committees for the National Institutes of Health and several pharmaceutical companies.

The permanent implantable cardiac heart pump was developed in the mid-20th century as an outgrowth of the success of heart-lung machines –which provided systemic support during cardiac arrest – required for valve replacement and later coronary bypass surgery.

The challenge to build a totally implantable heart has been the "holy grail" for almost half a century and occurred long before heart failure therapy was high on the agenda of cardiologists. It emerged as a result of the experimental perseverance and genius of Dr. Willem Kolff, who in 1957 was able to totally support dogs using an artificial heart device. Other surgeons, working in separate laboratories – including Dr. Adrian Kantrowitz, Dr. Denton Cooley, and Dr. Robert Jarvik – provided additional research support for the ultimate creation of the artificial heart. However, it wasn’t until 15 years later, in 1982, that Dr. Kolff captured the attention of the medical and lay press by supporting a Seattle dentist suffering from severe heart failure, Dr. Barney Clark, for 112 days with the heart that he and Dr. Jarvik had developed.

Since then, research on the totally implantable heart led to the approval in 2004 the SynCardia temporary Total Artificial Heart as a bridge to transplantation in patients with biventricular failure. In 2001, the first AbioCor totally implantable pump with an external power source was implanted. Initially approved by the FDA as a bridge to transplant for patients with biventricular failure, more recently it has been approved for patients with end stage heart failure as destination therapy.

As work went forward on the totally implantable heart, left ventricular assist devices (LVAD) were also being developed. The pharmacologic support of end stage left ventricular failure with vasodilators and inotropic agents has provided modest temporary benefit; but it has become obvious that we have reached a therapeutic wall with very few new medical options on the horizon. LVADs appeared to be our current best hope of providing additional short- and long-term support for the failing left ventricle.

Dr. E. Stanley Crawford and Dr. Domingo Liotta performed the first LVAD implant in 1966 in a patient who had cardiac arrest after surgery. Since then, there have been a variety of LVADs developed that were initially pulsatile, but now are more commonly continuous flow. Both types of devices are externally powered via drive lines and able to achieve flows up to 10 L/min and are interposed between a left ventricular apical conduit and an ascending aorta conduit. The initial LVADs were pulsatile devices based on the presumption that pulsatile flow was important for systemic perfusion and normal physiology. However, continuous-flow LVAD has proven to be quite compatible with normal organ function and perfusion, and shown better durability and lower mortality and morbidity compared to the pulsatile flow devices. (J. Am. Coll. Cardiol. 2011;57:1890-8).

In addition, as noted in "The Lead," LVADs have shown superiority over medical therapy in patients with advanced heart failure as destination therapy, and the 1-year mortality with continuous flow LVADs now approximates the experience with the 1-year mortality of patients receiving a heart transplant.

The expanded use of LVADs from creating a bridge for transplantation to destination therapy has opened an entirely new opportunity for the use of LVADs in the treatment of acute, but most importantly, chronic heart failure. The limitation of heart transplantation as a function of donor availability together with the limitation of medical therapy for heart failure patients has generated increased interest in LVADs for chronic therapy in patients with end-stage heart failure. The observation that in some patients, particularly those with reversible heart failure like myocarditis, the heart may actually recover during LVAD therapy and allow for its removal, provides a window into future clinical applications (N. Engl. J. Med. 2006:355;1873-84)

The potential for further miniaturization of these devices and the potential for total implantability also open new horizons for LVAD therapy. Total implantability hinges on the ability to apply technology of transcutaneous power source that is already available in a number of electronic implantable devices, including the total heart implant. The resolution of these technical issues will allow for further expansion of the clinical indications for LVAD therapy.

Dr. Goldstein, medical editor of Cardiology News, is a professor of medicine at Wayne State University and division head emeritus of cardiovascular medicine at Henry Ford Hospital, both in Detroit. He is on data safety monitoring committees for the National Institutes of Health and several pharmaceutical companies.

The permanent implantable cardiac heart pump was developed in the mid-20th century as an outgrowth of the success of heart-lung machines –which provided systemic support during cardiac arrest – required for valve replacement and later coronary bypass surgery.

The challenge to build a totally implantable heart has been the "holy grail" for almost half a century and occurred long before heart failure therapy was high on the agenda of cardiologists. It emerged as a result of the experimental perseverance and genius of Dr. Willem Kolff, who in 1957 was able to totally support dogs using an artificial heart device. Other surgeons, working in separate laboratories – including Dr. Adrian Kantrowitz, Dr. Denton Cooley, and Dr. Robert Jarvik – provided additional research support for the ultimate creation of the artificial heart. However, it wasn’t until 15 years later, in 1982, that Dr. Kolff captured the attention of the medical and lay press by supporting a Seattle dentist suffering from severe heart failure, Dr. Barney Clark, for 112 days with the heart that he and Dr. Jarvik had developed.

Since then, research on the totally implantable heart led to the approval in 2004 the SynCardia temporary Total Artificial Heart as a bridge to transplantation in patients with biventricular failure. In 2001, the first AbioCor totally implantable pump with an external power source was implanted. Initially approved by the FDA as a bridge to transplant for patients with biventricular failure, more recently it has been approved for patients with end stage heart failure as destination therapy.

As work went forward on the totally implantable heart, left ventricular assist devices (LVAD) were also being developed. The pharmacologic support of end stage left ventricular failure with vasodilators and inotropic agents has provided modest temporary benefit; but it has become obvious that we have reached a therapeutic wall with very few new medical options on the horizon. LVADs appeared to be our current best hope of providing additional short- and long-term support for the failing left ventricle.

Dr. E. Stanley Crawford and Dr. Domingo Liotta performed the first LVAD implant in 1966 in a patient who had cardiac arrest after surgery. Since then, there have been a variety of LVADs developed that were initially pulsatile, but now are more commonly continuous flow. Both types of devices are externally powered via drive lines and able to achieve flows up to 10 L/min and are interposed between a left ventricular apical conduit and an ascending aorta conduit. The initial LVADs were pulsatile devices based on the presumption that pulsatile flow was important for systemic perfusion and normal physiology. However, continuous-flow LVAD has proven to be quite compatible with normal organ function and perfusion, and shown better durability and lower mortality and morbidity compared to the pulsatile flow devices. (J. Am. Coll. Cardiol. 2011;57:1890-8).

In addition, as noted in "The Lead," LVADs have shown superiority over medical therapy in patients with advanced heart failure as destination therapy, and the 1-year mortality with continuous flow LVADs now approximates the experience with the 1-year mortality of patients receiving a heart transplant.

The expanded use of LVADs from creating a bridge for transplantation to destination therapy has opened an entirely new opportunity for the use of LVADs in the treatment of acute, but most importantly, chronic heart failure. The limitation of heart transplantation as a function of donor availability together with the limitation of medical therapy for heart failure patients has generated increased interest in LVADs for chronic therapy in patients with end-stage heart failure. The observation that in some patients, particularly those with reversible heart failure like myocarditis, the heart may actually recover during LVAD therapy and allow for its removal, provides a window into future clinical applications (N. Engl. J. Med. 2006:355;1873-84)

The potential for further miniaturization of these devices and the potential for total implantability also open new horizons for LVAD therapy. Total implantability hinges on the ability to apply technology of transcutaneous power source that is already available in a number of electronic implantable devices, including the total heart implant. The resolution of these technical issues will allow for further expansion of the clinical indications for LVAD therapy.

Dr. Goldstein, medical editor of Cardiology News, is a professor of medicine at Wayne State University and division head emeritus of cardiovascular medicine at Henry Ford Hospital, both in Detroit. He is on data safety monitoring committees for the National Institutes of Health and several pharmaceutical companies.

Physicians struggle every day to pick the right drug dosage for the treatment and prevention of disease. For the acute illnesses, efficacy is evident within hours or days. For the prevention of chronic disease, however, the outcome is uncertain at best. Therefore, we rely on randomized clinical trials to provide evidence that a specific drug and dosage are safe and effective.

