Sidney Goldstein

Dr. George Burch, one of the great leaders in cardiology in the mid-20th century, wrote in a 1954 monograph that “the patient with moderate or severe congestive heart failure should be placed at bed rest immediately.” As a result, many patients were kept in bed for many weeks. This was the considered recommendation of many cardiologists, who had at the time little else to offer to their patients.

In the half century that followed, we learned a great deal about exercise physiology and its role in rehabilitating patients after an acute myocardial infarction. It is now part of the standard care of such patients.

More recently, a large body of clinical data has emerged providing insight into the role of exercise in the patient with heart failure. These studies suggest that, contrary to previous concerns, exercise training may be safe and can lead to improved cardiac physiology. There is now significant evidence that exercise training improves exercise performance, increases peak oxygen consumption, reduces both muscle and systemic sympathetic activity, and favorably modifies systemic and tissue inflammatory markers.

On the basis of these physiologic studies, several clinical trials were performed in the past decade and reported clinical benefits associated with exercise training in heart failure. Although most of the studies have been small, they tended to reinforce the safety and physiologic benefits of exercise training. These studies were designed to include a broad spectrum of patients with varying degrees of heart failure, such as elderly patients, who are becoming an increasingly large part of the heart failure population.

As a result of the progress in this field, in 2002 the National Heart, Lung, and Blood Institute embarked on HF-ACTION (Heart Failure: A Controlled Trial Investigating Outcomes of Exercise Training). The trial, involving more than 2,300 patients with New York Heart Association class I-IV heart failure with ejection fractions of less than 35%, tested the relative morbidity and mortality benefit of exercise training in those who also were receiving optimal medical therapy.

Patients were randomized to usual care or a supervised exercise program for a concentrated 3-month period of exercise 3 days a week for 4 months, followed by home exercise 5 days a week for 2 years (CARDIOLOGY NEWS, Dec. 2008, p. 24).

Although the trial did not achieve statistical significance in its primary goal of decreasing all-cause mortality or all-cause hospitalization, it did demonstrate a significant 14% decrease in the disease-specific clinical outcome of cardiovascular mortality or heart failure hospitalization. This effect on outcome is similar to that achieved with angiotensin receptor blockade when added to de novo heart failure patients. In addition, the trial further supported the safety of exercise therapy in heart failure.

Many institutions have cardiac rehabilitation programs that include patients with heart failure. In some programs, the therapy is paid for by a third party. In light of the outcomes of HF-ACTION, an important question arises as to whether this therapy, with an expense that might be similar to the cost of providing cardiac rehabilitation for acute myocardial infarction patients, should become part of our standard reimbursement for Medicare and all third parties as an intrinsic part of heart failure therapy. This will be an important issue at a time when the escalating cost of health care is under increasing scrutiny.

Nevertheless, the result of HF-ACTION provides an important additional modality of treatment for heart failure patients and answers the question regarding the safety of exercise. The HF-ACTION investigators will need to provide the information, and some guidance, as to which patients with heart failure can benefit the most from exercise therapy.

It's time to consider making exercise therapy a standard, reimbursable treatment for heart failure. ©Pavel

Dr. George Burch, one of the great leaders in cardiology in the mid-20th century, wrote in a 1954 monograph that “the patient with moderate or severe congestive heart failure should be placed at bed rest immediately.” As a result, many patients were kept in bed for many weeks. This was the considered recommendation of many cardiologists, who had at the time little else to offer to their patients.

In the half century that followed, we learned a great deal about exercise physiology and its role in rehabilitating patients after an acute myocardial infarction. It is now part of the standard care of such patients.

More recently, a large body of clinical data has emerged providing insight into the role of exercise in the patient with heart failure. These studies suggest that, contrary to previous concerns, exercise training may be safe and can lead to improved cardiac physiology. There is now significant evidence that exercise training improves exercise performance, increases peak oxygen consumption, reduces both muscle and systemic sympathetic activity, and favorably modifies systemic and tissue inflammatory markers.

On the basis of these physiologic studies, several clinical trials were performed in the past decade and reported clinical benefits associated with exercise training in heart failure. Although most of the studies have been small, they tended to reinforce the safety and physiologic benefits of exercise training. These studies were designed to include a broad spectrum of patients with varying degrees of heart failure, such as elderly patients, who are becoming an increasingly large part of the heart failure population.

As a result of the progress in this field, in 2002 the National Heart, Lung, and Blood Institute embarked on HF-ACTION (Heart Failure: A Controlled Trial Investigating Outcomes of Exercise Training). The trial, involving more than 2,300 patients with New York Heart Association class I-IV heart failure with ejection fractions of less than 35%, tested the relative morbidity and mortality benefit of exercise training in those who also were receiving optimal medical therapy.

Patients were randomized to usual care or a supervised exercise program for a concentrated 3-month period of exercise 3 days a week for 4 months, followed by home exercise 5 days a week for 2 years (CARDIOLOGY NEWS, Dec. 2008, p. 24).

Although the trial did not achieve statistical significance in its primary goal of decreasing all-cause mortality or all-cause hospitalization, it did demonstrate a significant 14% decrease in the disease-specific clinical outcome of cardiovascular mortality or heart failure hospitalization. This effect on outcome is similar to that achieved with angiotensin receptor blockade when added to de novo heart failure patients. In addition, the trial further supported the safety of exercise therapy in heart failure.

Many institutions have cardiac rehabilitation programs that include patients with heart failure. In some programs, the therapy is paid for by a third party. In light of the outcomes of HF-ACTION, an important question arises as to whether this therapy, with an expense that might be similar to the cost of providing cardiac rehabilitation for acute myocardial infarction patients, should become part of our standard reimbursement for Medicare and all third parties as an intrinsic part of heart failure therapy. This will be an important issue at a time when the escalating cost of health care is under increasing scrutiny.

