Sidney Goldstein

It is projected that we will need from 85,000 to 200,000 more physicians by 2020 to meet clinical needs. Unless prevention programs become more effective, we will require this increase to provide the primary care for patients with acute coronary syndrome arriving in our emergency departments. At the same time, projections indicate that there will also be a significant increase in chronic heart disease patients and in heart failure patients.

To serve these patients, we will need to increase the number of medical graduates. We cannot continue to outsource medical education by importing doctors from abroad. This resource is becoming more tenuous as third world countries become increasingly sophisticated and their medical care improves.

The output of medical graduates from American medical schools has changed very little over the last quarter century. This year, however, there has been a major increase of 2.3% in first-year class size, compared with 2006. The applicant pool has also increased by 8.2%, and its quality has improved. This year's applicant had the highest MCAT scores and grade point averages on record.

As a result of the anticipated increase in medical graduates, the Council on Graduate Medial Education is asking for an increase of 15% in residency and fellowship slots to accommodate the new graduates. To achieve this, Congress must lift the cap on Medicare general medical education funding.

Health planners, anticipating these new graduates, are trying to model graduate education to affect the future makeup of American medicine. In the past, they have been reluctant to allow further growth of specialties, yet there will be an increase need for specialists such as cardiologists particularly as the population ages. Some are advocating the shunting of more graduates into primary care and general practice. Others argue that the purchasers of health care should decide the medical training needs. If they have their way, the emphasis will be on the training of more specialists. It seems there is little appreciation of the role that cardiologists play in providing primary care for the thousands of patients experiencing an acute MI every year.

At this time, it is appropriate to plan the future growth of cardiology and the makeup of its workforce. Over the past decade, there has been a gradual decrease in cardiology training programs and fellowship slots. However, there was an increase in training programs and fellowship slots from a low of 170 programs and 2,184 fellowship slots in 2004 to 177 programs and 2,334 fellowship slots this year. Associated with the increase in trainees, there had been an increase in interventional training from a plateau of 551 in 2001 to 630 in 2003.

The 35th Bethesda Conference report on the cardiology workforce crisis called attention to the pressing need for more cardiologists (J. Am. Coll. Cardiol. 2004;44:216). A previous Bethesda Conference, in 1993, suggested that in the age of managed care, there would be a decreased need for specialists in general and cardiologists in particular. Those estimates were far off base and failed to anticipate the effect of new technology that occurred in interventional cardiology, which entirely changed how we treat ACS and its resultant workforce requirements.

The obvious answer to this anticipated shortage is to increase the number of training programs and fellowship positions. However, the major obstacle to increasing the number of fellowship positions is the Balanced Budget Act of 1997, which froze the number and the funding of postgraduate medical education positions. As a result, hospitals have been reluctant to support training programs without an increase in Medicare general medical education support. The number of applicants for training programs is sure to increase in the future as the medical graduate pool increases. Some have suggested modification of the duration of internal medicine training and the creation of shortened training for cardiologists interested exclusively in clinical cardiology. Another impediment to expanding the number of training programs has been the increase in administrative burdens placed on program directors as a result of added certification requirements. These increased requirements have dampened the enthusiasm of program directors to expand their programs. Nevertheless, it is imperative that cardiology deal with the increased workforce requirements and constructs an aggressive program to meet those needs.

It is projected that we will need from 85,000 to 200,000 more physicians by 2020 to meet clinical needs. Unless prevention programs become more effective, we will require this increase to provide the primary care for patients with acute coronary syndrome arriving in our emergency departments. At the same time, projections indicate that there will also be a significant increase in chronic heart disease patients and in heart failure patients.

To serve these patients, we will need to increase the number of medical graduates. We cannot continue to outsource medical education by importing doctors from abroad. This resource is becoming more tenuous as third world countries become increasingly sophisticated and their medical care improves.

The output of medical graduates from American medical schools has changed very little over the last quarter century. This year, however, there has been a major increase of 2.3% in first-year class size, compared with 2006. The applicant pool has also increased by 8.2%, and its quality has improved. This year's applicant had the highest MCAT scores and grade point averages on record.

As a result of the anticipated increase in medical graduates, the Council on Graduate Medial Education is asking for an increase of 15% in residency and fellowship slots to accommodate the new graduates. To achieve this, Congress must lift the cap on Medicare general medical education funding.

Health planners, anticipating these new graduates, are trying to model graduate education to affect the future makeup of American medicine. In the past, they have been reluctant to allow further growth of specialties, yet there will be an increase need for specialists such as cardiologists particularly as the population ages. Some are advocating the shunting of more graduates into primary care and general practice. Others argue that the purchasers of health care should decide the medical training needs. If they have their way, the emphasis will be on the training of more specialists. It seems there is little appreciation of the role that cardiologists play in providing primary care for the thousands of patients experiencing an acute MI every year.

At this time, it is appropriate to plan the future growth of cardiology and the makeup of its workforce. Over the past decade, there has been a gradual decrease in cardiology training programs and fellowship slots. However, there was an increase in training programs and fellowship slots from a low of 170 programs and 2,184 fellowship slots in 2004 to 177 programs and 2,334 fellowship slots this year. Associated with the increase in trainees, there had been an increase in interventional training from a plateau of 551 in 2001 to 630 in 2003.

The 35th Bethesda Conference report on the cardiology workforce crisis called attention to the pressing need for more cardiologists (J. Am. Coll. Cardiol. 2004;44:216). A previous Bethesda Conference, in 1993, suggested that in the age of managed care, there would be a decreased need for specialists in general and cardiologists in particular. Those estimates were far off base and failed to anticipate the effect of new technology that occurred in interventional cardiology, which entirely changed how we treat ACS and its resultant workforce requirements.

The obvious answer to this anticipated shortage is to increase the number of training programs and fellowship positions. However, the major obstacle to increasing the number of fellowship positions is the Balanced Budget Act of 1997, which froze the number and the funding of postgraduate medical education positions. As a result, hospitals have been reluctant to support training programs without an increase in Medicare general medical education support. The number of applicants for training programs is sure to increase in the future as the medical graduate pool increases. Some have suggested modification of the duration of internal medicine training and the creation of shortened training for cardiologists interested exclusively in clinical cardiology. Another impediment to expanding the number of training programs has been the increase in administrative burdens placed on program directors as a result of added certification requirements. These increased requirements have dampened the enthusiasm of program directors to expand their programs. Nevertheless, it is imperative that cardiology deal with the increased workforce requirements and constructs an aggressive program to meet those needs.

It is projected that we will need from 85,000 to 200,000 more physicians by 2020 to meet clinical needs. Unless prevention programs become more effective, we will require this increase to provide the primary care for patients with acute coronary syndrome arriving in our emergency departments. At the same time, projections indicate that there will also be a significant increase in chronic heart disease patients and in heart failure patients.

To serve these patients, we will need to increase the number of medical graduates. We cannot continue to outsource medical education by importing doctors from abroad. This resource is becoming more tenuous as third world countries become increasingly sophisticated and their medical care improves.

The output of medical graduates from American medical schools has changed very little over the last quarter century. This year, however, there has been a major increase of 2.3% in first-year class size, compared with 2006. The applicant pool has also increased by 8.2%, and its quality has improved. This year's applicant had the highest MCAT scores and grade point averages on record.

As a result of the anticipated increase in medical graduates, the Council on Graduate Medial Education is asking for an increase of 15% in residency and fellowship slots to accommodate the new graduates. To achieve this, Congress must lift the cap on Medicare general medical education funding.

Health planners, anticipating these new graduates, are trying to model graduate education to affect the future makeup of American medicine. In the past, they have been reluctant to allow further growth of specialties, yet there will be an increase need for specialists such as cardiologists particularly as the population ages. Some are advocating the shunting of more graduates into primary care and general practice. Others argue that the purchasers of health care should decide the medical training needs. If they have their way, the emphasis will be on the training of more specialists. It seems there is little appreciation of the role that cardiologists play in providing primary care for the thousands of patients experiencing an acute MI every year.

At this time, it is appropriate to plan the future growth of cardiology and the makeup of its workforce. Over the past decade, there has been a gradual decrease in cardiology training programs and fellowship slots. However, there was an increase in training programs and fellowship slots from a low of 170 programs and 2,184 fellowship slots in 2004 to 177 programs and 2,334 fellowship slots this year. Associated with the increase in trainees, there had been an increase in interventional training from a plateau of 551 in 2001 to 630 in 2003.

The 35th Bethesda Conference report on the cardiology workforce crisis called attention to the pressing need for more cardiologists (J. Am. Coll. Cardiol. 2004;44:216). A previous Bethesda Conference, in 1993, suggested that in the age of managed care, there would be a decreased need for specialists in general and cardiologists in particular. Those estimates were far off base and failed to anticipate the effect of new technology that occurred in interventional cardiology, which entirely changed how we treat ACS and its resultant workforce requirements.