Unfortunately, because of the limited average follow-up of 3-5 years, randomized clinical trials (RCTs) do not provide efficacy and safety information for lifetime therapy that is often advocated for the prevention of chronic disease.

For both the patient and physician, the side effects become the deciding factor. The physician usually chooses the smallest dose in order to avoid toxicity and presumably to achieve some benefit. The patient takes the drug irregularly at best.

As an example, consider the appropriate dosage for statin therapy for the prevention of atherosclerotic cardiovascular disease. Although numerous RCTs have defined the effective dose of a number of statins, recent trends in therapeutics have advocated that rather than using the dose that was used in RCTs, clinicians should increase the dose in order to reach a specific LDL cholesterol blood level.

Choosing the dosage of a drug in an RCT is a less-than-perfect exercise. Here’s how it usually goes:

Phase I trials – often based on pharmacokinetic data derived from animal studies – examine the physiological characteristics of the drug in healthy human volunteers in order to determine an effective and safe dosage prior to a phase II trial.

Phase II trials are larger; they usually examine the effect of several different dosages on a target population, and are focused not on physiological effects but on clinical outcomes and safety, in order to choose the best dosage for a phase III study. Because of their small size, these phase II studies are underpowered and prone to providing misleading dose choices.

Nevertheless, one or two doses are chosen to be used in the definitive phase III RCT, which includes enough patients to provide proof of benefit and safety of the drug based solely on its effect on mortality and morbidity.

Information is often collected in regard to the physiological effects of the drug on, for example, LDL cholesterol (in the case of statins) or heart rate (in the case of beta-blocking drugs). The proof of benefit, however, is determined by clinical outcomes, not on the physiological or "surrogate" measurements.

In the process of designing an RCT, we often make presumptions about mechanisms and will identify certain parameters that theoretically provide insight into the presumed benefit. However, many of the drugs we use have physiological effects that extend beyond the specific therapeutic target. We often remain ignorant about the mechanism by which drugs express their benefit long after their proof of benefit is demonstrated.

Statins, for instance, have a variety of pleiotropic effects. One of the most interesting is their ability to modulate inflammation, a process that is thought to be central to the progression of atherosclerotic disease. Although we presume that their effect is on LDL cholesterol, that presumption may be incorrect. Similarly, beta-blockers have well-known effects on heart rate and blood pressure, but their effect on modulating the up-regulated sympathetic nervous system in heart failure has presumed importance well beyond their effect on heart rate and blood pressure.

It is tempting to make presumptions about the effect of a drug intervention on the basis of surrogate measures like heart rate or LDL cholesterol effects, but their mechanisms of action on mortality and morbidity of disease may be unrelated to that measure.

RCTs have come a long way from relying on "surrogate" end points as the basis for making therapeutic decisions. More than 20 years ago, the CAST (Cardiac Arrhythmia Suppression Trial) was the watershed RCT that excluded the surrogate as a measure of therapeutic efficacy (J. Am. Coll. Cardiol. 1991;18:14-9). At a time when ventricular premature contraction (VPC) suppression was the "mantra" to prevent sudden death, CAST examined the pharmacologic suppression of VPCs in post–MI patients and found that, as the drugs decreased ventricular ectopy, mortality increased.

The use of the seemingly appropriate and obvious "surrogate" of LDL cholesterol lowering as a measure of therapeutic efficacy may be just as illusory. As enticing as surrogates are, the contemporary drive to lower LDL cholesterol may be as misdirected as the target to decrease the frequency of VPCs to prevent sudden death.

Like many things in life and science, things may not be what they seem.

Dr. Goldstein, the medical editor of Cardiology News, is a professor of medicine at Wayne State University and division head emeritus of cardiovascular medicine at Henry Ford Hospital, both in Detroit. He is on data safety monitoring committees for the National Institutes of Health and several pharmaceutical companies.

Physicians struggle every day to pick the right drug dosage for the treatment and prevention of disease. For the acute illnesses, efficacy is evident within hours or days. For the prevention of chronic disease, however, the outcome is uncertain at best. Therefore, we rely on randomized clinical trials to provide evidence that a specific drug and dosage are safe and effective.

Unfortunately, because of the limited average follow-up of 3-5 years, randomized clinical trials (RCTs) do not provide efficacy and safety information for lifetime therapy that is often advocated for the prevention of chronic disease.

For both the patient and physician, the side effects become the deciding factor. The physician usually chooses the smallest dose in order to avoid toxicity and presumably to achieve some benefit. The patient takes the drug irregularly at best.

As an example, consider the appropriate dosage for statin therapy for the prevention of atherosclerotic cardiovascular disease. Although numerous RCTs have defined the effective dose of a number of statins, recent trends in therapeutics have advocated that rather than using the dose that was used in RCTs, clinicians should increase the dose in order to reach a specific LDL cholesterol blood level.

Choosing the dosage of a drug in an RCT is a less-than-perfect exercise. Here’s how it usually goes:

Phase I trials – often based on pharmacokinetic data derived from animal studies – examine the physiological characteristics of the drug in healthy human volunteers in order to determine an effective and safe dosage prior to a phase II trial.

Phase II trials are larger; they usually examine the effect of several different dosages on a target population, and are focused not on physiological effects but on clinical outcomes and safety, in order to choose the best dosage for a phase III study. Because of their small size, these phase II studies are underpowered and prone to providing misleading dose choices.

Nevertheless, one or two doses are chosen to be used in the definitive phase III RCT, which includes enough patients to provide proof of benefit and safety of the drug based solely on its effect on mortality and morbidity.

Information is often collected in regard to the physiological effects of the drug on, for example, LDL cholesterol (in the case of statins) or heart rate (in the case of beta-blocking drugs). The proof of benefit, however, is determined by clinical outcomes, not on the physiological or "surrogate" measurements.

In the process of designing an RCT, we often make presumptions about mechanisms and will identify certain parameters that theoretically provide insight into the presumed benefit. However, many of the drugs we use have physiological effects that extend beyond the specific therapeutic target. We often remain ignorant about the mechanism by which drugs express their benefit long after their proof of benefit is demonstrated.

Statins, for instance, have a variety of pleiotropic effects. One of the most interesting is their ability to modulate inflammation, a process that is thought to be central to the progression of atherosclerotic disease. Although we presume that their effect is on LDL cholesterol, that presumption may be incorrect. Similarly, beta-blockers have well-known effects on heart rate and blood pressure, but their effect on modulating the up-regulated sympathetic nervous system in heart failure has presumed importance well beyond their effect on heart rate and blood pressure.

It is tempting to make presumptions about the effect of a drug intervention on the basis of surrogate measures like heart rate or LDL cholesterol effects, but their mechanisms of action on mortality and morbidity of disease may be unrelated to that measure.

RCTs have come a long way from relying on "surrogate" end points as the basis for making therapeutic decisions. More than 20 years ago, the CAST (Cardiac Arrhythmia Suppression Trial) was the watershed RCT that excluded the surrogate as a measure of therapeutic efficacy (J. Am. Coll. Cardiol. 1991;18:14-9). At a time when ventricular premature contraction (VPC) suppression was the "mantra" to prevent sudden death, CAST examined the pharmacologic suppression of VPCs in post–MI patients and found that, as the drugs decreased ventricular ectopy, mortality increased.

The use of the seemingly appropriate and obvious "surrogate" of LDL cholesterol lowering as a measure of therapeutic efficacy may be just as illusory. As enticing as surrogates are, the contemporary drive to lower LDL cholesterol may be as misdirected as the target to decrease the frequency of VPCs to prevent sudden death.

Like many things in life and science, things may not be what they seem.

Dr. Goldstein, the medical editor of Cardiology News, is a professor of medicine at Wayne State University and division head emeritus of cardiovascular medicine at Henry Ford Hospital, both in Detroit. He is on data safety monitoring committees for the National Institutes of Health and several pharmaceutical companies.