Nevertheless, the result of HF-ACTION provides an important additional modality of treatment for heart failure patients and answers the question regarding the safety of exercise. The HF-ACTION investigators will need to provide the information, and some guidance, as to which patients with heart failure can benefit the most from exercise therapy.

It's time to consider making exercise therapy a standard, reimbursable treatment for heart failure. ©Pavel

Dr. George Burch, one of the great leaders in cardiology in the mid-20th century, wrote in a 1954 monograph that “the patient with moderate or severe congestive heart failure should be placed at bed rest immediately.” As a result, many patients were kept in bed for many weeks. This was the considered recommendation of many cardiologists, who had at the time little else to offer to their patients.

In the half century that followed, we learned a great deal about exercise physiology and its role in rehabilitating patients after an acute myocardial infarction. It is now part of the standard care of such patients.

More recently, a large body of clinical data has emerged providing insight into the role of exercise in the patient with heart failure. These studies suggest that, contrary to previous concerns, exercise training may be safe and can lead to improved cardiac physiology. There is now significant evidence that exercise training improves exercise performance, increases peak oxygen consumption, reduces both muscle and systemic sympathetic activity, and favorably modifies systemic and tissue inflammatory markers.

On the basis of these physiologic studies, several clinical trials were performed in the past decade and reported clinical benefits associated with exercise training in heart failure. Although most of the studies have been small, they tended to reinforce the safety and physiologic benefits of exercise training. These studies were designed to include a broad spectrum of patients with varying degrees of heart failure, such as elderly patients, who are becoming an increasingly large part of the heart failure population.

As a result of the progress in this field, in 2002 the National Heart, Lung, and Blood Institute embarked on HF-ACTION (Heart Failure: A Controlled Trial Investigating Outcomes of Exercise Training). The trial, involving more than 2,300 patients with New York Heart Association class I-IV heart failure with ejection fractions of less than 35%, tested the relative morbidity and mortality benefit of exercise training in those who also were receiving optimal medical therapy.

Patients were randomized to usual care or a supervised exercise program for a concentrated 3-month period of exercise 3 days a week for 4 months, followed by home exercise 5 days a week for 2 years (CARDIOLOGY NEWS, Dec. 2008, p. 24).

Although the trial did not achieve statistical significance in its primary goal of decreasing all-cause mortality or all-cause hospitalization, it did demonstrate a significant 14% decrease in the disease-specific clinical outcome of cardiovascular mortality or heart failure hospitalization. This effect on outcome is similar to that achieved with angiotensin receptor blockade when added to de novo heart failure patients. In addition, the trial further supported the safety of exercise therapy in heart failure.

Many institutions have cardiac rehabilitation programs that include patients with heart failure. In some programs, the therapy is paid for by a third party. In light of the outcomes of HF-ACTION, an important question arises as to whether this therapy, with an expense that might be similar to the cost of providing cardiac rehabilitation for acute myocardial infarction patients, should become part of our standard reimbursement for Medicare and all third parties as an intrinsic part of heart failure therapy. This will be an important issue at a time when the escalating cost of health care is under increasing scrutiny.

Nevertheless, the result of HF-ACTION provides an important additional modality of treatment for heart failure patients and answers the question regarding the safety of exercise. The HF-ACTION investigators will need to provide the information, and some guidance, as to which patients with heart failure can benefit the most from exercise therapy.

It's time to consider making exercise therapy a standard, reimbursable treatment for heart failure. ©Pavel

Among individuals who experience an acute myocardial infarction, approximately half will die of sudden death, and it often occurs outside of the hospital. The benefit of automatic implantable cardioverter defibrillators (ICDs) in high-risk patients with left ventricular dysfunction with chronic ischemic heart failure has focused our attention on ways of preventing sudden death.

Unfortunately, ICDs have been found to be ineffective and perhaps dangerous in the first 30 days after an acute MI, when such patients are at the greatest risk of sudden death (N. Engl. J. Med. 2004;351:2481–8).

A recent epidemiologic study from the Mayo Clinic of the population in Olmsted County, Minn., examined the occurrence of sudden death in the 30 days after an acute MI. It provides some interesting insight into the change in the frequency of sudden death during the last 25 years and underscores the importance of β-blocker therapy in patients experiencing an acute MI (JAMA 2008;300:2022–9).

In the Mayo Clinic study, sudden death was the cause of 24% of all deaths that occurred in acute MI patients between 1987 and 2005. Of the 59 sudden deaths that occurred in the first year after an acute MI, 35 (59%) occurred in the first 30 days after the MI. However, during the 27 years of the study, the incidence of sudden death decreased significantly. Compared with the period of 1979 to 1987, the risk of sudden death was reduced by 20% during 1988–1997, and by 38% during 1998–2005. The concomitant occurrence of heart failure doubled the rate of sudden death.

Many changes in the therapy of patients experiencing an acute myocardial infarction have occurred since that study began in 1979, including the use of thrombolytics, percutaneous coronary intervention, and coronary artery bypass surgery. All of these interventions have had an important impact on decreasing post-acute MI mortality. However, the only intervention initiated in that period that has been shown to affect sudden death is β-blocker therapy.

First reported in 1981, β-blocker therapy in large multicenter clinical trials both in the United States and Europe indicated that these drugs have a profound effect on total mortality after an acute MI and are particularly effective in preventing sudden death.

In the Beta-Blocker Heart Attack Trial (BHAT), β-blockers initiated within 7 days of hospitalization for an acute myocardial infarction decreased all mortality by 26% and sudden death by 28%. In BHAT patients with heart failure, therapy with β-blockers resulted in a 47% decrease in sudden death. Propranolol was used in BHAT, initiated at a dose of 120 mg daily and increased to 160–180 mg at 4 weeks.