The obvious answer to this anticipated shortage is to increase the number of training programs and fellowship positions. However, the major obstacle to increasing the number of fellowship positions is the Balanced Budget Act of 1997, which froze the number and the funding of postgraduate medical education positions. As a result, hospitals have been reluctant to support training programs without an increase in Medicare general medical education support. The number of applicants for training programs is sure to increase in the future as the medical graduate pool increases. Some have suggested modification of the duration of internal medicine training and the creation of shortened training for cardiologists interested exclusively in clinical cardiology. Another impediment to expanding the number of training programs has been the increase in administrative burdens placed on program directors as a result of added certification requirements. These increased requirements have dampened the enthusiasm of program directors to expand their programs. Nevertheless, it is imperative that cardiology deal with the increased workforce requirements and constructs an aggressive program to meet those needs.

Over the last half century, the support of clinical trials has shifted from the National Institutes of Health to the pharmaceutical and device industries. Federal funding for the basic research still remains the foundation upon which clinical research and clinical trials are built. However, the translation of basic research to the bedside has largely become the domain of industry.

In its newly acquired role, industry has relied upon clinical investigators to advise and design clinical trials that will responsibly and accurately answer the question posed by new scientific discoveries that derive from the laboratory and small clinical studies. The design of these trials depends largely on the mutual cooperation of the scientist and the industry sponsor. Although both participants come from different backgrounds, there is a confluence of motives on the part of the investigators and industry. Nevertheless, industry, not devoid of altruism, has as its motivation the corporate profits it needs for survival. The clinical investigators, usually specialists in a particular area, enter this alliance trying to answer important medical questions, using the clinical trial as a platform on which these questions can be answered.

This symbiosis between independent scientists and industry has been immensely successful. It has provided physicians and patients with a multitude of drugs and devices that have resulted in the impressive decrease in cardiac mortality in the past 50 years. At the same time, these trials have provided important science that has defined the natural history of disease, explained mechanism of action of new molecules and devices, and raised important questions for future avenues of scientific exploration.

There is a common understanding that motivates both participants to continue moving forward in the pursuit of new medical knowledge. Part of that understanding is the responsibility for expeditious reporting of clinical trial results. The aroma that emanates from the recent ENHANCE study, widely covered in the lay press and on the front page of CARDIOLOGY NEWS, raises serious concerns about how that study was carried out and the future direction of randomized clinical trials.

In this case, the data on the proof of efficacy of the study drug are not our main concern. Those data will require much further inquiry. However, we are concerned about the delay in reporting and the apparent conflict that has arisen between the industry sponsor and the clinical scientists chosen to direct the study. Much of what we know is derived from comments in the lay press and statements from congressional sources. There may be more relevant information yet to come. However, with what we now know, there was an inordinate delay of more than a year in reporting these data.

Often within the framework of the Science-Industry agreements, there is a moratorium on reporting of 30–60 days on the part of both sides. But a year is excessive. During that time, the principal investigators protested the delay as the industrial sponsor accelerated its advertising of the particular drug.

As the results of randomized clinical trials draw near, the participants have mixed emotions. If the study is positive, all the players are eager to report the result. If negative, the scientist who has worked on the study still may see science coming from negative results. The sponsor, federally or industry funded, would like to bury the data. Like it or not, the responsibility to report the data is undeniable. Either way, the results traditionally end up on the program of the circus that we know as the Late Breaking Clinical Trials at one or another of our national meetings.

The delay in reporting the results of ENHANCE, for whatever reason, has had a chilling effect on the continued support of randomized clinical trials on the part of both the scientist and the public. This methodology is so central to the attainment of improvement in quality care of cardiac patients that anything that challenges its authenticity and reliability diminished those efforts. Recruitment of American patients into randomized clinical trials has driven many of these studies to Europe and Asia, where the relevancy of outcome data to the American patients can be challenged. It has also limited the ability of young American clinical scientists to participate in these studies.

This may be a time to begin to codify the relationships between the sponsor and the clinical scientists who participate in randomized clinical trials. Perhaps we have taken that relationship for granted for too long without fully articulating the motivation and responsibilities of all the participants in this very important method of clinical research.

Over the last half century, the support of clinical trials has shifted from the National Institutes of Health to the pharmaceutical and device industries. Federal funding for the basic research still remains the foundation upon which clinical research and clinical trials are built. However, the translation of basic research to the bedside has largely become the domain of industry.

In its newly acquired role, industry has relied upon clinical investigators to advise and design clinical trials that will responsibly and accurately answer the question posed by new scientific discoveries that derive from the laboratory and small clinical studies. The design of these trials depends largely on the mutual cooperation of the scientist and the industry sponsor. Although both participants come from different backgrounds, there is a confluence of motives on the part of the investigators and industry. Nevertheless, industry, not devoid of altruism, has as its motivation the corporate profits it needs for survival. The clinical investigators, usually specialists in a particular area, enter this alliance trying to answer important medical questions, using the clinical trial as a platform on which these questions can be answered.

This symbiosis between independent scientists and industry has been immensely successful. It has provided physicians and patients with a multitude of drugs and devices that have resulted in the impressive decrease in cardiac mortality in the past 50 years. At the same time, these trials have provided important science that has defined the natural history of disease, explained mechanism of action of new molecules and devices, and raised important questions for future avenues of scientific exploration.

There is a common understanding that motivates both participants to continue moving forward in the pursuit of new medical knowledge. Part of that understanding is the responsibility for expeditious reporting of clinical trial results. The aroma that emanates from the recent ENHANCE study, widely covered in the lay press and on the front page of CARDIOLOGY NEWS, raises serious concerns about how that study was carried out and the future direction of randomized clinical trials.

In this case, the data on the proof of efficacy of the study drug are not our main concern. Those data will require much further inquiry. However, we are concerned about the delay in reporting and the apparent conflict that has arisen between the industry sponsor and the clinical scientists chosen to direct the study. Much of what we know is derived from comments in the lay press and statements from congressional sources. There may be more relevant information yet to come. However, with what we now know, there was an inordinate delay of more than a year in reporting these data.

Often within the framework of the Science-Industry agreements, there is a moratorium on reporting of 30–60 days on the part of both sides. But a year is excessive. During that time, the principal investigators protested the delay as the industrial sponsor accelerated its advertising of the particular drug.

As the results of randomized clinical trials draw near, the participants have mixed emotions. If the study is positive, all the players are eager to report the result. If negative, the scientist who has worked on the study still may see science coming from negative results. The sponsor, federally or industry funded, would like to bury the data. Like it or not, the responsibility to report the data is undeniable. Either way, the results traditionally end up on the program of the circus that we know as the Late Breaking Clinical Trials at one or another of our national meetings.

The delay in reporting the results of ENHANCE, for whatever reason, has had a chilling effect on the continued support of randomized clinical trials on the part of both the scientist and the public. This methodology is so central to the attainment of improvement in quality care of cardiac patients that anything that challenges its authenticity and reliability diminished those efforts. Recruitment of American patients into randomized clinical trials has driven many of these studies to Europe and Asia, where the relevancy of outcome data to the American patients can be challenged. It has also limited the ability of young American clinical scientists to participate in these studies.

This may be a time to begin to codify the relationships between the sponsor and the clinical scientists who participate in randomized clinical trials. Perhaps we have taken that relationship for granted for too long without fully articulating the motivation and responsibilities of all the participants in this very important method of clinical research.

Over the last half century, the support of clinical trials has shifted from the National Institutes of Health to the pharmaceutical and device industries. Federal funding for the basic research still remains the foundation upon which clinical research and clinical trials are built. However, the translation of basic research to the bedside has largely become the domain of industry.

In its newly acquired role, industry has relied upon clinical investigators to advise and design clinical trials that will responsibly and accurately answer the question posed by new scientific discoveries that derive from the laboratory and small clinical studies. The design of these trials depends largely on the mutual cooperation of the scientist and the industry sponsor. Although both participants come from different backgrounds, there is a confluence of motives on the part of the investigators and industry. Nevertheless, industry, not devoid of altruism, has as its motivation the corporate profits it needs for survival. The clinical investigators, usually specialists in a particular area, enter this alliance trying to answer important medical questions, using the clinical trial as a platform on which these questions can be answered.

This symbiosis between independent scientists and industry has been immensely successful. It has provided physicians and patients with a multitude of drugs and devices that have resulted in the impressive decrease in cardiac mortality in the past 50 years. At the same time, these trials have provided important science that has defined the natural history of disease, explained mechanism of action of new molecules and devices, and raised important questions for future avenues of scientific exploration.