Physicians struggle every day to pick the right drug dosage for the treatment and prevention of disease. For the acute illnesses, efficacy is evident within hours or days. For the prevention of chronic disease, however, the outcome is uncertain at best. Therefore, we rely on randomized clinical trials to provide evidence that a specific drug and dosage are safe and effective.

Unfortunately, because of the limited average follow-up of 3-5 years, randomized clinical trials (RCTs) do not provide efficacy and safety information for lifetime therapy that is often advocated for the prevention of chronic disease.

For both the patient and physician, the side effects become the deciding factor. The physician usually chooses the smallest dose in order to avoid toxicity and presumably to achieve some benefit. The patient takes the drug irregularly at best.

As an example, consider the appropriate dosage for statin therapy for the prevention of atherosclerotic cardiovascular disease. Although numerous RCTs have defined the effective dose of a number of statins, recent trends in therapeutics have advocated that rather than using the dose that was used in RCTs, clinicians should increase the dose in order to reach a specific LDL cholesterol blood level.

Choosing the dosage of a drug in an RCT is a less-than-perfect exercise. Here’s how it usually goes:

Phase I trials – often based on pharmacokinetic data derived from animal studies – examine the physiological characteristics of the drug in healthy human volunteers in order to determine an effective and safe dosage prior to a phase II trial.

Phase II trials are larger; they usually examine the effect of several different dosages on a target population, and are focused not on physiological effects but on clinical outcomes and safety, in order to choose the best dosage for a phase III study. Because of their small size, these phase II studies are underpowered and prone to providing misleading dose choices.

Nevertheless, one or two doses are chosen to be used in the definitive phase III RCT, which includes enough patients to provide proof of benefit and safety of the drug based solely on its effect on mortality and morbidity.

Information is often collected in regard to the physiological effects of the drug on, for example, LDL cholesterol (in the case of statins) or heart rate (in the case of beta-blocking drugs). The proof of benefit, however, is determined by clinical outcomes, not on the physiological or "surrogate" measurements.

In the process of designing an RCT, we often make presumptions about mechanisms and will identify certain parameters that theoretically provide insight into the presumed benefit. However, many of the drugs we use have physiological effects that extend beyond the specific therapeutic target. We often remain ignorant about the mechanism by which drugs express their benefit long after their proof of benefit is demonstrated.

Statins, for instance, have a variety of pleiotropic effects. One of the most interesting is their ability to modulate inflammation, a process that is thought to be central to the progression of atherosclerotic disease. Although we presume that their effect is on LDL cholesterol, that presumption may be incorrect. Similarly, beta-blockers have well-known effects on heart rate and blood pressure, but their effect on modulating the up-regulated sympathetic nervous system in heart failure has presumed importance well beyond their effect on heart rate and blood pressure.

It is tempting to make presumptions about the effect of a drug intervention on the basis of surrogate measures like heart rate or LDL cholesterol effects, but their mechanisms of action on mortality and morbidity of disease may be unrelated to that measure.

RCTs have come a long way from relying on "surrogate" end points as the basis for making therapeutic decisions. More than 20 years ago, the CAST (Cardiac Arrhythmia Suppression Trial) was the watershed RCT that excluded the surrogate as a measure of therapeutic efficacy (J. Am. Coll. Cardiol. 1991;18:14-9). At a time when ventricular premature contraction (VPC) suppression was the "mantra" to prevent sudden death, CAST examined the pharmacologic suppression of VPCs in post–MI patients and found that, as the drugs decreased ventricular ectopy, mortality increased.

The use of the seemingly appropriate and obvious "surrogate" of LDL cholesterol lowering as a measure of therapeutic efficacy may be just as illusory. As enticing as surrogates are, the contemporary drive to lower LDL cholesterol may be as misdirected as the target to decrease the frequency of VPCs to prevent sudden death.

Like many things in life and science, things may not be what they seem.

Dr. Goldstein, the medical editor of Cardiology News, is a professor of medicine at Wayne State University and division head emeritus of cardiovascular medicine at Henry Ford Hospital, both in Detroit. He is on data safety monitoring committees for the National Institutes of Health and several pharmaceutical companies.

Rehospitalization within 30 days of an initial acute coronary syndrome or heart failure event has now become a CMS quality measure that will affect overall hospital Medicare payments. It has been appreciated for some time that rehospitalization for these diagnoses has been unacceptably high.

A recent report indicates that a greater percentage of U.S. patients who experienced a STEMI are more likely to be rehospitalized within 30 days, compared with other Western countries (14.5% vs. 9.9%, respectively). That report (JAMA 2012;307:66-74) indicates that the increase is directly related to the shorter length of hospital stay in the United States. Among the 17 countries included in the report, the average duration was shortest in the United States (3 days) and longest in Germany (8 days). Predictors of readmission other than length of stay include the age of the patient and the presence of heart failure. The most interesting part of the story is how we arrived at this state of affairs.

For those of you who were not yet born or are too young to remember when Medicare was passed into law in 1965, I will give you a little history. And for those of you who were around at the time, I will provide a reminder.

As you undoubtedly know, Medicare, in addition to paying physicians’ fees also pays hospital costs. In the period between 1965 and 1983, using a payment system that was defined as "reasonable and allowable costs," Medicare payments to hospitals increased 10-fold, from $3 billion to $37 billion. In consequence, Congress passed a law in 1982 that created a prospective payment system for hospitals using diagnosis-related groups establishing a payment schedule for specific diagnoses, which included acute myocardial infarction and heart failure. With this schedule, hospitals were paid a fixed rate regardless of the number of procedures performed or duration of hospitalization. In order to minimize costs, hospitals accelerated discharges and shortened hospital length of stay. Emergency admissions resulted in urgent discharge.

In order to expedite the process of admission and discharge, hospitalists were hired to accelerate that process since practicing internists and cardiologists were not available to push the paperwork through fast enough to get the patients discharged quickly. Hospitals saw this additional layer of doctors caring for patients as financially profitable. As a result, hospital stays decreased markedly and payments to hospitals decreased by 52% from 1985 to 1990 and by an additional 37% between 1990 and 1995. Everyone seemed to be very happy with this, including the hospitals, Medicare, and doctors. As far as I know, patients were not consulted.

Cardiologists at that time were telling themselves how benign an acute MI is and began doing accelerated discharge after percutaneous coronary intervention. We prided ourselves on how patients could be discharged to home within 24-36 hours, but never actually reached the ultimate goal of a "drive-through PCI." The fact that patients with acute MI and heart failure were frequently readmitted was good business since each admission resulted in further Medicare payments both to the hospital and the doctors. Urging by some physicians to develop plans that could educate patients and develop discharge follow-up systems was met with incredulity by hospital administrators who saw readmission as a revenue source and discharge planning as costly.

It is important to emphasize that readmission not only reflects an important morbidity event, it also carries with it the potential for increased risk of mortality. In the report cited above, one-third of the deaths after hospitalization for a STEMI occurred within the same 30-day post-event period. The recent emphasis on decreasing door-to-balloon time, although effective in shortening that period, has had little effect on the mortality associated with an acute myocardial infarction. It is reasonable to assume that in placing a greater emphasis on insuring that patients are ready to leave the hospital, we can improve mortality and morbidity of both the ACS and heart failure patient. There really is no urgency to discharge patients other than improving the bottom line, and that imperative may no longer be relevant.

Dr. Goldstein, medical editor of Cardiology News, is professor of medicine at Wayne State University and division head emeritus of cardiovascular medicine at Henry Ford Hospital, both in Detroit. He is on data safety monitoring committees for the National Institutes of Health and several pharmaceutical companies.

Rehospitalization within 30 days of an initial acute coronary syndrome or heart failure event has now become a CMS quality measure that will affect overall hospital Medicare payments. It has been appreciated for some time that rehospitalization for these diagnoses has been unacceptably high.