Despite these reported effects, β-blocker therapy was poorly accepted for the routine treatment after an acute MI. Well into the 1990s, fewer than 50% of patients who had experienced an acute myocardial infarction received that therapy. It was not until the incorporation of β-blocker therapy as a quality measure by the National Committee for Quality Assurance (NCQA) in 1996 and the subsequent inclusion in American Heart Association-American College of Cardiology guidelines in 2000 that they were more widely used. Now, well over 90% of patients discharged from the hospital after an acute myocardial infarction are treated with β-blockers. It is often a low dose, but they are receiving some therapy nonetheless.

Although we cannot be certain what led to the decrease in sudden death in Olmsted County, it is tempting to presume that at least it can be attributed in part to the temporal changes in β-blocker usage.

Quality improvement programs provide a measure of whether or not a drug is ordered, but they do not measure the dose used. Equating the propranolol doses in BHAT to the contemporary β-blockers carvedilol and metoprolol succinate, both of which have been shown to provide benefits similar to that of propranolol, calls for daily doses up to 50 mg and 200 mg, respectively. The NCQA has recently introduced a new measure to ensure continuing therapy after 6 months, after a study in 2006 indicated that only 71% of patients after an acute myocardial infarction were still receiving β-blockers.

The observations from Olmsted County place in perspective the success of the quality improvement process in mitigating mortality in acute myocardial infarction. They also should provide an important encouragement for the practitioner to use full doses of contemporary β-blockers and to continue therapy.

Among individuals who experience an acute myocardial infarction, approximately half will die of sudden death, and it often occurs outside of the hospital. The benefit of automatic implantable cardioverter defibrillators (ICDs) in high-risk patients with left ventricular dysfunction with chronic ischemic heart failure has focused our attention on ways of preventing sudden death.

Unfortunately, ICDs have been found to be ineffective and perhaps dangerous in the first 30 days after an acute MI, when such patients are at the greatest risk of sudden death (N. Engl. J. Med. 2004;351:2481–8).

A recent epidemiologic study from the Mayo Clinic of the population in Olmsted County, Minn., examined the occurrence of sudden death in the 30 days after an acute MI. It provides some interesting insight into the change in the frequency of sudden death during the last 25 years and underscores the importance of β-blocker therapy in patients experiencing an acute MI (JAMA 2008;300:2022–9).

In the Mayo Clinic study, sudden death was the cause of 24% of all deaths that occurred in acute MI patients between 1987 and 2005. Of the 59 sudden deaths that occurred in the first year after an acute MI, 35 (59%) occurred in the first 30 days after the MI. However, during the 27 years of the study, the incidence of sudden death decreased significantly. Compared with the period of 1979 to 1987, the risk of sudden death was reduced by 20% during 1988–1997, and by 38% during 1998–2005. The concomitant occurrence of heart failure doubled the rate of sudden death.

Many changes in the therapy of patients experiencing an acute myocardial infarction have occurred since that study began in 1979, including the use of thrombolytics, percutaneous coronary intervention, and coronary artery bypass surgery. All of these interventions have had an important impact on decreasing post-acute MI mortality. However, the only intervention initiated in that period that has been shown to affect sudden death is β-blocker therapy.

First reported in 1981, β-blocker therapy in large multicenter clinical trials both in the United States and Europe indicated that these drugs have a profound effect on total mortality after an acute MI and are particularly effective in preventing sudden death.

In the Beta-Blocker Heart Attack Trial (BHAT), β-blockers initiated within 7 days of hospitalization for an acute myocardial infarction decreased all mortality by 26% and sudden death by 28%. In BHAT patients with heart failure, therapy with β-blockers resulted in a 47% decrease in sudden death. Propranolol was used in BHAT, initiated at a dose of 120 mg daily and increased to 160–180 mg at 4 weeks.

Despite these reported effects, β-blocker therapy was poorly accepted for the routine treatment after an acute MI. Well into the 1990s, fewer than 50% of patients who had experienced an acute myocardial infarction received that therapy. It was not until the incorporation of β-blocker therapy as a quality measure by the National Committee for Quality Assurance (NCQA) in 1996 and the subsequent inclusion in American Heart Association-American College of Cardiology guidelines in 2000 that they were more widely used. Now, well over 90% of patients discharged from the hospital after an acute myocardial infarction are treated with β-blockers. It is often a low dose, but they are receiving some therapy nonetheless.

Although we cannot be certain what led to the decrease in sudden death in Olmsted County, it is tempting to presume that at least it can be attributed in part to the temporal changes in β-blocker usage.

Quality improvement programs provide a measure of whether or not a drug is ordered, but they do not measure the dose used. Equating the propranolol doses in BHAT to the contemporary β-blockers carvedilol and metoprolol succinate, both of which have been shown to provide benefits similar to that of propranolol, calls for daily doses up to 50 mg and 200 mg, respectively. The NCQA has recently introduced a new measure to ensure continuing therapy after 6 months, after a study in 2006 indicated that only 71% of patients after an acute myocardial infarction were still receiving β-blockers.

The observations from Olmsted County place in perspective the success of the quality improvement process in mitigating mortality in acute myocardial infarction. They also should provide an important encouragement for the practitioner to use full doses of contemporary β-blockers and to continue therapy.

Among individuals who experience an acute myocardial infarction, approximately half will die of sudden death, and it often occurs outside of the hospital. The benefit of automatic implantable cardioverter defibrillators (ICDs) in high-risk patients with left ventricular dysfunction with chronic ischemic heart failure has focused our attention on ways of preventing sudden death.