There is a common understanding that motivates both participants to continue moving forward in the pursuit of new medical knowledge. Part of that understanding is the responsibility for expeditious reporting of clinical trial results. The aroma that emanates from the recent ENHANCE study, widely covered in the lay press and on the front page of CARDIOLOGY NEWS, raises serious concerns about how that study was carried out and the future direction of randomized clinical trials.

In this case, the data on the proof of efficacy of the study drug are not our main concern. Those data will require much further inquiry. However, we are concerned about the delay in reporting and the apparent conflict that has arisen between the industry sponsor and the clinical scientists chosen to direct the study. Much of what we know is derived from comments in the lay press and statements from congressional sources. There may be more relevant information yet to come. However, with what we now know, there was an inordinate delay of more than a year in reporting these data.

Often within the framework of the Science-Industry agreements, there is a moratorium on reporting of 30–60 days on the part of both sides. But a year is excessive. During that time, the principal investigators protested the delay as the industrial sponsor accelerated its advertising of the particular drug.

As the results of randomized clinical trials draw near, the participants have mixed emotions. If the study is positive, all the players are eager to report the result. If negative, the scientist who has worked on the study still may see science coming from negative results. The sponsor, federally or industry funded, would like to bury the data. Like it or not, the responsibility to report the data is undeniable. Either way, the results traditionally end up on the program of the circus that we know as the Late Breaking Clinical Trials at one or another of our national meetings.

The delay in reporting the results of ENHANCE, for whatever reason, has had a chilling effect on the continued support of randomized clinical trials on the part of both the scientist and the public. This methodology is so central to the attainment of improvement in quality care of cardiac patients that anything that challenges its authenticity and reliability diminished those efforts. Recruitment of American patients into randomized clinical trials has driven many of these studies to Europe and Asia, where the relevancy of outcome data to the American patients can be challenged. It has also limited the ability of young American clinical scientists to participate in these studies.

This may be a time to begin to codify the relationships between the sponsor and the clinical scientists who participate in randomized clinical trials. Perhaps we have taken that relationship for granted for too long without fully articulating the motivation and responsibilities of all the participants in this very important method of clinical research.

As cardiologists struggle to shorten “door to balloon” time, the reality of emergency department overcrowding and delays in receiving care is working against us. Research from the Cambridge Alliance and Harvard Medical School (Health Affairs, January 2008) indicates that heart attack patients' waiting time to see a physician increased by 12 minutes in the period from 1997 to 2004.

My recent experience on a Saturday afternoon with a friend at an emergency department in a county hospital in upstate New York that provides regional emergency services attests to that observation. When we arrived in the waiting room of the ED, a sign indicated that we should wait until the triage nurse finished admitting a patient in an adjoining room, as she carefully catalogued his list of medications and past medical history before attending to my companion. Fortunately, my friend was not experiencing chest pain.

Nationwide, emergency department visits have increased by 18% and the number of EDs in this country has decreased by 12%. This recent research indicates that median wait time in the ED has increased by 36% for an increase of 30 minutes.

For patients needing urgent care, waiting time increased from 14 to 20 minutes. For patients with an acute myocardial infarction, it increased by 150% for a typical delay of 20 minutes before seeing a doctor. Over a quarter of the patients with an acute myocardial infarction had wait times that increased by 50 minutes or more. With the exception of urban hospitals, which had longer waits than did rural hospitals, the delays to see a doctor were fairly uniform across the nation, regardless of insurability and demographic characteristics.

Much of the delay can be explained by an increase in the volume of patients who use the emergency department for both acute and chronic care.

The survey also indicates that there has been a change in the mix of patients coming to the ED, with a decrease in the number of patients coming for urgent care and an increase in those arriving seeking nonurgent care. For the more than 45 million Americans without insurance, the emergency department has become the family physician. As the uninsured population continues to expand, the ED burden will increase.

The decrease in the number of U.S. emergency departments has resulted in part from the closure of hospitals in both urban and rural America. Few of us consider the consequence of these closures on the availability of ED facilities. Often, we see this process as a reallocation of hospital resources to areas in need. However, this reallocation often results in the closure of an urban hospital and the transfer of beds from the inner city to the affluent suburbs. As the number of hospital beds decreases and the age of patients increases, more sick, nonurgent patients will be spending more time waiting in the ED for hospital beds.

Considering the tenuous nature of our urban hospitals, the potential effect on the availability of emergency care should be of great community concern. Hospitals that have not closed have tried to cut back on emergency care because of financial losses incurred by providing that care. The projected decrease in budgeted Medicaid payments represents a further disincentive for the provision of emergency care. At the same time, there has been a decrease in physicians willing to take ED call because of a decrease in reimbursement and increase in medical liability.

For those patients with obvious acute signs and symptoms, emergent care is often prompt, but for those with chest pain and less overt evidence of disease, time to medical response is slower. As the cardiology community attempts to shorten the time between the onset of symptoms and the treatment for acute coronary syndromes, we need to be more attentive to the state of emergency care that we practice in. Each hospital merger or closure leads to further decreases in the number of ED facilities available to our cardiac patients. It is clear that the state of emergency care in America is going from bad to worse and requires urgent solutions.

As cardiologists struggle to shorten “door to balloon” time, the reality of emergency department overcrowding and delays in receiving care is working against us. Research from the Cambridge Alliance and Harvard Medical School (Health Affairs, January 2008) indicates that heart attack patients' waiting time to see a physician increased by 12 minutes in the period from 1997 to 2004.

My recent experience on a Saturday afternoon with a friend at an emergency department in a county hospital in upstate New York that provides regional emergency services attests to that observation. When we arrived in the waiting room of the ED, a sign indicated that we should wait until the triage nurse finished admitting a patient in an adjoining room, as she carefully catalogued his list of medications and past medical history before attending to my companion. Fortunately, my friend was not experiencing chest pain.

Nationwide, emergency department visits have increased by 18% and the number of EDs in this country has decreased by 12%. This recent research indicates that median wait time in the ED has increased by 36% for an increase of 30 minutes.

For patients needing urgent care, waiting time increased from 14 to 20 minutes. For patients with an acute myocardial infarction, it increased by 150% for a typical delay of 20 minutes before seeing a doctor. Over a quarter of the patients with an acute myocardial infarction had wait times that increased by 50 minutes or more. With the exception of urban hospitals, which had longer waits than did rural hospitals, the delays to see a doctor were fairly uniform across the nation, regardless of insurability and demographic characteristics.

Much of the delay can be explained by an increase in the volume of patients who use the emergency department for both acute and chronic care.

The survey also indicates that there has been a change in the mix of patients coming to the ED, with a decrease in the number of patients coming for urgent care and an increase in those arriving seeking nonurgent care. For the more than 45 million Americans without insurance, the emergency department has become the family physician. As the uninsured population continues to expand, the ED burden will increase.

The decrease in the number of U.S. emergency departments has resulted in part from the closure of hospitals in both urban and rural America. Few of us consider the consequence of these closures on the availability of ED facilities. Often, we see this process as a reallocation of hospital resources to areas in need. However, this reallocation often results in the closure of an urban hospital and the transfer of beds from the inner city to the affluent suburbs. As the number of hospital beds decreases and the age of patients increases, more sick, nonurgent patients will be spending more time waiting in the ED for hospital beds.

Considering the tenuous nature of our urban hospitals, the potential effect on the availability of emergency care should be of great community concern. Hospitals that have not closed have tried to cut back on emergency care because of financial losses incurred by providing that care. The projected decrease in budgeted Medicaid payments represents a further disincentive for the provision of emergency care. At the same time, there has been a decrease in physicians willing to take ED call because of a decrease in reimbursement and increase in medical liability.

For those patients with obvious acute signs and symptoms, emergent care is often prompt, but for those with chest pain and less overt evidence of disease, time to medical response is slower. As the cardiology community attempts to shorten the time between the onset of symptoms and the treatment for acute coronary syndromes, we need to be more attentive to the state of emergency care that we practice in. Each hospital merger or closure leads to further decreases in the number of ED facilities available to our cardiac patients. It is clear that the state of emergency care in America is going from bad to worse and requires urgent solutions.

As cardiologists struggle to shorten “door to balloon” time, the reality of emergency department overcrowding and delays in receiving care is working against us. Research from the Cambridge Alliance and Harvard Medical School (Health Affairs, January 2008) indicates that heart attack patients' waiting time to see a physician increased by 12 minutes in the period from 1997 to 2004.

My recent experience on a Saturday afternoon with a friend at an emergency department in a county hospital in upstate New York that provides regional emergency services attests to that observation. When we arrived in the waiting room of the ED, a sign indicated that we should wait until the triage nurse finished admitting a patient in an adjoining room, as she carefully catalogued his list of medications and past medical history before attending to my companion. Fortunately, my friend was not experiencing chest pain.