A recent report indicates that a greater percentage of U.S. patients who experienced a STEMI are more likely to be rehospitalized within 30 days, compared with other Western countries (14.5% vs. 9.9%, respectively). That report (JAMA 2012;307:66-74) indicates that the increase is directly related to the shorter length of hospital stay in the United States. Among the 17 countries included in the report, the average duration was shortest in the United States (3 days) and longest in Germany (8 days). Predictors of readmission other than length of stay include the age of the patient and the presence of heart failure. The most interesting part of the story is how we arrived at this state of affairs.

For those of you who were not yet born or are too young to remember when Medicare was passed into law in 1965, I will give you a little history. And for those of you who were around at the time, I will provide a reminder.

As you undoubtedly know, Medicare, in addition to paying physicians’ fees also pays hospital costs. In the period between 1965 and 1983, using a payment system that was defined as "reasonable and allowable costs," Medicare payments to hospitals increased 10-fold, from $3 billion to $37 billion. In consequence, Congress passed a law in 1982 that created a prospective payment system for hospitals using diagnosis-related groups establishing a payment schedule for specific diagnoses, which included acute myocardial infarction and heart failure. With this schedule, hospitals were paid a fixed rate regardless of the number of procedures performed or duration of hospitalization. In order to minimize costs, hospitals accelerated discharges and shortened hospital length of stay. Emergency admissions resulted in urgent discharge.

In order to expedite the process of admission and discharge, hospitalists were hired to accelerate that process since practicing internists and cardiologists were not available to push the paperwork through fast enough to get the patients discharged quickly. Hospitals saw this additional layer of doctors caring for patients as financially profitable. As a result, hospital stays decreased markedly and payments to hospitals decreased by 52% from 1985 to 1990 and by an additional 37% between 1990 and 1995. Everyone seemed to be very happy with this, including the hospitals, Medicare, and doctors. As far as I know, patients were not consulted.

Cardiologists at that time were telling themselves how benign an acute MI is and began doing accelerated discharge after percutaneous coronary intervention. We prided ourselves on how patients could be discharged to home within 24-36 hours, but never actually reached the ultimate goal of a "drive-through PCI." The fact that patients with acute MI and heart failure were frequently readmitted was good business since each admission resulted in further Medicare payments both to the hospital and the doctors. Urging by some physicians to develop plans that could educate patients and develop discharge follow-up systems was met with incredulity by hospital administrators who saw readmission as a revenue source and discharge planning as costly.

It is important to emphasize that readmission not only reflects an important morbidity event, it also carries with it the potential for increased risk of mortality. In the report cited above, one-third of the deaths after hospitalization for a STEMI occurred within the same 30-day post-event period. The recent emphasis on decreasing door-to-balloon time, although effective in shortening that period, has had little effect on the mortality associated with an acute myocardial infarction. It is reasonable to assume that in placing a greater emphasis on insuring that patients are ready to leave the hospital, we can improve mortality and morbidity of both the ACS and heart failure patient. There really is no urgency to discharge patients other than improving the bottom line, and that imperative may no longer be relevant.

Dr. Goldstein, medical editor of Cardiology News, is professor of medicine at Wayne State University and division head emeritus of cardiovascular medicine at Henry Ford Hospital, both in Detroit. He is on data safety monitoring committees for the National Institutes of Health and several pharmaceutical companies.

Rehospitalization within 30 days of an initial acute coronary syndrome or heart failure event has now become a CMS quality measure that will affect overall hospital Medicare payments. It has been appreciated for some time that rehospitalization for these diagnoses has been unacceptably high.

A recent report indicates that a greater percentage of U.S. patients who experienced a STEMI are more likely to be rehospitalized within 30 days, compared with other Western countries (14.5% vs. 9.9%, respectively). That report (JAMA 2012;307:66-74) indicates that the increase is directly related to the shorter length of hospital stay in the United States. Among the 17 countries included in the report, the average duration was shortest in the United States (3 days) and longest in Germany (8 days). Predictors of readmission other than length of stay include the age of the patient and the presence of heart failure. The most interesting part of the story is how we arrived at this state of affairs.

For those of you who were not yet born or are too young to remember when Medicare was passed into law in 1965, I will give you a little history. And for those of you who were around at the time, I will provide a reminder.

As you undoubtedly know, Medicare, in addition to paying physicians’ fees also pays hospital costs. In the period between 1965 and 1983, using a payment system that was defined as "reasonable and allowable costs," Medicare payments to hospitals increased 10-fold, from $3 billion to $37 billion. In consequence, Congress passed a law in 1982 that created a prospective payment system for hospitals using diagnosis-related groups establishing a payment schedule for specific diagnoses, which included acute myocardial infarction and heart failure. With this schedule, hospitals were paid a fixed rate regardless of the number of procedures performed or duration of hospitalization. In order to minimize costs, hospitals accelerated discharges and shortened hospital length of stay. Emergency admissions resulted in urgent discharge.

In order to expedite the process of admission and discharge, hospitalists were hired to accelerate that process since practicing internists and cardiologists were not available to push the paperwork through fast enough to get the patients discharged quickly. Hospitals saw this additional layer of doctors caring for patients as financially profitable. As a result, hospital stays decreased markedly and payments to hospitals decreased by 52% from 1985 to 1990 and by an additional 37% between 1990 and 1995. Everyone seemed to be very happy with this, including the hospitals, Medicare, and doctors. As far as I know, patients were not consulted.

Cardiologists at that time were telling themselves how benign an acute MI is and began doing accelerated discharge after percutaneous coronary intervention. We prided ourselves on how patients could be discharged to home within 24-36 hours, but never actually reached the ultimate goal of a "drive-through PCI." The fact that patients with acute MI and heart failure were frequently readmitted was good business since each admission resulted in further Medicare payments both to the hospital and the doctors. Urging by some physicians to develop plans that could educate patients and develop discharge follow-up systems was met with incredulity by hospital administrators who saw readmission as a revenue source and discharge planning as costly.

It is important to emphasize that readmission not only reflects an important morbidity event, it also carries with it the potential for increased risk of mortality. In the report cited above, one-third of the deaths after hospitalization for a STEMI occurred within the same 30-day post-event period. The recent emphasis on decreasing door-to-balloon time, although effective in shortening that period, has had little effect on the mortality associated with an acute myocardial infarction. It is reasonable to assume that in placing a greater emphasis on insuring that patients are ready to leave the hospital, we can improve mortality and morbidity of both the ACS and heart failure patient. There really is no urgency to discharge patients other than improving the bottom line, and that imperative may no longer be relevant.

Dr. Goldstein, medical editor of Cardiology News, is professor of medicine at Wayne State University and division head emeritus of cardiovascular medicine at Henry Ford Hospital, both in Detroit. He is on data safety monitoring committees for the National Institutes of Health and several pharmaceutical companies.

The annual meetings of the American College of Cardiology and the American Heart Association have been the centerpiece for the international exchange of ideas in clinical and basic cardiology for the last half century. They have attracted research scientists from around the world as a result of their preeminence as a platform for the presentation of new concepts.

They provided the setting for Mason Sones to show the first direct angiographic imaging of the coronary artery, for Andreis Grunzig to demonstrate the first percutaneous dilatation of the coronary artery, and for Michel Mirowski to present the first demonstration of the automatic implanted defibrillator. Those events caused gasps in the audience as we all saw, for the first time, a major breakthrough in cardiovascular medicine.

The scramble to get onto that platform or to be in that audience when the newest discovery was presented drew large audiences. The decrease in attendance in the past few years can be viewed as an index of the decrease in the importance of that platform.

The decreased attendance in the AHA and ACC annual scientific sessions provides ample evidence of the reduced role of American leadership and the ascendancy of European leadership in the world of cardiology. As the attendance at American meetings has ebbed, the European Society of Cardiology has seen a progressive increase in attendance of its annual meeting.

The AHA reached its highest attendance in the later part of the last century when its professional attendance in 1999 topped just over 20,000. It gradually slipped to 19,169 in 2010, and was 15,553 in Orlando in 2011. The ACC professional attendance has also fallen, from 18,542 in 2008 to 12,980 in 2011. At the same time, the attendance at the European Society of Cardiology has increased from 18,413 in 2002 in Berlin to almost 27,080 professional attendees in 2011 in Paris.