Unfortunately, ICDs have been found to be ineffective and perhaps dangerous in the first 30 days after an acute MI, when such patients are at the greatest risk of sudden death (N. Engl. J. Med. 2004;351:2481–8).

A recent epidemiologic study from the Mayo Clinic of the population in Olmsted County, Minn., examined the occurrence of sudden death in the 30 days after an acute MI. It provides some interesting insight into the change in the frequency of sudden death during the last 25 years and underscores the importance of β-blocker therapy in patients experiencing an acute MI (JAMA 2008;300:2022–9).

In the Mayo Clinic study, sudden death was the cause of 24% of all deaths that occurred in acute MI patients between 1987 and 2005. Of the 59 sudden deaths that occurred in the first year after an acute MI, 35 (59%) occurred in the first 30 days after the MI. However, during the 27 years of the study, the incidence of sudden death decreased significantly. Compared with the period of 1979 to 1987, the risk of sudden death was reduced by 20% during 1988–1997, and by 38% during 1998–2005. The concomitant occurrence of heart failure doubled the rate of sudden death.

Many changes in the therapy of patients experiencing an acute myocardial infarction have occurred since that study began in 1979, including the use of thrombolytics, percutaneous coronary intervention, and coronary artery bypass surgery. All of these interventions have had an important impact on decreasing post-acute MI mortality. However, the only intervention initiated in that period that has been shown to affect sudden death is β-blocker therapy.

First reported in 1981, β-blocker therapy in large multicenter clinical trials both in the United States and Europe indicated that these drugs have a profound effect on total mortality after an acute MI and are particularly effective in preventing sudden death.

In the Beta-Blocker Heart Attack Trial (BHAT), β-blockers initiated within 7 days of hospitalization for an acute myocardial infarction decreased all mortality by 26% and sudden death by 28%. In BHAT patients with heart failure, therapy with β-blockers resulted in a 47% decrease in sudden death. Propranolol was used in BHAT, initiated at a dose of 120 mg daily and increased to 160–180 mg at 4 weeks.

Despite these reported effects, β-blocker therapy was poorly accepted for the routine treatment after an acute MI. Well into the 1990s, fewer than 50% of patients who had experienced an acute myocardial infarction received that therapy. It was not until the incorporation of β-blocker therapy as a quality measure by the National Committee for Quality Assurance (NCQA) in 1996 and the subsequent inclusion in American Heart Association-American College of Cardiology guidelines in 2000 that they were more widely used. Now, well over 90% of patients discharged from the hospital after an acute myocardial infarction are treated with β-blockers. It is often a low dose, but they are receiving some therapy nonetheless.

Although we cannot be certain what led to the decrease in sudden death in Olmsted County, it is tempting to presume that at least it can be attributed in part to the temporal changes in β-blocker usage.

Quality improvement programs provide a measure of whether or not a drug is ordered, but they do not measure the dose used. Equating the propranolol doses in BHAT to the contemporary β-blockers carvedilol and metoprolol succinate, both of which have been shown to provide benefits similar to that of propranolol, calls for daily doses up to 50 mg and 200 mg, respectively. The NCQA has recently introduced a new measure to ensure continuing therapy after 6 months, after a study in 2006 indicated that only 71% of patients after an acute myocardial infarction were still receiving β-blockers.

The observations from Olmsted County place in perspective the success of the quality improvement process in mitigating mortality in acute myocardial infarction. They also should provide an important encouragement for the practitioner to use full doses of contemporary β-blockers and to continue therapy.

Treatment of acute coronary syndromes has come a long way since 1969, when Dr. Arthur Moss and I held a symposium at the University of Rochester titled, The Prehospital Phase of Acute Myocardial Infarction. It was one of the first such events focused on the early pathophysiologic events and care of patients with symptoms of an acute myocardial infarction (Am. J. Card. 1969;24:609–11).

This meeting was held about 4 years after Prof. Desmond Julian in Edinburgh proposed the concept of a coronary care unit and a few years after Dr. Frank Partridge had organized the first mobile coronary care unit in Belfast, Northern Ireland, and Dr. Hughes Day established the first CCU in Bethany, Kan. These seminal efforts showed that patients with an acute MI were best cared for in the setting of a unit dedicated to the treatment of the pathophysiologic events associated with acute myocardial ischemia. Prior to the development of CCUs, patients with acute MIs were hospitalized in the general hospital ward without any special monitoring.

We became interested at that time in the prodromal symptoms leading up to the event and factors that lead to the decision to come to the hospital. We observed that approximately 3.5 hours elapsed from the onset of symptoms to hospital arrival (Circulation 1970;41:737–42). More than half of that time was taken up with the patient and or family making a decision to come to the hospital. It is more than likely that many patients who experienced an acute MI could have died in that time.

To deal with hospital delay, we among others urged for the first time that patients come promptly to the emergency department without consulting their physicians. This was a sharp departure from the standard of practice at that time. The rest, of course, is history. The floodgates were opened and the emergency departments (EDs) were deluged with the myriad of medical causes of chest pain, real and fancied. The emergency physicians were left to sort it all out.

Fast forward to the development of biomarkers, exercise technology, and imaging that developed from the need to define and identify the individual with an acute coronary event. Today there are approximately 8 million visits to the ED for chest pain and related symptoms. Of these, approximately 20% are defined as an acute coronary syndrome (ACS) event. Of the estimated 1.1 million myocardial infarctions annually in the United States, about half the patients survive and make it to the ED for care. Recent studies indicate that the diagnosis of acute MI is missed in 2.1% of them (N. Engl. J. Med. 2000;342:1163–70). Similarly, 2.3% of patients seen in the ED for unstable angina are discharged and their diagnosis is missed. The risk-adjusted mortality rate in those patients in whom the diagnosis was missed is associated with an increased mortality risk.