Nationwide, emergency department visits have increased by 18% and the number of EDs in this country has decreased by 12%. This recent research indicates that median wait time in the ED has increased by 36% for an increase of 30 minutes.

For patients needing urgent care, waiting time increased from 14 to 20 minutes. For patients with an acute myocardial infarction, it increased by 150% for a typical delay of 20 minutes before seeing a doctor. Over a quarter of the patients with an acute myocardial infarction had wait times that increased by 50 minutes or more. With the exception of urban hospitals, which had longer waits than did rural hospitals, the delays to see a doctor were fairly uniform across the nation, regardless of insurability and demographic characteristics.

Much of the delay can be explained by an increase in the volume of patients who use the emergency department for both acute and chronic care.

The survey also indicates that there has been a change in the mix of patients coming to the ED, with a decrease in the number of patients coming for urgent care and an increase in those arriving seeking nonurgent care. For the more than 45 million Americans without insurance, the emergency department has become the family physician. As the uninsured population continues to expand, the ED burden will increase.

The decrease in the number of U.S. emergency departments has resulted in part from the closure of hospitals in both urban and rural America. Few of us consider the consequence of these closures on the availability of ED facilities. Often, we see this process as a reallocation of hospital resources to areas in need. However, this reallocation often results in the closure of an urban hospital and the transfer of beds from the inner city to the affluent suburbs. As the number of hospital beds decreases and the age of patients increases, more sick, nonurgent patients will be spending more time waiting in the ED for hospital beds.

Considering the tenuous nature of our urban hospitals, the potential effect on the availability of emergency care should be of great community concern. Hospitals that have not closed have tried to cut back on emergency care because of financial losses incurred by providing that care. The projected decrease in budgeted Medicaid payments represents a further disincentive for the provision of emergency care. At the same time, there has been a decrease in physicians willing to take ED call because of a decrease in reimbursement and increase in medical liability.

For those patients with obvious acute signs and symptoms, emergent care is often prompt, but for those with chest pain and less overt evidence of disease, time to medical response is slower. As the cardiology community attempts to shorten the time between the onset of symptoms and the treatment for acute coronary syndromes, we need to be more attentive to the state of emergency care that we practice in. Each hospital merger or closure leads to further decreases in the number of ED facilities available to our cardiac patients. It is clear that the state of emergency care in America is going from bad to worse and requires urgent solutions.

In the beginning, there were very few cardiologists. At another time and in almost another world, a cardiologist could do very little more than could an internist. After all, an internist could give digitalis and quinidine just as well as a cardiologist, and the fee was the same: very little. Cardiologists could do catheterization of the heart, but then again so could some internists. But to what purpose, since we hadn't yet discovered that you could actually get an angiogram of the coronary vessel by placing a catheter in a vessel where you were told to never go?

A lot has changed since then. We have about 30,000 cardiologists in this country, and now we have a new secondary subspecialty proposed that will deal with advanced heart failure and transplantation. The new subspecialty was recently approved by the American Board of Internal Medicine and awaits approval by the American Board of Medical Specialists and the subsequent development of training programs (CARDIOLOGY NEWS, November 2007, p. 1). It joins the other subspecialties in our midst—interventional cardiology and electrophysiology. There are probably others waiting in the wings.

The need to develop expertise in a given field is driven by developing technology and by the increase in the number of patients, both actual and projected. In response to the growing patient population, new drugs and devices have been developed to deal with heart failure. Few of us are familiar with the care and maintenance of left ventricular assist devices and even fewer have the expertise to manage the aftercare of heart transplant recipients. Therefore, to provide competency in these special areas, it is essential that we train a cadre of our colleagues to respond to the exigencies of the technology and support our therapeutic programs as the dimension of our care expands.

Many express their dismay at the further balkanization of internal medicine and, to a lesser extent, cardiology. They point to the fact that about 80% of patients with heart failure are cared for by general internists, family practitioners, and the occasional cardiologist. Indeed, most of these patients can be cared for by using accepted guidelines.

Nevertheless, therapy for heart failure has become more complex as new drugs and devices have become available to optimize treatment of this heterogeneous patient population. The heart failure specialist can help to individualize therapy in more complex patients.

It is clear that the prevalence of heart failure is increasing rapidly as our population ages. It is estimated that the number of heart failure patients will swell from 5.2 million in 2004 to more than 30 million in 2037. Many of these patients will be getting chronic cardiac support and terminal therapy from devices that we now use as a temporary bridge to transplant. Other devices are yet to be fully developed.

It can be anticipated that just as we have thousands of patients who depend on renal dialysis for survival, we will have patients relying on implantable ventricular assist or replacement devices for permanent heart failure therapy. The availability of donor hearts will never equal the need for heart replacement, given the escalating incidence of heart failure in the future.

The training of heart failure specialists will not occur without some pain. It will require an additional year of cardiology training. Although a number of institutions are equipped to provide the necessary training, many training programs will not be able to provide the dimension of experience necessary to adequately train these new specialists. Their training will require the integration of their experience into a program that has easy access to electrophysiology and surgical specialties. It will unfortunately prolong cardiology training at a time when we are falling short in meeting the needs of our society for general cardiologists.

An additional aspect of the development of this subspecialty will bring recognition of heart failure as an important cost center in the referral network and lead to more institutional infrastructure support for heart failure therapy. The development of the advanced heart failure and transplant specialty will lead to an improvement in the care of our growing and aging patient population.

In the beginning, there were very few cardiologists. At another time and in almost another world, a cardiologist could do very little more than could an internist. After all, an internist could give digitalis and quinidine just as well as a cardiologist, and the fee was the same: very little. Cardiologists could do catheterization of the heart, but then again so could some internists. But to what purpose, since we hadn't yet discovered that you could actually get an angiogram of the coronary vessel by placing a catheter in a vessel where you were told to never go?

A lot has changed since then. We have about 30,000 cardiologists in this country, and now we have a new secondary subspecialty proposed that will deal with advanced heart failure and transplantation. The new subspecialty was recently approved by the American Board of Internal Medicine and awaits approval by the American Board of Medical Specialists and the subsequent development of training programs (CARDIOLOGY NEWS, November 2007, p. 1). It joins the other subspecialties in our midst—interventional cardiology and electrophysiology. There are probably others waiting in the wings.

The need to develop expertise in a given field is driven by developing technology and by the increase in the number of patients, both actual and projected. In response to the growing patient population, new drugs and devices have been developed to deal with heart failure. Few of us are familiar with the care and maintenance of left ventricular assist devices and even fewer have the expertise to manage the aftercare of heart transplant recipients. Therefore, to provide competency in these special areas, it is essential that we train a cadre of our colleagues to respond to the exigencies of the technology and support our therapeutic programs as the dimension of our care expands.

Many express their dismay at the further balkanization of internal medicine and, to a lesser extent, cardiology. They point to the fact that about 80% of patients with heart failure are cared for by general internists, family practitioners, and the occasional cardiologist. Indeed, most of these patients can be cared for by using accepted guidelines.

Nevertheless, therapy for heart failure has become more complex as new drugs and devices have become available to optimize treatment of this heterogeneous patient population. The heart failure specialist can help to individualize therapy in more complex patients.

It is clear that the prevalence of heart failure is increasing rapidly as our population ages. It is estimated that the number of heart failure patients will swell from 5.2 million in 2004 to more than 30 million in 2037. Many of these patients will be getting chronic cardiac support and terminal therapy from devices that we now use as a temporary bridge to transplant. Other devices are yet to be fully developed.

It can be anticipated that just as we have thousands of patients who depend on renal dialysis for survival, we will have patients relying on implantable ventricular assist or replacement devices for permanent heart failure therapy. The availability of donor hearts will never equal the need for heart replacement, given the escalating incidence of heart failure in the future.

The training of heart failure specialists will not occur without some pain. It will require an additional year of cardiology training. Although a number of institutions are equipped to provide the necessary training, many training programs will not be able to provide the dimension of experience necessary to adequately train these new specialists. Their training will require the integration of their experience into a program that has easy access to electrophysiology and surgical specialties. It will unfortunately prolong cardiology training at a time when we are falling short in meeting the needs of our society for general cardiologists.

An additional aspect of the development of this subspecialty will bring recognition of heart failure as an important cost center in the referral network and lead to more institutional infrastructure support for heart failure therapy. The development of the advanced heart failure and transplant specialty will lead to an improvement in the care of our growing and aging patient population.

In the beginning, there were very few cardiologists. At another time and in almost another world, a cardiologist could do very little more than could an internist. After all, an internist could give digitalis and quinidine just as well as a cardiologist, and the fee was the same: very little. Cardiologists could do catheterization of the heart, but then again so could some internists. But to what purpose, since we hadn't yet discovered that you could actually get an angiogram of the coronary vessel by placing a catheter in a vessel where you were told to never go?