This decrease has not been observed in all American medical specialties. The Radiological Society of North America has had approximately 27,000 professional attendees for the last 5 years, and it advertises nearly eight football fields of exhibits.

One factor limiting attendance at some meetings is the expense, including the increase in admission fees, which now have gotten well into the four-figure level even if you are a member.

One of the most striking changes at the recent AHA and ACC meetings was the stark decrease in exhibitors. Exhibits that seemed to go on for miles in previous years, requiring rest stops at coffee stands along the way, have now became accessible with a casual walk. Many of the high-tech exhibitors either shrank their exhibit space or were entirely absent. Attendance and the number of exhibitors at the recent AHA meeting were impacted by the annual meeting of Transcatheter Cardiovascular Therapeutics, which had more than 12,000 attendees and was being held almost simultaneously a continent away. In order to fill the exhibition space at the recent AHA meeting, booth space was given over to displays of costume jewelry and pashmina scarves.

It is estimated by representatives of the ACC that international attendance at American meetings has decreased by at least one-third. This decrease is open to different interpretations. It has become increasingly difficult, for example, for many Asian and Eastern European cardiologists to obtain U.S. visas. But the fact that the Europeans do have an excellent meeting on their own soil has made that meeting more accessible to them. It is also clear that more Asian and American cardiologists are attending the European meeting. Part of this attraction has been related to a friendlier environment for the performance and consequent presentation of clinical trials in Europe.

The decrease in attendance at the American meetings is, in large part, a result of the balkanization of the "big tent" of cardiology. The creation of specialty associations by electrophysiologists, interventionalists, and heart failure specialists, to name but a few, has impacted on the appeal of – and need to engage in – the large annual meeting in order to satisfy professional requirements. Specialty cardiologists now have not only their own meeting platforms, but also their own specialty journals, which are in direct competition with JACC and Circulation.

What is lost, however, is the integrated educational experience that the practicing cardiologist needs in order to bring the entirety of cardiovascular science to the individual patient. When the field of cardiology was smaller and its scientific and clinical horizons were nearer at hand, this could be accomplished at one meeting.

We have, unfortunately, outgrown our "tent," but the Internet is now there to help us. Access to the meeting’s scientific presentations is now readily available through a variety of electronic media sites, including Cardiology News.

The annual meetings of the American College of Cardiology and the American Heart Association have been the centerpiece for the international exchange of ideas in clinical and basic cardiology for the last half century. They have attracted research scientists from around the world as a result of their preeminence as a platform for the presentation of new concepts.

They provided the setting for Mason Sones to show the first direct angiographic imaging of the coronary artery, for Andreis Grunzig to demonstrate the first percutaneous dilatation of the coronary artery, and for Michel Mirowski to present the first demonstration of the automatic implanted defibrillator. Those events caused gasps in the audience as we all saw, for the first time, a major breakthrough in cardiovascular medicine.

The scramble to get onto that platform or to be in that audience when the newest discovery was presented drew large audiences. The decrease in attendance in the past few years can be viewed as an index of the decrease in the importance of that platform.

The decreased attendance in the AHA and ACC annual scientific sessions provides ample evidence of the reduced role of American leadership and the ascendancy of European leadership in the world of cardiology. As the attendance at American meetings has ebbed, the European Society of Cardiology has seen a progressive increase in attendance of its annual meeting.

The AHA reached its highest attendance in the later part of the last century when its professional attendance in 1999 topped just over 20,000. It gradually slipped to 19,169 in 2010, and was 15,553 in Orlando in 2011. The ACC professional attendance has also fallen, from 18,542 in 2008 to 12,980 in 2011. At the same time, the attendance at the European Society of Cardiology has increased from 18,413 in 2002 in Berlin to almost 27,080 professional attendees in 2011 in Paris.

This decrease has not been observed in all American medical specialties. The Radiological Society of North America has had approximately 27,000 professional attendees for the last 5 years, and it advertises nearly eight football fields of exhibits.

One factor limiting attendance at some meetings is the expense, including the increase in admission fees, which now have gotten well into the four-figure level even if you are a member.

One of the most striking changes at the recent AHA and ACC meetings was the stark decrease in exhibitors. Exhibits that seemed to go on for miles in previous years, requiring rest stops at coffee stands along the way, have now became accessible with a casual walk. Many of the high-tech exhibitors either shrank their exhibit space or were entirely absent. Attendance and the number of exhibitors at the recent AHA meeting were impacted by the annual meeting of Transcatheter Cardiovascular Therapeutics, which had more than 12,000 attendees and was being held almost simultaneously a continent away. In order to fill the exhibition space at the recent AHA meeting, booth space was given over to displays of costume jewelry and pashmina scarves.

It is estimated by representatives of the ACC that international attendance at American meetings has decreased by at least one-third. This decrease is open to different interpretations. It has become increasingly difficult, for example, for many Asian and Eastern European cardiologists to obtain U.S. visas. But the fact that the Europeans do have an excellent meeting on their own soil has made that meeting more accessible to them. It is also clear that more Asian and American cardiologists are attending the European meeting. Part of this attraction has been related to a friendlier environment for the performance and consequent presentation of clinical trials in Europe.

The decrease in attendance at the American meetings is, in large part, a result of the balkanization of the "big tent" of cardiology. The creation of specialty associations by electrophysiologists, interventionalists, and heart failure specialists, to name but a few, has impacted on the appeal of – and need to engage in – the large annual meeting in order to satisfy professional requirements. Specialty cardiologists now have not only their own meeting platforms, but also their own specialty journals, which are in direct competition with JACC and Circulation.

What is lost, however, is the integrated educational experience that the practicing cardiologist needs in order to bring the entirety of cardiovascular science to the individual patient. When the field of cardiology was smaller and its scientific and clinical horizons were nearer at hand, this could be accomplished at one meeting.

We have, unfortunately, outgrown our "tent," but the Internet is now there to help us. Access to the meeting’s scientific presentations is now readily available through a variety of electronic media sites, including Cardiology News.

The annual meetings of the American College of Cardiology and the American Heart Association have been the centerpiece for the international exchange of ideas in clinical and basic cardiology for the last half century. They have attracted research scientists from around the world as a result of their preeminence as a platform for the presentation of new concepts.

They provided the setting for Mason Sones to show the first direct angiographic imaging of the coronary artery, for Andreis Grunzig to demonstrate the first percutaneous dilatation of the coronary artery, and for Michel Mirowski to present the first demonstration of the automatic implanted defibrillator. Those events caused gasps in the audience as we all saw, for the first time, a major breakthrough in cardiovascular medicine.

The scramble to get onto that platform or to be in that audience when the newest discovery was presented drew large audiences. The decrease in attendance in the past few years can be viewed as an index of the decrease in the importance of that platform.

The decreased attendance in the AHA and ACC annual scientific sessions provides ample evidence of the reduced role of American leadership and the ascendancy of European leadership in the world of cardiology. As the attendance at American meetings has ebbed, the European Society of Cardiology has seen a progressive increase in attendance of its annual meeting.

The AHA reached its highest attendance in the later part of the last century when its professional attendance in 1999 topped just over 20,000. It gradually slipped to 19,169 in 2010, and was 15,553 in Orlando in 2011. The ACC professional attendance has also fallen, from 18,542 in 2008 to 12,980 in 2011. At the same time, the attendance at the European Society of Cardiology has increased from 18,413 in 2002 in Berlin to almost 27,080 professional attendees in 2011 in Paris.

This decrease has not been observed in all American medical specialties. The Radiological Society of North America has had approximately 27,000 professional attendees for the last 5 years, and it advertises nearly eight football fields of exhibits.

One factor limiting attendance at some meetings is the expense, including the increase in admission fees, which now have gotten well into the four-figure level even if you are a member.