In response to this deluge of patients coming to EDs, more than 1,500 chest pain units have been established, most of them attached to an ED where patients can be monitored and evaluated outside of the hurly-burly atmosphere characteristic of emergency departments. These units were first established by the American College of Cardiovascular Administrators in 1991, which later merged into the Society of Chest Pain Centers and Providers (SCPCP). The organization is made up predominately of ED physicians and bridges the fields of emergency medicine, cardiology, and critical care nursing. Although often located within emergency facilities, they provide an atmosphere where patients can be evaluated using current diagnostic facilities at a cost less than that of the traditional CCU. They also expedite early therapy for patients with ACS by shortening door-to-needle time and by early administration of thrombolytic and pharmacologic therapy to minimize ischemia. The chest pain centers are now undergoing an accreditation process under the direction of the SCPCP.

To deal with this increased volume of patients coming to the ED for evaluation of chest pain, hospitals have modified emergency department facilities and procedures. The establishment of chest pain centers has provided a model of how chest pain patients can be expeditiously managed and treated in the face of increasing patient volume in an era of decreasing numbers of EDs nationwide.

Treatment of acute coronary syndromes has come a long way since 1969, when Dr. Arthur Moss and I held a symposium at the University of Rochester titled, The Prehospital Phase of Acute Myocardial Infarction. It was one of the first such events focused on the early pathophysiologic events and care of patients with symptoms of an acute myocardial infarction (Am. J. Card. 1969;24:609–11).

This meeting was held about 4 years after Prof. Desmond Julian in Edinburgh proposed the concept of a coronary care unit and a few years after Dr. Frank Partridge had organized the first mobile coronary care unit in Belfast, Northern Ireland, and Dr. Hughes Day established the first CCU in Bethany, Kan. These seminal efforts showed that patients with an acute MI were best cared for in the setting of a unit dedicated to the treatment of the pathophysiologic events associated with acute myocardial ischemia. Prior to the development of CCUs, patients with acute MIs were hospitalized in the general hospital ward without any special monitoring.

We became interested at that time in the prodromal symptoms leading up to the event and factors that lead to the decision to come to the hospital. We observed that approximately 3.5 hours elapsed from the onset of symptoms to hospital arrival (Circulation 1970;41:737–42). More than half of that time was taken up with the patient and or family making a decision to come to the hospital. It is more than likely that many patients who experienced an acute MI could have died in that time.

To deal with hospital delay, we among others urged for the first time that patients come promptly to the emergency department without consulting their physicians. This was a sharp departure from the standard of practice at that time. The rest, of course, is history. The floodgates were opened and the emergency departments (EDs) were deluged with the myriad of medical causes of chest pain, real and fancied. The emergency physicians were left to sort it all out.

Fast forward to the development of biomarkers, exercise technology, and imaging that developed from the need to define and identify the individual with an acute coronary event. Today there are approximately 8 million visits to the ED for chest pain and related symptoms. Of these, approximately 20% are defined as an acute coronary syndrome (ACS) event. Of the estimated 1.1 million myocardial infarctions annually in the United States, about half the patients survive and make it to the ED for care. Recent studies indicate that the diagnosis of acute MI is missed in 2.1% of them (N. Engl. J. Med. 2000;342:1163–70). Similarly, 2.3% of patients seen in the ED for unstable angina are discharged and their diagnosis is missed. The risk-adjusted mortality rate in those patients in whom the diagnosis was missed is associated with an increased mortality risk.

In response to this deluge of patients coming to EDs, more than 1,500 chest pain units have been established, most of them attached to an ED where patients can be monitored and evaluated outside of the hurly-burly atmosphere characteristic of emergency departments. These units were first established by the American College of Cardiovascular Administrators in 1991, which later merged into the Society of Chest Pain Centers and Providers (SCPCP). The organization is made up predominately of ED physicians and bridges the fields of emergency medicine, cardiology, and critical care nursing. Although often located within emergency facilities, they provide an atmosphere where patients can be evaluated using current diagnostic facilities at a cost less than that of the traditional CCU. They also expedite early therapy for patients with ACS by shortening door-to-needle time and by early administration of thrombolytic and pharmacologic therapy to minimize ischemia. The chest pain centers are now undergoing an accreditation process under the direction of the SCPCP.

To deal with this increased volume of patients coming to the ED for evaluation of chest pain, hospitals have modified emergency department facilities and procedures. The establishment of chest pain centers has provided a model of how chest pain patients can be expeditiously managed and treated in the face of increasing patient volume in an era of decreasing numbers of EDs nationwide.

Treatment of acute coronary syndromes has come a long way since 1969, when Dr. Arthur Moss and I held a symposium at the University of Rochester titled, The Prehospital Phase of Acute Myocardial Infarction. It was one of the first such events focused on the early pathophysiologic events and care of patients with symptoms of an acute myocardial infarction (Am. J. Card. 1969;24:609–11).

This meeting was held about 4 years after Prof. Desmond Julian in Edinburgh proposed the concept of a coronary care unit and a few years after Dr. Frank Partridge had organized the first mobile coronary care unit in Belfast, Northern Ireland, and Dr. Hughes Day established the first CCU in Bethany, Kan. These seminal efforts showed that patients with an acute MI were best cared for in the setting of a unit dedicated to the treatment of the pathophysiologic events associated with acute myocardial ischemia. Prior to the development of CCUs, patients with acute MIs were hospitalized in the general hospital ward without any special monitoring.