A lot has changed since then. We have about 30,000 cardiologists in this country, and now we have a new secondary subspecialty proposed that will deal with advanced heart failure and transplantation. The new subspecialty was recently approved by the American Board of Internal Medicine and awaits approval by the American Board of Medical Specialists and the subsequent development of training programs (CARDIOLOGY NEWS, November 2007, p. 1). It joins the other subspecialties in our midst—interventional cardiology and electrophysiology. There are probably others waiting in the wings.

The need to develop expertise in a given field is driven by developing technology and by the increase in the number of patients, both actual and projected. In response to the growing patient population, new drugs and devices have been developed to deal with heart failure. Few of us are familiar with the care and maintenance of left ventricular assist devices and even fewer have the expertise to manage the aftercare of heart transplant recipients. Therefore, to provide competency in these special areas, it is essential that we train a cadre of our colleagues to respond to the exigencies of the technology and support our therapeutic programs as the dimension of our care expands.

Many express their dismay at the further balkanization of internal medicine and, to a lesser extent, cardiology. They point to the fact that about 80% of patients with heart failure are cared for by general internists, family practitioners, and the occasional cardiologist. Indeed, most of these patients can be cared for by using accepted guidelines.

Nevertheless, therapy for heart failure has become more complex as new drugs and devices have become available to optimize treatment of this heterogeneous patient population. The heart failure specialist can help to individualize therapy in more complex patients.

It is clear that the prevalence of heart failure is increasing rapidly as our population ages. It is estimated that the number of heart failure patients will swell from 5.2 million in 2004 to more than 30 million in 2037. Many of these patients will be getting chronic cardiac support and terminal therapy from devices that we now use as a temporary bridge to transplant. Other devices are yet to be fully developed.

It can be anticipated that just as we have thousands of patients who depend on renal dialysis for survival, we will have patients relying on implantable ventricular assist or replacement devices for permanent heart failure therapy. The availability of donor hearts will never equal the need for heart replacement, given the escalating incidence of heart failure in the future.

The training of heart failure specialists will not occur without some pain. It will require an additional year of cardiology training. Although a number of institutions are equipped to provide the necessary training, many training programs will not be able to provide the dimension of experience necessary to adequately train these new specialists. Their training will require the integration of their experience into a program that has easy access to electrophysiology and surgical specialties. It will unfortunately prolong cardiology training at a time when we are falling short in meeting the needs of our society for general cardiologists.

An additional aspect of the development of this subspecialty will bring recognition of heart failure as an important cost center in the referral network and lead to more institutional infrastructure support for heart failure therapy. The development of the advanced heart failure and transplant specialty will lead to an improvement in the care of our growing and aging patient population.

More than 25 years ago, the benefit of the routine treatment of patients with β-adrenergic blocking agents who experienced a myocardial infarction was established by the Norwegian Multicenter Study on Timolol After Myocardial Infarction and the Beta Blocker Heart Attack Trial (BHAT). At that time, the placebo mortality in BHAT was 8.9% compared with 6.6% in patients treated with propranolol and represented a 26% decrease in all cause mortality.

Since then, our targets for the successful treatment in patients experiencing an acute MI and more recently for an acute coronary syndrome have changed. Over the years, the mortality rate in acute MI in ACS has decreased to 2%–3% as a result of therapy with a variety of agents, including β-blockers.

At the same time, our diagnostic criteria for acute MI have changed. Patients with lesser degrees of myocardial necrosis can now be identified using sensitive biomarkers such as the troponin assays. As a result, the incidence of nonfatal MIs, repeat hospitalizations, and revascularization events has increased markedly.

In contemporary trials for the treatment of ACS, nonfatal MIs represent four to five times the number of mortality events. To adequately measure significant and modest treatment effects, current trials often require more than 10,000 patients. The primary therapeutic goal in these trials is a composite end point that includes both cardiac deaths and nonfatal MIs. Since a mortality benefit is difficult to demonstrate because of relatively few events, most of the benefit is measured by a decrease in nonfatal MIs. They are defined in part by the TIMI clinical definition but driven to an even greater extent by elevated troponin concentrations above the upper limit of normal. The degree of elevation is not reported. We are all aware of the uncertainty of this highly sensitive determination of cell death and its relative lack of specificity, particularly at the lower concentrations.

The importance of nonfatal MI frequency in determining clinical trial efficacy was dramatically shown recently in TRITON (Trial to Assess Improvement in Therapeutic Outcomes by Optimizing Platelet Inhibition With Prasugrel—Thrombolysis in Myocardial Infarction), which compared prasugrel to clopidogrel for the treatment of ACS patients undergoing percutaneous coronary intervention. In that study of 13,608 patients, there were 183 cardiovascular deaths and 1,095 nonfatal MIs. The combined end point was significantly reduced with prasugrel, compared with clopidogrel, determined mainly by a significant decrease in nonfatal MI with prasugrel. Yet prasugrel had no significant effect on mortality, compared with clopidogrel. In the trial prasugrel was, however, associated with a significant increase in life-threatening and fatal bleeding events. It is therefore clear from these data that in TRITON we are using a potent agent with significant bleeding risks for the prevention of recurrent nonfatal MIs, the nature and importance of which is unclear.

A subgroup analysis of TRITON suggested that patients with certain characteristics were at an increased risk of bleeding if given prasugrel: those who had a previous stroke, those who were aged over 75, or those who were underweight. Although this analysis might provide comfort to some physicians, it does not provide insight into what long-term benefit can be achieved by preventing a nonfatal MI.

A recent market survey of 85 interventional and clinical cardiologists reported in Forbes.com surprisingly showed that 36% of their patients would receive prasugrel following angioplasty. Even more striking was the fact that some physicians might use prasugrel for the long-term treatment of ACS patients who did not undergo percutaneous coronary intervention (www.forbes.com/healthcare/2007/11/29/prasugrel-plavix-lilly-biz-healthcare-cx_mh_1129lilly.html

It is clear that patients with suspected ACS with elevated troponin represent a very heterogeneous group. The need to know more about this group of patients is emphasized in the recent consensus document establishing a universal definition of MI, which focuses particularly on the uncertain definition of nonfatal MI in randomized clinical trials. The document emphasizes that we know little about the long term outcome in this mixed patient population. The new definition provides a classification of nonfatal MI for future clinical trials based on the degree of troponin elevation and the mechanism of infarction.

Before we proceed in the direction of prevention of all nonfatal MIs with drugs that have major downside risks, we need to know more about who will benefit. It is imperative that future clinical trials better define nonfatal MI and provide information about the therapeutic benefit of preventing that event.

More than 25 years ago, the benefit of the routine treatment of patients with β-adrenergic blocking agents who experienced a myocardial infarction was established by the Norwegian Multicenter Study on Timolol After Myocardial Infarction and the Beta Blocker Heart Attack Trial (BHAT). At that time, the placebo mortality in BHAT was 8.9% compared with 6.6% in patients treated with propranolol and represented a 26% decrease in all cause mortality.

Since then, our targets for the successful treatment in patients experiencing an acute MI and more recently for an acute coronary syndrome have changed. Over the years, the mortality rate in acute MI in ACS has decreased to 2%–3% as a result of therapy with a variety of agents, including β-blockers.

At the same time, our diagnostic criteria for acute MI have changed. Patients with lesser degrees of myocardial necrosis can now be identified using sensitive biomarkers such as the troponin assays. As a result, the incidence of nonfatal MIs, repeat hospitalizations, and revascularization events has increased markedly.

In contemporary trials for the treatment of ACS, nonfatal MIs represent four to five times the number of mortality events. To adequately measure significant and modest treatment effects, current trials often require more than 10,000 patients. The primary therapeutic goal in these trials is a composite end point that includes both cardiac deaths and nonfatal MIs. Since a mortality benefit is difficult to demonstrate because of relatively few events, most of the benefit is measured by a decrease in nonfatal MIs. They are defined in part by the TIMI clinical definition but driven to an even greater extent by elevated troponin concentrations above the upper limit of normal. The degree of elevation is not reported. We are all aware of the uncertainty of this highly sensitive determination of cell death and its relative lack of specificity, particularly at the lower concentrations.

The importance of nonfatal MI frequency in determining clinical trial efficacy was dramatically shown recently in TRITON (Trial to Assess Improvement in Therapeutic Outcomes by Optimizing Platelet Inhibition With Prasugrel—Thrombolysis in Myocardial Infarction), which compared prasugrel to clopidogrel for the treatment of ACS patients undergoing percutaneous coronary intervention. In that study of 13,608 patients, there were 183 cardiovascular deaths and 1,095 nonfatal MIs. The combined end point was significantly reduced with prasugrel, compared with clopidogrel, determined mainly by a significant decrease in nonfatal MI with prasugrel. Yet prasugrel had no significant effect on mortality, compared with clopidogrel. In the trial prasugrel was, however, associated with a significant increase in life-threatening and fatal bleeding events. It is therefore clear from these data that in TRITON we are using a potent agent with significant bleeding risks for the prevention of recurrent nonfatal MIs, the nature and importance of which is unclear.