One of the most striking changes at the recent AHA and ACC meetings was the stark decrease in exhibitors. Exhibits that seemed to go on for miles in previous years, requiring rest stops at coffee stands along the way, have now became accessible with a casual walk. Many of the high-tech exhibitors either shrank their exhibit space or were entirely absent. Attendance and the number of exhibitors at the recent AHA meeting were impacted by the annual meeting of Transcatheter Cardiovascular Therapeutics, which had more than 12,000 attendees and was being held almost simultaneously a continent away. In order to fill the exhibition space at the recent AHA meeting, booth space was given over to displays of costume jewelry and pashmina scarves.

It is estimated by representatives of the ACC that international attendance at American meetings has decreased by at least one-third. This decrease is open to different interpretations. It has become increasingly difficult, for example, for many Asian and Eastern European cardiologists to obtain U.S. visas. But the fact that the Europeans do have an excellent meeting on their own soil has made that meeting more accessible to them. It is also clear that more Asian and American cardiologists are attending the European meeting. Part of this attraction has been related to a friendlier environment for the performance and consequent presentation of clinical trials in Europe.

The decrease in attendance at the American meetings is, in large part, a result of the balkanization of the "big tent" of cardiology. The creation of specialty associations by electrophysiologists, interventionalists, and heart failure specialists, to name but a few, has impacted on the appeal of – and need to engage in – the large annual meeting in order to satisfy professional requirements. Specialty cardiologists now have not only their own meeting platforms, but also their own specialty journals, which are in direct competition with JACC and Circulation.

What is lost, however, is the integrated educational experience that the practicing cardiologist needs in order to bring the entirety of cardiovascular science to the individual patient. When the field of cardiology was smaller and its scientific and clinical horizons were nearer at hand, this could be accomplished at one meeting.

We have, unfortunately, outgrown our "tent," but the Internet is now there to help us. Access to the meeting’s scientific presentations is now readily available through a variety of electronic media sites, including Cardiology News.

It has been 100 years since Sir William Osler outlined his concept of the relationship of the hospital to the university and to the education of physicians and nurses in an address to the Northumberland and Durham Medical Society in England. He stated that the hospital stands "primarily for the cure of the sick and the relief of suffering; secondly, for the study of the problems of disease; and thirdly, for the training of men and of women to serve the public as doctors and nurses. A majority of hospitals deal only with the first of these objects, and incidentally with the third" (Lancet 1911;177:211-3).

Of course, much has changed over the subsequent century, but much remains the same. The integration of the hospital into its role of a teaching institution was difficult even in the Oslerian age of the early 20th century. That relationship has become even more complex in contemporary medicine, in which the hospital has increasingly become the center of community and national health care.

Dr. Osler’s comments came to mind while I was reading a recent article about the development of concierge care in America’s most prestigious hospitals (New York Times, Jan. 22, 2012, p. 3A). A money manager recuperating from back pain is shown relaxing in a $1,600-a-day luxurious hospital room dressed in a spa-type bathrobe in New York City’s Mount Sinai Medical Center, where amenities include gourmet food service. "I have a primary care physician who acts as ringmaster for all my other doctors. And I see no people in training – only the best of the best," the patient said.

The hospital’s spokesperson indicated that the lack of house staff was a result of training limitations and not the preference of the rich patients. Mount Sinai has a long history of excellence in medical education, but the ambience now provided for its wealthy clientele protects them from any intrusion by medical students and house staff.

The American hospital has evolved over the last century from a place of last resort for the poor sick to a high-technology institution created for intensive medical and surgical therapy. Funded initially by community and religious benevolence, the hospital has now become big business and heavily dependent on private insurers, Medicare and Medicaid, and whatever evolves from the new health care laws.

Now divested of minor illnesses and routine surgical procedures that can be dealt with in the outpatient setting, it is filled with critically sick patients.

There has always been a tenuous balance between the goals of the community hospital and its educational responsibilities. The contemporary community hospital has enjoyed a profitable environment fed by private health insurance and sustained by federal dollars. Medicare, since its inception almost 50 years ago, has generously supported education through indirect funding for house staff education. This support has recently been significantly decreased, and realistic forecasts suggest that the previous profit margins will be a thing of the past as the federal and state budget puts constraints on both Medicare and Medicaid. Dr. Osler argued for the hospital financial supporters of teaching faculty and challenged local communities to dig deep into their pockets to support the education of medical students and house staff.

Now, with the increasing development of hospital-centric health care, the hospital has also become the focus of community health. The need to train more health professionals will put more pressure on hospitals to provide facilities for the whole dimension of caregivers, including medical students, house officers, nurses, and a variety of physician assistants. With increases in both the number of medical schools and the matriculating class sizes of current medical schools, more community hospitals will be called upon to provide clinical facilities to provide the training grounds for these new students. These changes will place financial pressures on the hospitals in order to meet that challenge. Even now, fast-track admissions and discharge practice, already a part of the patient experience in many hospitals and a source of their profit margin, adversely affects the quality of medical education.

To cushion the effects of the decrease in private and governmental support for medical education, hospitals will be have to seek other sources of income – like concierge services – in order to meet their social and educational responsibilities.

How they meet both of these challenges in the contemporary entrepreneurial world of health care will require a great degree of agility. But no matter what changes do occur, there will always be room for concierge care.

It has been 100 years since Sir William Osler outlined his concept of the relationship of the hospital to the university and to the education of physicians and nurses in an address to the Northumberland and Durham Medical Society in England. He stated that the hospital stands "primarily for the cure of the sick and the relief of suffering; secondly, for the study of the problems of disease; and thirdly, for the training of men and of women to serve the public as doctors and nurses. A majority of hospitals deal only with the first of these objects, and incidentally with the third" (Lancet 1911;177:211-3).

Of course, much has changed over the subsequent century, but much remains the same. The integration of the hospital into its role of a teaching institution was difficult even in the Oslerian age of the early 20th century. That relationship has become even more complex in contemporary medicine, in which the hospital has increasingly become the center of community and national health care.

Dr. Osler’s comments came to mind while I was reading a recent article about the development of concierge care in America’s most prestigious hospitals (New York Times, Jan. 22, 2012, p. 3A). A money manager recuperating from back pain is shown relaxing in a $1,600-a-day luxurious hospital room dressed in a spa-type bathrobe in New York City’s Mount Sinai Medical Center, where amenities include gourmet food service. "I have a primary care physician who acts as ringmaster for all my other doctors. And I see no people in training – only the best of the best," the patient said.

The hospital’s spokesperson indicated that the lack of house staff was a result of training limitations and not the preference of the rich patients. Mount Sinai has a long history of excellence in medical education, but the ambience now provided for its wealthy clientele protects them from any intrusion by medical students and house staff.

The American hospital has evolved over the last century from a place of last resort for the poor sick to a high-technology institution created for intensive medical and surgical therapy. Funded initially by community and religious benevolence, the hospital has now become big business and heavily dependent on private insurers, Medicare and Medicaid, and whatever evolves from the new health care laws.

Now divested of minor illnesses and routine surgical procedures that can be dealt with in the outpatient setting, it is filled with critically sick patients.

There has always been a tenuous balance between the goals of the community hospital and its educational responsibilities. The contemporary community hospital has enjoyed a profitable environment fed by private health insurance and sustained by federal dollars. Medicare, since its inception almost 50 years ago, has generously supported education through indirect funding for house staff education. This support has recently been significantly decreased, and realistic forecasts suggest that the previous profit margins will be a thing of the past as the federal and state budget puts constraints on both Medicare and Medicaid. Dr. Osler argued for the hospital financial supporters of teaching faculty and challenged local communities to dig deep into their pockets to support the education of medical students and house staff.