We became interested at that time in the prodromal symptoms leading up to the event and factors that lead to the decision to come to the hospital. We observed that approximately 3.5 hours elapsed from the onset of symptoms to hospital arrival (Circulation 1970;41:737–42). More than half of that time was taken up with the patient and or family making a decision to come to the hospital. It is more than likely that many patients who experienced an acute MI could have died in that time.

To deal with hospital delay, we among others urged for the first time that patients come promptly to the emergency department without consulting their physicians. This was a sharp departure from the standard of practice at that time. The rest, of course, is history. The floodgates were opened and the emergency departments (EDs) were deluged with the myriad of medical causes of chest pain, real and fancied. The emergency physicians were left to sort it all out.

Fast forward to the development of biomarkers, exercise technology, and imaging that developed from the need to define and identify the individual with an acute coronary event. Today there are approximately 8 million visits to the ED for chest pain and related symptoms. Of these, approximately 20% are defined as an acute coronary syndrome (ACS) event. Of the estimated 1.1 million myocardial infarctions annually in the United States, about half the patients survive and make it to the ED for care. Recent studies indicate that the diagnosis of acute MI is missed in 2.1% of them (N. Engl. J. Med. 2000;342:1163–70). Similarly, 2.3% of patients seen in the ED for unstable angina are discharged and their diagnosis is missed. The risk-adjusted mortality rate in those patients in whom the diagnosis was missed is associated with an increased mortality risk.

In response to this deluge of patients coming to EDs, more than 1,500 chest pain units have been established, most of them attached to an ED where patients can be monitored and evaluated outside of the hurly-burly atmosphere characteristic of emergency departments. These units were first established by the American College of Cardiovascular Administrators in 1991, which later merged into the Society of Chest Pain Centers and Providers (SCPCP). The organization is made up predominately of ED physicians and bridges the fields of emergency medicine, cardiology, and critical care nursing. Although often located within emergency facilities, they provide an atmosphere where patients can be evaluated using current diagnostic facilities at a cost less than that of the traditional CCU. They also expedite early therapy for patients with ACS by shortening door-to-needle time and by early administration of thrombolytic and pharmacologic therapy to minimize ischemia. The chest pain centers are now undergoing an accreditation process under the direction of the SCPCP.

To deal with this increased volume of patients coming to the ED for evaluation of chest pain, hospitals have modified emergency department facilities and procedures. The establishment of chest pain centers has provided a model of how chest pain patients can be expeditiously managed and treated in the face of increasing patient volume in an era of decreasing numbers of EDs nationwide.

As this column is being written, America's quadrennial self-flagellation over choosing a new president is underway, and by the time it arrives in your mailbox, a new president will have been elected.

That president will be facing numerous problems, one of which is providing health care to the 300 million Americans in the face of a failing economy, a huge budget deficit, and increasing unemployment, particularly in the manufacturing sector. Because employers laid the foundation upon which health insurance has been built, economic collapse, particularly of the auto industry and its related support industries, would leave thousands of workers without health insurance. Those who are employed will face increasing personal costs to participate in their coverage. In this environment, our ability as physicians to meet the standards of cardiac care will become increasingly difficult.

How either candidate meets the expectations in the next 4 years remains uncertain regardless of who becomes president. If we have a Democratic president along with the presumed ascendancy of a Democratic majority in Congress, it is possible but not certain that significant changes will occur. Sen. Barack Obama has promised a $2,500 decrease in insurance premiums and providing health care to everyone by achieving efficiencies in care.

With a Republican president, it is more than likely we will continue to deal with a stalemate in the face of a Democratic Congress. Nevertheless, Sen. John McCain plans to provide a tax credit for each individual of $2,500 and $5,000 to every family. Those who are uninsured can take their tax credit and apply it to the insurance of their choice when they become insured.

It is clear, however, that no one is totally happy with how health care is provided at the present. There is considerable anxiety about our individual ability to pay for health insurance as the cost of these plans continues to increase. At the same time, the number of uninsured remains unacceptably large—almost 45 million Americans are without health insurance. There has been a slight decrease in the number of Americans without insurance as more families are turning to Medicare and Medicaid as incomes decrease and the population ages. In 2008, as unemployment has risen and individuals have lost their employer-supported insurance, there has been a 2.1% nationwide increase in patients going into Medicaid. In Michigan, where unemployment is approximately 10%, Medicaid enrollment increased by 3.8%. As unemployment increases, we can anticipate this expansion of government coverage to increase.

The recent huge advances made in clinical science with its resultant increase in expensive drugs and devices represent a paradox in an atmosphere of diminishing economic resources. The calls for more aggressive preventive measures to decrease the incidence of coronary heart disease, hypertension, and diabetes is occurring in the face of an expanding population of uninsured patients and decreasing financial resources. Preventive medicine is lacking even for insured Americans.

However, throughout the country, alternative ways to pay and organize health insurance and provide a more inclusive system are emerging.

The Massachusetts health plan is one of those alternatives. It requires that each resident be enrolled in a private, state, or federal insurance program. It mandates universal coverage to those with lower incomes, using a sliding scale of premiums for families who are earning less than three times the poverty level or $63,000. Many of the insured have purchased private insurance, participate in the subsidized plan, or have enrolled in Medicaid. By providing state-sponsored health insurance programs, Massachusetts has seen the uninsured rate decrease to about 5% (N. Engl. J. Med. 2008:358;2757–60). This program, which relies on funding from the Centers for Medicare and Medicaid Services, provides a foundation upon which preventive medicine can be built, as well as an opportunity to mitigate the forces that lead to annually increasing acute care expenses. Whether or not this model can be applied to a larger population, particularly in view of the problematic national economy, our next president faces a significant challenge indeed.

As this column is being written, America's quadrennial self-flagellation over choosing a new president is underway, and by the time it arrives in your mailbox, a new president will have been elected.