A subgroup analysis of TRITON suggested that patients with certain characteristics were at an increased risk of bleeding if given prasugrel: those who had a previous stroke, those who were aged over 75, or those who were underweight. Although this analysis might provide comfort to some physicians, it does not provide insight into what long-term benefit can be achieved by preventing a nonfatal MI.

A recent market survey of 85 interventional and clinical cardiologists reported in Forbes.com surprisingly showed that 36% of their patients would receive prasugrel following angioplasty. Even more striking was the fact that some physicians might use prasugrel for the long-term treatment of ACS patients who did not undergo percutaneous coronary intervention (www.forbes.com/healthcare/2007/11/29/prasugrel-plavix-lilly-biz-healthcare-cx_mh_1129lilly.html

It is clear that patients with suspected ACS with elevated troponin represent a very heterogeneous group. The need to know more about this group of patients is emphasized in the recent consensus document establishing a universal definition of MI, which focuses particularly on the uncertain definition of nonfatal MI in randomized clinical trials. The document emphasizes that we know little about the long term outcome in this mixed patient population. The new definition provides a classification of nonfatal MI for future clinical trials based on the degree of troponin elevation and the mechanism of infarction.

Before we proceed in the direction of prevention of all nonfatal MIs with drugs that have major downside risks, we need to know more about who will benefit. It is imperative that future clinical trials better define nonfatal MI and provide information about the therapeutic benefit of preventing that event.

More than 25 years ago, the benefit of the routine treatment of patients with β-adrenergic blocking agents who experienced a myocardial infarction was established by the Norwegian Multicenter Study on Timolol After Myocardial Infarction and the Beta Blocker Heart Attack Trial (BHAT). At that time, the placebo mortality in BHAT was 8.9% compared with 6.6% in patients treated with propranolol and represented a 26% decrease in all cause mortality.

Since then, our targets for the successful treatment in patients experiencing an acute MI and more recently for an acute coronary syndrome have changed. Over the years, the mortality rate in acute MI in ACS has decreased to 2%–3% as a result of therapy with a variety of agents, including β-blockers.

At the same time, our diagnostic criteria for acute MI have changed. Patients with lesser degrees of myocardial necrosis can now be identified using sensitive biomarkers such as the troponin assays. As a result, the incidence of nonfatal MIs, repeat hospitalizations, and revascularization events has increased markedly.

In contemporary trials for the treatment of ACS, nonfatal MIs represent four to five times the number of mortality events. To adequately measure significant and modest treatment effects, current trials often require more than 10,000 patients. The primary therapeutic goal in these trials is a composite end point that includes both cardiac deaths and nonfatal MIs. Since a mortality benefit is difficult to demonstrate because of relatively few events, most of the benefit is measured by a decrease in nonfatal MIs. They are defined in part by the TIMI clinical definition but driven to an even greater extent by elevated troponin concentrations above the upper limit of normal. The degree of elevation is not reported. We are all aware of the uncertainty of this highly sensitive determination of cell death and its relative lack of specificity, particularly at the lower concentrations.

The importance of nonfatal MI frequency in determining clinical trial efficacy was dramatically shown recently in TRITON (Trial to Assess Improvement in Therapeutic Outcomes by Optimizing Platelet Inhibition With Prasugrel—Thrombolysis in Myocardial Infarction), which compared prasugrel to clopidogrel for the treatment of ACS patients undergoing percutaneous coronary intervention. In that study of 13,608 patients, there were 183 cardiovascular deaths and 1,095 nonfatal MIs. The combined end point was significantly reduced with prasugrel, compared with clopidogrel, determined mainly by a significant decrease in nonfatal MI with prasugrel. Yet prasugrel had no significant effect on mortality, compared with clopidogrel. In the trial prasugrel was, however, associated with a significant increase in life-threatening and fatal bleeding events. It is therefore clear from these data that in TRITON we are using a potent agent with significant bleeding risks for the prevention of recurrent nonfatal MIs, the nature and importance of which is unclear.

A subgroup analysis of TRITON suggested that patients with certain characteristics were at an increased risk of bleeding if given prasugrel: those who had a previous stroke, those who were aged over 75, or those who were underweight. Although this analysis might provide comfort to some physicians, it does not provide insight into what long-term benefit can be achieved by preventing a nonfatal MI.

A recent market survey of 85 interventional and clinical cardiologists reported in Forbes.com surprisingly showed that 36% of their patients would receive prasugrel following angioplasty. Even more striking was the fact that some physicians might use prasugrel for the long-term treatment of ACS patients who did not undergo percutaneous coronary intervention (www.forbes.com/healthcare/2007/11/29/prasugrel-plavix-lilly-biz-healthcare-cx_mh_1129lilly.html

It is clear that patients with suspected ACS with elevated troponin represent a very heterogeneous group. The need to know more about this group of patients is emphasized in the recent consensus document establishing a universal definition of MI, which focuses particularly on the uncertain definition of nonfatal MI in randomized clinical trials. The document emphasizes that we know little about the long term outcome in this mixed patient population. The new definition provides a classification of nonfatal MI for future clinical trials based on the degree of troponin elevation and the mechanism of infarction.

Before we proceed in the direction of prevention of all nonfatal MIs with drugs that have major downside risks, we need to know more about who will benefit. It is imperative that future clinical trials better define nonfatal MI and provide information about the therapeutic benefit of preventing that event.

Readers of this column know that we cardiologists have become addicted to the late-breaking clinical trial. Played out in an auditorium large enough to hold at least a quarter of the attendees of the annual scientific sessions of the American Heart Association, the LBCTs are selected as the most important clinical trials of the season. They are presented with huge fanfare to an attentive and anticipating audience of cardiologists, nurses, and Wall Street “gurus” waiting for the latest trend and the next “blockbuster.” When none are revealed, which is often the case, the disappointed audience retires to the nearest coffee shop waiting for the next session.

This fall, 23 LBCTs were presented at the AHA meeting, compared with 13 regular LBCTs and 18 mini-LBCTs at the spring meeting of the American College of Cardiology. Much of the anticipation hinges on the possibility that the presentation of a trial will open new avenues of therapy. Disappointment ensues if none occur. Yet important clinical information is always revealed. Some are explorations up the blind alleys of science; others are either confirmatory or expansive of previous observations. This season, although there was no blockbuster revealed, there was a lot of important clinical science.

Some studies achieved their primary objectives; some failed and others added information about previous studies. A substudy of reperfusion imaging conducted in 314 of the more than 2,000 patients with stable coronary artery disease in the Clinical Outcomes Using Revascularization and Aggressive Drug Evaluation (COURAGE) trial provided new data about a previously negative trial. It compared nuclear reperfusion imaging in patients receiving percutaneous coronary intervention plus standard medical therapy with that in patients receiving standard medical therapy alone. Not surprisingly, PCI was significantly better at restoring flow to ischemic areas than was standard medical therapy alone. However, the observation that a full 20% of patients with standard medical therapy improved flow without a PCI, compared with 33% of those who received PCI, was particularly encouraging.

The Controlled Rosuvastatin Multinational Trial in Heart Failure (CORONA) study, however, surprised many when it failed to reach a positive outcome in patients receiving rosuvastatin with heart failure secondary to ischemic heart disease. Patients with proven ischemic heart disease with an average ejection fraction of 31% and increased serum LDL cholesterol levels were randomized to receive either rosuvastatin or placebo. Although a significant decrease in LDL cholesterol was achieved with rosuvastatin, the combined end point of cardiovascular death, nonfatal MI, and nonfatal stroke was unaffected by the therapy. (See article on p. 8.) This is one of the first studies that failed to show any benefit of statin therapy in patients with ischemic heart disease.

The application of 64-slice CT angiography was examined in the CORE 64 study, which compared that technology to standard angiography and showed a close relationship of the two methodologies. However, the discussant of the report chastised the presenter for showing benefit in a study that put patients at risk of radiation-induced cancer without providing any morbidity of mortality benefit to patients. (See article on p. 1 and editorial on p. 11.)

Another trial, Resynchronization Therapy in Normal QRS (RethinQ), examined the importance of atrial fibrillation in heart failure (AF-HF) and observed no adverse effects associated with the arrhythmia in patients with heart failure. Resynchronization of patients with normal QRS time, considered to be the next horizon in biventricular synchronized pacing, also failed to show any benefit in patients with QRS times of less than 130 msec in patients with left ventricular systolic dysfunction.