Now, with the increasing development of hospital-centric health care, the hospital has also become the focus of community health. The need to train more health professionals will put more pressure on hospitals to provide facilities for the whole dimension of caregivers, including medical students, house officers, nurses, and a variety of physician assistants. With increases in both the number of medical schools and the matriculating class sizes of current medical schools, more community hospitals will be called upon to provide clinical facilities to provide the training grounds for these new students. These changes will place financial pressures on the hospitals in order to meet that challenge. Even now, fast-track admissions and discharge practice, already a part of the patient experience in many hospitals and a source of their profit margin, adversely affects the quality of medical education.

To cushion the effects of the decrease in private and governmental support for medical education, hospitals will be have to seek other sources of income – like concierge services – in order to meet their social and educational responsibilities.

How they meet both of these challenges in the contemporary entrepreneurial world of health care will require a great degree of agility. But no matter what changes do occur, there will always be room for concierge care.

It has been 100 years since Sir William Osler outlined his concept of the relationship of the hospital to the university and to the education of physicians and nurses in an address to the Northumberland and Durham Medical Society in England. He stated that the hospital stands "primarily for the cure of the sick and the relief of suffering; secondly, for the study of the problems of disease; and thirdly, for the training of men and of women to serve the public as doctors and nurses. A majority of hospitals deal only with the first of these objects, and incidentally with the third" (Lancet 1911;177:211-3).

Of course, much has changed over the subsequent century, but much remains the same. The integration of the hospital into its role of a teaching institution was difficult even in the Oslerian age of the early 20th century. That relationship has become even more complex in contemporary medicine, in which the hospital has increasingly become the center of community and national health care.

Dr. Osler’s comments came to mind while I was reading a recent article about the development of concierge care in America’s most prestigious hospitals (New York Times, Jan. 22, 2012, p. 3A). A money manager recuperating from back pain is shown relaxing in a $1,600-a-day luxurious hospital room dressed in a spa-type bathrobe in New York City’s Mount Sinai Medical Center, where amenities include gourmet food service. "I have a primary care physician who acts as ringmaster for all my other doctors. And I see no people in training – only the best of the best," the patient said.

The hospital’s spokesperson indicated that the lack of house staff was a result of training limitations and not the preference of the rich patients. Mount Sinai has a long history of excellence in medical education, but the ambience now provided for its wealthy clientele protects them from any intrusion by medical students and house staff.

The American hospital has evolved over the last century from a place of last resort for the poor sick to a high-technology institution created for intensive medical and surgical therapy. Funded initially by community and religious benevolence, the hospital has now become big business and heavily dependent on private insurers, Medicare and Medicaid, and whatever evolves from the new health care laws.

Now divested of minor illnesses and routine surgical procedures that can be dealt with in the outpatient setting, it is filled with critically sick patients.

There has always been a tenuous balance between the goals of the community hospital and its educational responsibilities. The contemporary community hospital has enjoyed a profitable environment fed by private health insurance and sustained by federal dollars. Medicare, since its inception almost 50 years ago, has generously supported education through indirect funding for house staff education. This support has recently been significantly decreased, and realistic forecasts suggest that the previous profit margins will be a thing of the past as the federal and state budget puts constraints on both Medicare and Medicaid. Dr. Osler argued for the hospital financial supporters of teaching faculty and challenged local communities to dig deep into their pockets to support the education of medical students and house staff.

Now, with the increasing development of hospital-centric health care, the hospital has also become the focus of community health. The need to train more health professionals will put more pressure on hospitals to provide facilities for the whole dimension of caregivers, including medical students, house officers, nurses, and a variety of physician assistants. With increases in both the number of medical schools and the matriculating class sizes of current medical schools, more community hospitals will be called upon to provide clinical facilities to provide the training grounds for these new students. These changes will place financial pressures on the hospitals in order to meet that challenge. Even now, fast-track admissions and discharge practice, already a part of the patient experience in many hospitals and a source of their profit margin, adversely affects the quality of medical education.

To cushion the effects of the decrease in private and governmental support for medical education, hospitals will be have to seek other sources of income – like concierge services – in order to meet their social and educational responsibilities.

How they meet both of these challenges in the contemporary entrepreneurial world of health care will require a great degree of agility. But no matter what changes do occur, there will always be room for concierge care.

It has been 17 years since the first publication of the Scandinavian Simvastatin Survival Study (Lancet 1994;344;1383-9) describing the benefit of coenzyme A reductase inhibitors (statins) on cardiovascular events in patients with coronary heart disease.

During this period, statins have become a major part of our strategy for the treatment and prevention of acute and chronic coronary heart disease. A number of statins have been introduced in a variety of clinical settings, and all have shown a consistent benefit. Although associated with some side effects, they have been relatively well tolerated by patients requiring either dose adjustment or switching to other drugs within the class.

Along the way, questions have been raised about the long-term safety of statins, and their potential oncogenic potential. The impact of statins directly on the cardiovascular intima has been elucidated using angiographic and intravascular imaging techniques. These studies have shown that statins mitigate to some degree the progression of localized intravascular abnormalities. Two recent studies provide important information both about the safety and long-term benefit of statins, and their remarkable effect on remodeling of the coronary arteries and regression of vascular lesions.

A recent intracoronary ultrasound study that compared high-dose rosuvastatin with atorvastatin in 1,039 patients with coronary disease provides striking evidence for the benefit of both of these drugs on regression of coronary plaque. In patients with residual lesions of 20%-50% by angiography, treatment with these drugs demonstrated a decrease in percent of atherosclerotic volume by 1.22% with rosuvastatin and by 0.99% with atorvastatin, and a decrease in total atheroma volume of 6.39 mm³ and 4.42 mm³, respectively. With doses of 40 mg atorvastatin and 80 mg rosuvastatin, low-density lipoprotein (LDL) cholesterol was decreased to 62.6 mg/dL and 70.2 mg/dL, respectively, and HDL cholesterol increased to 50.4 mg/dL and 48.6 mg/dL in the rosuvastatin and atorvastatin patients, respectively (N. Engl. J. Med. 2011;365;2078-87).

Regression of coronary lesions was observed in approximately two-thirds of the patients. Because of the short duration of the study, there were very few ischemic events and there was no difference between the two drug strategies. Since remodeling of the coronary artery is a surrogate indicator for clinical disease prevention, we cannot be certain that these ultrasound changes in plaques are directly related to the prevention of coronary events.

The second study of interest is the extended follow-up of the Heart Protection Study, which included more than 20,536 patients treated with 40 mg simvastatin or placebo for 5.3 years in-trial and a post-trial follow-up for a total 11 years (Lancet 2011:378;2013-20). There was an overall 23% decrease in major vascular events in the simvastatin-treated patients in the first year of the trial that continued to decrease annually during the trial phase. After study conclusion, when all patients were placed on therapy, there was a legacy benefit that persisted during the remaining 6 years of the study for the patients who were initially in the simvastatin arm of the study. The study confirms the long-term benefit of simvastatin and its safety without any evidence for an increase in cancer or other adverse events during the 11 years of follow-up.

The demonstration that statins can remodel the coronary artery provides pathologic support for their clinical benefit. Questions still remain in regard to mechanisms of action. The changes in the plaque volume theoretically could explain the therapeutic benefit of statins, but they must still be considered as surrogates for clinical benefit. Newer intravascular imaging technology using near-infrared spectroscopy is now able to characterize and measure the lipid core of the coronary plaque (JACC Cardiovasc. Imaging 2008;1:638-48), and may provide a better understanding of the mechanism by which statins modify plaque architecture.

Challenges still remain in regard to how the one-third of patients who did not experience any plaque regression should be approached. A treatment strategy for these presumably high-risk patients remains elusive.

Much has been learned from statin therapy, but many questions still remain in regard to the pathologic process by which the plaque progresses to cause an acute event, and how to prevent it.

This column, "Heart of the Matter," appears regularly in Cardiology News, a publication of Elsevier. Dr. Goldstein, medical editor of Cardiology News, is a professor of medicine at Wayne State University and division head emeritus of cardiovascular medicine at Henry Ford Hospital, both in Detroit. He is on data safety monitoring committees for the National Institutes of Health and several pharmaceutical companies.