That president will be facing numerous problems, one of which is providing health care to the 300 million Americans in the face of a failing economy, a huge budget deficit, and increasing unemployment, particularly in the manufacturing sector. Because employers laid the foundation upon which health insurance has been built, economic collapse, particularly of the auto industry and its related support industries, would leave thousands of workers without health insurance. Those who are employed will face increasing personal costs to participate in their coverage. In this environment, our ability as physicians to meet the standards of cardiac care will become increasingly difficult.

How either candidate meets the expectations in the next 4 years remains uncertain regardless of who becomes president. If we have a Democratic president along with the presumed ascendancy of a Democratic majority in Congress, it is possible but not certain that significant changes will occur. Sen. Barack Obama has promised a $2,500 decrease in insurance premiums and providing health care to everyone by achieving efficiencies in care.

With a Republican president, it is more than likely we will continue to deal with a stalemate in the face of a Democratic Congress. Nevertheless, Sen. John McCain plans to provide a tax credit for each individual of $2,500 and $5,000 to every family. Those who are uninsured can take their tax credit and apply it to the insurance of their choice when they become insured.

It is clear, however, that no one is totally happy with how health care is provided at the present. There is considerable anxiety about our individual ability to pay for health insurance as the cost of these plans continues to increase. At the same time, the number of uninsured remains unacceptably large—almost 45 million Americans are without health insurance. There has been a slight decrease in the number of Americans without insurance as more families are turning to Medicare and Medicaid as incomes decrease and the population ages. In 2008, as unemployment has risen and individuals have lost their employer-supported insurance, there has been a 2.1% nationwide increase in patients going into Medicaid. In Michigan, where unemployment is approximately 10%, Medicaid enrollment increased by 3.8%. As unemployment increases, we can anticipate this expansion of government coverage to increase.

The recent huge advances made in clinical science with its resultant increase in expensive drugs and devices represent a paradox in an atmosphere of diminishing economic resources. The calls for more aggressive preventive measures to decrease the incidence of coronary heart disease, hypertension, and diabetes is occurring in the face of an expanding population of uninsured patients and decreasing financial resources. Preventive medicine is lacking even for insured Americans.

However, throughout the country, alternative ways to pay and organize health insurance and provide a more inclusive system are emerging.

The Massachusetts health plan is one of those alternatives. It requires that each resident be enrolled in a private, state, or federal insurance program. It mandates universal coverage to those with lower incomes, using a sliding scale of premiums for families who are earning less than three times the poverty level or $63,000. Many of the insured have purchased private insurance, participate in the subsidized plan, or have enrolled in Medicaid. By providing state-sponsored health insurance programs, Massachusetts has seen the uninsured rate decrease to about 5% (N. Engl. J. Med. 2008:358;2757–60). This program, which relies on funding from the Centers for Medicare and Medicaid Services, provides a foundation upon which preventive medicine can be built, as well as an opportunity to mitigate the forces that lead to annually increasing acute care expenses. Whether or not this model can be applied to a larger population, particularly in view of the problematic national economy, our next president faces a significant challenge indeed.

As this column is being written, America's quadrennial self-flagellation over choosing a new president is underway, and by the time it arrives in your mailbox, a new president will have been elected.

That president will be facing numerous problems, one of which is providing health care to the 300 million Americans in the face of a failing economy, a huge budget deficit, and increasing unemployment, particularly in the manufacturing sector. Because employers laid the foundation upon which health insurance has been built, economic collapse, particularly of the auto industry and its related support industries, would leave thousands of workers without health insurance. Those who are employed will face increasing personal costs to participate in their coverage. In this environment, our ability as physicians to meet the standards of cardiac care will become increasingly difficult.

How either candidate meets the expectations in the next 4 years remains uncertain regardless of who becomes president. If we have a Democratic president along with the presumed ascendancy of a Democratic majority in Congress, it is possible but not certain that significant changes will occur. Sen. Barack Obama has promised a $2,500 decrease in insurance premiums and providing health care to everyone by achieving efficiencies in care.

With a Republican president, it is more than likely we will continue to deal with a stalemate in the face of a Democratic Congress. Nevertheless, Sen. John McCain plans to provide a tax credit for each individual of $2,500 and $5,000 to every family. Those who are uninsured can take their tax credit and apply it to the insurance of their choice when they become insured.

It is clear, however, that no one is totally happy with how health care is provided at the present. There is considerable anxiety about our individual ability to pay for health insurance as the cost of these plans continues to increase. At the same time, the number of uninsured remains unacceptably large—almost 45 million Americans are without health insurance. There has been a slight decrease in the number of Americans without insurance as more families are turning to Medicare and Medicaid as incomes decrease and the population ages. In 2008, as unemployment has risen and individuals have lost their employer-supported insurance, there has been a 2.1% nationwide increase in patients going into Medicaid. In Michigan, where unemployment is approximately 10%, Medicaid enrollment increased by 3.8%. As unemployment increases, we can anticipate this expansion of government coverage to increase.

The recent huge advances made in clinical science with its resultant increase in expensive drugs and devices represent a paradox in an atmosphere of diminishing economic resources. The calls for more aggressive preventive measures to decrease the incidence of coronary heart disease, hypertension, and diabetes is occurring in the face of an expanding population of uninsured patients and decreasing financial resources. Preventive medicine is lacking even for insured Americans.

However, throughout the country, alternative ways to pay and organize health insurance and provide a more inclusive system are emerging.