The Master I trial unfortunately failed to provide any significant predictors for life-threatening ventricular events in patients with implantable cardioverter defibrillators, but the MASS Stent study (see p. 12) dispelled much of the concern about drug-eluting stents in a nonrandomized population study. It compared outcomes of mortality and revascularization in more than 17,000 patients who received bare-metal or drug-eluting stents over a 2-year period in Massachusetts. They observed that, despite recent reports, drug-eluting stents appeared to show safety and benefit.

LBCTs have become fixtures of national scientific meetings. In them, unfortunately, large studies are overemphasized while very important, but less glamorous, research reports are eclipsed.

I vow to overcome my addiction and skip the LBCTs at the next meeting and listen in on some of the science being presented in the back rooms of the meeting. Stay tuned.

Readers of this column know that we cardiologists have become addicted to the late-breaking clinical trial. Played out in an auditorium large enough to hold at least a quarter of the attendees of the annual scientific sessions of the American Heart Association, the LBCTs are selected as the most important clinical trials of the season. They are presented with huge fanfare to an attentive and anticipating audience of cardiologists, nurses, and Wall Street “gurus” waiting for the latest trend and the next “blockbuster.” When none are revealed, which is often the case, the disappointed audience retires to the nearest coffee shop waiting for the next session.

This fall, 23 LBCTs were presented at the AHA meeting, compared with 13 regular LBCTs and 18 mini-LBCTs at the spring meeting of the American College of Cardiology. Much of the anticipation hinges on the possibility that the presentation of a trial will open new avenues of therapy. Disappointment ensues if none occur. Yet important clinical information is always revealed. Some are explorations up the blind alleys of science; others are either confirmatory or expansive of previous observations. This season, although there was no blockbuster revealed, there was a lot of important clinical science.

Some studies achieved their primary objectives; some failed and others added information about previous studies. A substudy of reperfusion imaging conducted in 314 of the more than 2,000 patients with stable coronary artery disease in the Clinical Outcomes Using Revascularization and Aggressive Drug Evaluation (COURAGE) trial provided new data about a previously negative trial. It compared nuclear reperfusion imaging in patients receiving percutaneous coronary intervention plus standard medical therapy with that in patients receiving standard medical therapy alone. Not surprisingly, PCI was significantly better at restoring flow to ischemic areas than was standard medical therapy alone. However, the observation that a full 20% of patients with standard medical therapy improved flow without a PCI, compared with 33% of those who received PCI, was particularly encouraging.

The Controlled Rosuvastatin Multinational Trial in Heart Failure (CORONA) study, however, surprised many when it failed to reach a positive outcome in patients receiving rosuvastatin with heart failure secondary to ischemic heart disease. Patients with proven ischemic heart disease with an average ejection fraction of 31% and increased serum LDL cholesterol levels were randomized to receive either rosuvastatin or placebo. Although a significant decrease in LDL cholesterol was achieved with rosuvastatin, the combined end point of cardiovascular death, nonfatal MI, and nonfatal stroke was unaffected by the therapy. (See article on p. 8.) This is one of the first studies that failed to show any benefit of statin therapy in patients with ischemic heart disease.

The application of 64-slice CT angiography was examined in the CORE 64 study, which compared that technology to standard angiography and showed a close relationship of the two methodologies. However, the discussant of the report chastised the presenter for showing benefit in a study that put patients at risk of radiation-induced cancer without providing any morbidity of mortality benefit to patients. (See article on p. 1 and editorial on p. 11.)

Another trial, Resynchronization Therapy in Normal QRS (RethinQ), examined the importance of atrial fibrillation in heart failure (AF-HF) and observed no adverse effects associated with the arrhythmia in patients with heart failure. Resynchronization of patients with normal QRS time, considered to be the next horizon in biventricular synchronized pacing, also failed to show any benefit in patients with QRS times of less than 130 msec in patients with left ventricular systolic dysfunction.

The Master I trial unfortunately failed to provide any significant predictors for life-threatening ventricular events in patients with implantable cardioverter defibrillators, but the MASS Stent study (see p. 12) dispelled much of the concern about drug-eluting stents in a nonrandomized population study. It compared outcomes of mortality and revascularization in more than 17,000 patients who received bare-metal or drug-eluting stents over a 2-year period in Massachusetts. They observed that, despite recent reports, drug-eluting stents appeared to show safety and benefit.

LBCTs have become fixtures of national scientific meetings. In them, unfortunately, large studies are overemphasized while very important, but less glamorous, research reports are eclipsed.

I vow to overcome my addiction and skip the LBCTs at the next meeting and listen in on some of the science being presented in the back rooms of the meeting. Stay tuned.

Readers of this column know that we cardiologists have become addicted to the late-breaking clinical trial. Played out in an auditorium large enough to hold at least a quarter of the attendees of the annual scientific sessions of the American Heart Association, the LBCTs are selected as the most important clinical trials of the season. They are presented with huge fanfare to an attentive and anticipating audience of cardiologists, nurses, and Wall Street “gurus” waiting for the latest trend and the next “blockbuster.” When none are revealed, which is often the case, the disappointed audience retires to the nearest coffee shop waiting for the next session.

This fall, 23 LBCTs were presented at the AHA meeting, compared with 13 regular LBCTs and 18 mini-LBCTs at the spring meeting of the American College of Cardiology. Much of the anticipation hinges on the possibility that the presentation of a trial will open new avenues of therapy. Disappointment ensues if none occur. Yet important clinical information is always revealed. Some are explorations up the blind alleys of science; others are either confirmatory or expansive of previous observations. This season, although there was no blockbuster revealed, there was a lot of important clinical science.

Some studies achieved their primary objectives; some failed and others added information about previous studies. A substudy of reperfusion imaging conducted in 314 of the more than 2,000 patients with stable coronary artery disease in the Clinical Outcomes Using Revascularization and Aggressive Drug Evaluation (COURAGE) trial provided new data about a previously negative trial. It compared nuclear reperfusion imaging in patients receiving percutaneous coronary intervention plus standard medical therapy with that in patients receiving standard medical therapy alone. Not surprisingly, PCI was significantly better at restoring flow to ischemic areas than was standard medical therapy alone. However, the observation that a full 20% of patients with standard medical therapy improved flow without a PCI, compared with 33% of those who received PCI, was particularly encouraging.

The Controlled Rosuvastatin Multinational Trial in Heart Failure (CORONA) study, however, surprised many when it failed to reach a positive outcome in patients receiving rosuvastatin with heart failure secondary to ischemic heart disease. Patients with proven ischemic heart disease with an average ejection fraction of 31% and increased serum LDL cholesterol levels were randomized to receive either rosuvastatin or placebo. Although a significant decrease in LDL cholesterol was achieved with rosuvastatin, the combined end point of cardiovascular death, nonfatal MI, and nonfatal stroke was unaffected by the therapy. (See article on p. 8.) This is one of the first studies that failed to show any benefit of statin therapy in patients with ischemic heart disease.

The application of 64-slice CT angiography was examined in the CORE 64 study, which compared that technology to standard angiography and showed a close relationship of the two methodologies. However, the discussant of the report chastised the presenter for showing benefit in a study that put patients at risk of radiation-induced cancer without providing any morbidity of mortality benefit to patients. (See article on p. 1 and editorial on p. 11.)

Another trial, Resynchronization Therapy in Normal QRS (RethinQ), examined the importance of atrial fibrillation in heart failure (AF-HF) and observed no adverse effects associated with the arrhythmia in patients with heart failure. Resynchronization of patients with normal QRS time, considered to be the next horizon in biventricular synchronized pacing, also failed to show any benefit in patients with QRS times of less than 130 msec in patients with left ventricular systolic dysfunction.

The Master I trial unfortunately failed to provide any significant predictors for life-threatening ventricular events in patients with implantable cardioverter defibrillators, but the MASS Stent study (see p. 12) dispelled much of the concern about drug-eluting stents in a nonrandomized population study. It compared outcomes of mortality and revascularization in more than 17,000 patients who received bare-metal or drug-eluting stents over a 2-year period in Massachusetts. They observed that, despite recent reports, drug-eluting stents appeared to show safety and benefit.

LBCTs have become fixtures of national scientific meetings. In them, unfortunately, large studies are overemphasized while very important, but less glamorous, research reports are eclipsed.

I vow to overcome my addiction and skip the LBCTs at the next meeting and listen in on some of the science being presented in the back rooms of the meeting. Stay tuned.

Implantable cardioverter defibrillators have been rapidly incorporated into the standard therapy for patients with left ventricular failure in the United States where nearly 10,000s ICDs are implanted each month.

Now data sources are beginning to give us a glimpse of who these patients are and of the risks associated with ICD implantation. The first report of the National ICD Registry provides the cardiology community with rich and robust information regarding the demographics of the patients receiving ICDs and the medical environment in which they are being implanted. As such, it provides an opportunity to enlarge our knowledge about these ICD recipients and this special therapy. The registry also provides a model for future investigations using the Medicare database to evaluate various cardiac therapies.