It has been 17 years since the first publication of the Scandinavian Simvastatin Survival Study (Lancet 1994;344;1383-9) describing the benefit of coenzyme A reductase inhibitors (statins) on cardiovascular events in patients with coronary heart disease.

During this period, statins have become a major part of our strategy for the treatment and prevention of acute and chronic coronary heart disease. A number of statins have been introduced in a variety of clinical settings, and all have shown a consistent benefit. Although associated with some side effects, they have been relatively well tolerated by patients requiring either dose adjustment or switching to other drugs within the class.

Along the way, questions have been raised about the long-term safety of statins, and their potential oncogenic potential. The impact of statins directly on the cardiovascular intima has been elucidated using angiographic and intravascular imaging techniques. These studies have shown that statins mitigate to some degree the progression of localized intravascular abnormalities. Two recent studies provide important information both about the safety and long-term benefit of statins, and their remarkable effect on remodeling of the coronary arteries and regression of vascular lesions.

A recent intracoronary ultrasound study that compared high-dose rosuvastatin with atorvastatin in 1,039 patients with coronary disease provides striking evidence for the benefit of both of these drugs on regression of coronary plaque. In patients with residual lesions of 20%-50% by angiography, treatment with these drugs demonstrated a decrease in percent of atherosclerotic volume by 1.22% with rosuvastatin and by 0.99% with atorvastatin, and a decrease in total atheroma volume of 6.39 mm³ and 4.42 mm³, respectively. With doses of 40 mg atorvastatin and 80 mg rosuvastatin, low-density lipoprotein (LDL) cholesterol was decreased to 62.6 mg/dL and 70.2 mg/dL, respectively, and HDL cholesterol increased to 50.4 mg/dL and 48.6 mg/dL in the rosuvastatin and atorvastatin patients, respectively (N. Engl. J. Med. 2011;365;2078-87).

Regression of coronary lesions was observed in approximately two-thirds of the patients. Because of the short duration of the study, there were very few ischemic events and there was no difference between the two drug strategies. Since remodeling of the coronary artery is a surrogate indicator for clinical disease prevention, we cannot be certain that these ultrasound changes in plaques are directly related to the prevention of coronary events.

The second study of interest is the extended follow-up of the Heart Protection Study, which included more than 20,536 patients treated with 40 mg simvastatin or placebo for 5.3 years in-trial and a post-trial follow-up for a total 11 years (Lancet 2011:378;2013-20). There was an overall 23% decrease in major vascular events in the simvastatin-treated patients in the first year of the trial that continued to decrease annually during the trial phase. After study conclusion, when all patients were placed on therapy, there was a legacy benefit that persisted during the remaining 6 years of the study for the patients who were initially in the simvastatin arm of the study. The study confirms the long-term benefit of simvastatin and its safety without any evidence for an increase in cancer or other adverse events during the 11 years of follow-up.

The demonstration that statins can remodel the coronary artery provides pathologic support for their clinical benefit. Questions still remain in regard to mechanisms of action. The changes in the plaque volume theoretically could explain the therapeutic benefit of statins, but they must still be considered as surrogates for clinical benefit. Newer intravascular imaging technology using near-infrared spectroscopy is now able to characterize and measure the lipid core of the coronary plaque (JACC Cardiovasc. Imaging 2008;1:638-48), and may provide a better understanding of the mechanism by which statins modify plaque architecture.

Challenges still remain in regard to how the one-third of patients who did not experience any plaque regression should be approached. A treatment strategy for these presumably high-risk patients remains elusive.

Much has been learned from statin therapy, but many questions still remain in regard to the pathologic process by which the plaque progresses to cause an acute event, and how to prevent it.

This column, "Heart of the Matter," appears regularly in Cardiology News, a publication of Elsevier. Dr. Goldstein, medical editor of Cardiology News, is a professor of medicine at Wayne State University and division head emeritus of cardiovascular medicine at Henry Ford Hospital, both in Detroit. He is on data safety monitoring committees for the National Institutes of Health and several pharmaceutical companies.

It has been 17 years since the first publication of the Scandinavian Simvastatin Survival Study (Lancet 1994;344;1383-9) describing the benefit of coenzyme A reductase inhibitors (statins) on cardiovascular events in patients with coronary heart disease.

During this period, statins have become a major part of our strategy for the treatment and prevention of acute and chronic coronary heart disease. A number of statins have been introduced in a variety of clinical settings, and all have shown a consistent benefit. Although associated with some side effects, they have been relatively well tolerated by patients requiring either dose adjustment or switching to other drugs within the class.

Along the way, questions have been raised about the long-term safety of statins, and their potential oncogenic potential. The impact of statins directly on the cardiovascular intima has been elucidated using angiographic and intravascular imaging techniques. These studies have shown that statins mitigate to some degree the progression of localized intravascular abnormalities. Two recent studies provide important information both about the safety and long-term benefit of statins, and their remarkable effect on remodeling of the coronary arteries and regression of vascular lesions.

A recent intracoronary ultrasound study that compared high-dose rosuvastatin with atorvastatin in 1,039 patients with coronary disease provides striking evidence for the benefit of both of these drugs on regression of coronary plaque. In patients with residual lesions of 20%-50% by angiography, treatment with these drugs demonstrated a decrease in percent of atherosclerotic volume by 1.22% with rosuvastatin and by 0.99% with atorvastatin, and a decrease in total atheroma volume of 6.39 mm³ and 4.42 mm³, respectively. With doses of 40 mg atorvastatin and 80 mg rosuvastatin, low-density lipoprotein (LDL) cholesterol was decreased to 62.6 mg/dL and 70.2 mg/dL, respectively, and HDL cholesterol increased to 50.4 mg/dL and 48.6 mg/dL in the rosuvastatin and atorvastatin patients, respectively (N. Engl. J. Med. 2011;365;2078-87).

Regression of coronary lesions was observed in approximately two-thirds of the patients. Because of the short duration of the study, there were very few ischemic events and there was no difference between the two drug strategies. Since remodeling of the coronary artery is a surrogate indicator for clinical disease prevention, we cannot be certain that these ultrasound changes in plaques are directly related to the prevention of coronary events.

The second study of interest is the extended follow-up of the Heart Protection Study, which included more than 20,536 patients treated with 40 mg simvastatin or placebo for 5.3 years in-trial and a post-trial follow-up for a total 11 years (Lancet 2011:378;2013-20). There was an overall 23% decrease in major vascular events in the simvastatin-treated patients in the first year of the trial that continued to decrease annually during the trial phase. After study conclusion, when all patients were placed on therapy, there was a legacy benefit that persisted during the remaining 6 years of the study for the patients who were initially in the simvastatin arm of the study. The study confirms the long-term benefit of simvastatin and its safety without any evidence for an increase in cancer or other adverse events during the 11 years of follow-up.

The demonstration that statins can remodel the coronary artery provides pathologic support for their clinical benefit. Questions still remain in regard to mechanisms of action. The changes in the plaque volume theoretically could explain the therapeutic benefit of statins, but they must still be considered as surrogates for clinical benefit. Newer intravascular imaging technology using near-infrared spectroscopy is now able to characterize and measure the lipid core of the coronary plaque (JACC Cardiovasc. Imaging 2008;1:638-48), and may provide a better understanding of the mechanism by which statins modify plaque architecture.

Challenges still remain in regard to how the one-third of patients who did not experience any plaque regression should be approached. A treatment strategy for these presumably high-risk patients remains elusive.

Much has been learned from statin therapy, but many questions still remain in regard to the pathologic process by which the plaque progresses to cause an acute event, and how to prevent it.

This column, "Heart of the Matter," appears regularly in Cardiology News, a publication of Elsevier. Dr. Goldstein, medical editor of Cardiology News, is a professor of medicine at Wayne State University and division head emeritus of cardiovascular medicine at Henry Ford Hospital, both in Detroit. He is on data safety monitoring committees for the National Institutes of Health and several pharmaceutical companies.