Registries will become increasingly important as we proceed with gene and device therapies where our understanding of the long-term safety and efficacy will be required and where the usual clinical trial construct cannot provide the necessary information.

Since April 2006, the National ICD registry has collected data from more than 100,000 implants, most in Medicare patients as mandated by the Centers for Medicare and Medicaid Services, and an additional 30% from non-Medicare insured patients. Fortunately, the inclusion of privately insured patients provides information about patients aged younger than 65 years.

Most of the patients (79.2%) in the registry received the device for primary prevention using current class IIA guidelines advising implantation of the ICD in patients with a left ventricular ejection fraction of less than 30% at least 1 month after an acute myocardial infarction or 3 months after coronary bypass surgery. The remaining patients were implanted for secondary prevention, presumably having experienced previous life-threatening events. Very few adverse events were associated with implantation. The development of a pocket hematoma, the most frequent adverse effect, occurred in 1.3% of the implantations. Interestingly, slightly more that one-third of the patients had biventricular pacemakers implanted with the device.

Cardiologists, and particularly electrophysiologists, were the main players. Sixty percent of the devices were implanted by cardiologists who had undergone electrophysiology training; most had passed the board examination for that specialty. About 10% had completed surgical or thoracic residencies, and they implanted 2.7% of the devices. And 15% of the physicians, who placed 6.2% of the devices, had no training in implantation.

Additional information about the use of ICDs emerges from a recent examination of the Medicare database. In that analysis of ICD implantation for both primary and secondary prevention, there is striking disparity in the implantation by sex and race. In both the primary prevention and secondary prevention groups, there was more than a threefold increase in the implantation of ICDs in men compared with women. There was a similar disparity between white and black patients. Of particular interest, mortality data adjusted for a variety of comorbidities indicated no difference in benefit accrued to patients receiving the ICD for primary prevention. In contrast, those patients receiving the ICD for secondary prevention experienced a 35% decrease in mortality compared with the nonrecipients (JAMA 2007;298:1517–24).

The variations in the use of defibrillators based on race and sex are just examples of how a number of contemporary cardiovascular technologies are not equally applied. These disparities cannot be fully explained by insurance coverage differences but probably relate to differences in clinical factors as well as a number of sociologic differences.

We will learn more about the risks of implantation in the future, but unfortunately we will not gain any further precise information about the relative mortality and morbidity benefit of these devices other than what we received from the MADIT II and SCD-HeFT trials. That evaluation will depend upon the development of other methods for the treatment and prevention of sudden cardiac death.

Implantable cardioverter defibrillators have been rapidly incorporated into the standard therapy for patients with left ventricular failure in the United States where nearly 10,000s ICDs are implanted each month.

Now data sources are beginning to give us a glimpse of who these patients are and of the risks associated with ICD implantation. The first report of the National ICD Registry provides the cardiology community with rich and robust information regarding the demographics of the patients receiving ICDs and the medical environment in which they are being implanted. As such, it provides an opportunity to enlarge our knowledge about these ICD recipients and this special therapy. The registry also provides a model for future investigations using the Medicare database to evaluate various cardiac therapies.

Registries will become increasingly important as we proceed with gene and device therapies where our understanding of the long-term safety and efficacy will be required and where the usual clinical trial construct cannot provide the necessary information.

Since April 2006, the National ICD registry has collected data from more than 100,000 implants, most in Medicare patients as mandated by the Centers for Medicare and Medicaid Services, and an additional 30% from non-Medicare insured patients. Fortunately, the inclusion of privately insured patients provides information about patients aged younger than 65 years.

Most of the patients (79.2%) in the registry received the device for primary prevention using current class IIA guidelines advising implantation of the ICD in patients with a left ventricular ejection fraction of less than 30% at least 1 month after an acute myocardial infarction or 3 months after coronary bypass surgery. The remaining patients were implanted for secondary prevention, presumably having experienced previous life-threatening events. Very few adverse events were associated with implantation. The development of a pocket hematoma, the most frequent adverse effect, occurred in 1.3% of the implantations. Interestingly, slightly more that one-third of the patients had biventricular pacemakers implanted with the device.

Cardiologists, and particularly electrophysiologists, were the main players. Sixty percent of the devices were implanted by cardiologists who had undergone electrophysiology training; most had passed the board examination for that specialty. About 10% had completed surgical or thoracic residencies, and they implanted 2.7% of the devices. And 15% of the physicians, who placed 6.2% of the devices, had no training in implantation.

Additional information about the use of ICDs emerges from a recent examination of the Medicare database. In that analysis of ICD implantation for both primary and secondary prevention, there is striking disparity in the implantation by sex and race. In both the primary prevention and secondary prevention groups, there was more than a threefold increase in the implantation of ICDs in men compared with women. There was a similar disparity between white and black patients. Of particular interest, mortality data adjusted for a variety of comorbidities indicated no difference in benefit accrued to patients receiving the ICD for primary prevention. In contrast, those patients receiving the ICD for secondary prevention experienced a 35% decrease in mortality compared with the nonrecipients (JAMA 2007;298:1517–24).

The variations in the use of defibrillators based on race and sex are just examples of how a number of contemporary cardiovascular technologies are not equally applied. These disparities cannot be fully explained by insurance coverage differences but probably relate to differences in clinical factors as well as a number of sociologic differences.

We will learn more about the risks of implantation in the future, but unfortunately we will not gain any further precise information about the relative mortality and morbidity benefit of these devices other than what we received from the MADIT II and SCD-HeFT trials. That evaluation will depend upon the development of other methods for the treatment and prevention of sudden cardiac death.

Implantable cardioverter defibrillators have been rapidly incorporated into the standard therapy for patients with left ventricular failure in the United States where nearly 10,000s ICDs are implanted each month.

Now data sources are beginning to give us a glimpse of who these patients are and of the risks associated with ICD implantation. The first report of the National ICD Registry provides the cardiology community with rich and robust information regarding the demographics of the patients receiving ICDs and the medical environment in which they are being implanted. As such, it provides an opportunity to enlarge our knowledge about these ICD recipients and this special therapy. The registry also provides a model for future investigations using the Medicare database to evaluate various cardiac therapies.

Registries will become increasingly important as we proceed with gene and device therapies where our understanding of the long-term safety and efficacy will be required and where the usual clinical trial construct cannot provide the necessary information.

Since April 2006, the National ICD registry has collected data from more than 100,000 implants, most in Medicare patients as mandated by the Centers for Medicare and Medicaid Services, and an additional 30% from non-Medicare insured patients. Fortunately, the inclusion of privately insured patients provides information about patients aged younger than 65 years.

Most of the patients (79.2%) in the registry received the device for primary prevention using current class IIA guidelines advising implantation of the ICD in patients with a left ventricular ejection fraction of less than 30% at least 1 month after an acute myocardial infarction or 3 months after coronary bypass surgery. The remaining patients were implanted for secondary prevention, presumably having experienced previous life-threatening events. Very few adverse events were associated with implantation. The development of a pocket hematoma, the most frequent adverse effect, occurred in 1.3% of the implantations. Interestingly, slightly more that one-third of the patients had biventricular pacemakers implanted with the device.

Cardiologists, and particularly electrophysiologists, were the main players. Sixty percent of the devices were implanted by cardiologists who had undergone electrophysiology training; most had passed the board examination for that specialty. About 10% had completed surgical or thoracic residencies, and they implanted 2.7% of the devices. And 15% of the physicians, who placed 6.2% of the devices, had no training in implantation.

Additional information about the use of ICDs emerges from a recent examination of the Medicare database. In that analysis of ICD implantation for both primary and secondary prevention, there is striking disparity in the implantation by sex and race. In both the primary prevention and secondary prevention groups, there was more than a threefold increase in the implantation of ICDs in men compared with women. There was a similar disparity between white and black patients. Of particular interest, mortality data adjusted for a variety of comorbidities indicated no difference in benefit accrued to patients receiving the ICD for primary prevention. In contrast, those patients receiving the ICD for secondary prevention experienced a 35% decrease in mortality compared with the nonrecipients (JAMA 2007;298:1517–24).

The variations in the use of defibrillators based on race and sex are just examples of how a number of contemporary cardiovascular technologies are not equally applied. These disparities cannot be fully explained by insurance coverage differences but probably relate to differences in clinical factors as well as a number of sociologic differences.

We will learn more about the risks of implantation in the future, but unfortunately we will not gain any further precise information about the relative mortality and morbidity benefit of these devices other than what we received from the MADIT II and SCD-HeFT trials. That evaluation will depend upon the development of other methods for the treatment and prevention of sudden cardiac death.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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