The Massachusetts health plan is one of those alternatives. It requires that each resident be enrolled in a private, state, or federal insurance program. It mandates universal coverage to those with lower incomes, using a sliding scale of premiums for families who are earning less than three times the poverty level or $63,000. Many of the insured have purchased private insurance, participate in the subsidized plan, or have enrolled in Medicaid. By providing state-sponsored health insurance programs, Massachusetts has seen the uninsured rate decrease to about 5% (N. Engl. J. Med. 2008:358;2757–60). This program, which relies on funding from the Centers for Medicare and Medicaid Services, provides a foundation upon which preventive medicine can be built, as well as an opportunity to mitigate the forces that lead to annually increasing acute care expenses. Whether or not this model can be applied to a larger population, particularly in view of the problematic national economy, our next president faces a significant challenge indeed.

Let's face it: Diabetes management has been off the radar screen of most cardiologists. But the recent report of two major randomized clinical trials should reenergize research in the pathogenesis of macrovascular atherosclerotic disease in diabetes and increase our efforts in the prevention of cardiovascular sequelae of this disease.

These two trials, ACCORD (Action to Control Cardiovascular Risk in Diabetes) and ADVANCE (Action in Diabetes and Vascular Disease) (N. Engl. J. Med. 2008:358;2545-72), explored the role of intensive glucose control in the development of macrovascular and microvascular disease in type 2 diabetic patients with established cardiovascular disease or additional risk factors. Since previous clinical studies showed that hyperglycemic control modulated microvascular disease in diabetics, it seemed reasonable to further modify glucose control to prevent macrovascular disease. Both studies achieved a significant decrease in blood glucose levels, although researchers used different drug protocols to achieve their targets.

In addition to more precise insulin therapy, ACCORD used the thiazolidinedione rosiglitazone as additive therapy to achieve the target, whereas ADVANCE used the sulfonylurea gliclazide in addition to perindopril and indapamide.

Both studies were negative in their unique ways. ACCORD failed to have a positive effect on the primary outcome of a composite of nonfatal myocardial infarction and stroke in addition to cardiovascular mortality. Although the study showed a significant decrease in nonfatal myocardial infarction, this decrease was associated with an increase in all-cause mortality and morbidity due to cardiovascular disease, which led to the study's premature termination.

In contrast, ADVANCE observed a nonsignificant 10% reduction in a composite of micro- and macrovascular end points. In regard to the macrovascular end points, the major emphasis of these studies, there was no benefit observed as to nonfatal myocardial infarction, stroke, or death. The failure of the intensive glucose control strategy to limit the expression of macrovascular disease emphasizes the importance of a more aggressive approach to secondary prevention.

Diabetes continues to be a growing problem in cardiology and most certainly will increase in its incidence as our population ages and becomes more obese. The pathogenesis of the process that accelerates the deposition of cholesterol in the arterial wall in diabetes continues to elude our understanding. It is clear, however, that diabetic patients are at increased risk of atherosclerosis and coronary artery disease.

Many of the medications that have been shown to be effective in preventing the expression and progression of coronary artery disease in the general population are equally effective in diabetes patients, and are underutilized. It is estimated that fewer than 10% of diabetic patients are being treated to target for hypertension and hyperlipidemia (JAMA 2004;291:335-42). For example, ACE inhibitors were underutilized in ACCORD. And in the ADVANCE trial, fewer than 50% of the patients randomized to that study were receiving statins, and fewer than 60% were receiving aspirin. These therapies were much more widely used in ACCORD, and this increased use was associated with a lower mortality and morbidity in ACCORD than in ADVANCE.

It is possible that other targets for intervention in the diabetic patient will be developed from the further analysis of these two very important studies and subsequent research. However, it is clear from these studies that diabetic patients should be considered at high risk for the development of atherosclerosis, even if they have not expressed a clinical event. It is therefore imperative that we become more effective in instituting preventive therapies—proved effective in cardiac patients—in our diabetic patients. Even in well-organized clinical centers such as those used in these studies, these goals are difficult to achieve and are not being met.

Let's face it: Diabetes management has been off the radar screen of most cardiologists. But the recent report of two major randomized clinical trials should reenergize research in the pathogenesis of macrovascular atherosclerotic disease in diabetes and increase our efforts in the prevention of cardiovascular sequelae of this disease.

These two trials, ACCORD (Action to Control Cardiovascular Risk in Diabetes) and ADVANCE (Action in Diabetes and Vascular Disease) (N. Engl. J. Med. 2008:358;2545-72), explored the role of intensive glucose control in the development of macrovascular and microvascular disease in type 2 diabetic patients with established cardiovascular disease or additional risk factors. Since previous clinical studies showed that hyperglycemic control modulated microvascular disease in diabetics, it seemed reasonable to further modify glucose control to prevent macrovascular disease. Both studies achieved a significant decrease in blood glucose levels, although researchers used different drug protocols to achieve their targets.

In addition to more precise insulin therapy, ACCORD used the thiazolidinedione rosiglitazone as additive therapy to achieve the target, whereas ADVANCE used the sulfonylurea gliclazide in addition to perindopril and indapamide.

Both studies were negative in their unique ways. ACCORD failed to have a positive effect on the primary outcome of a composite of nonfatal myocardial infarction and stroke in addition to cardiovascular mortality. Although the study showed a significant decrease in nonfatal myocardial infarction, this decrease was associated with an increase in all-cause mortality and morbidity due to cardiovascular disease, which led to the study's premature termination.

In contrast, ADVANCE observed a nonsignificant 10% reduction in a composite of micro- and macrovascular end points. In regard to the macrovascular end points, the major emphasis of these studies, there was no benefit observed as to nonfatal myocardial infarction, stroke, or death. The failure of the intensive glucose control strategy to limit the expression of macrovascular disease emphasizes the importance of a more aggressive approach to secondary prevention.

Diabetes continues to be a growing problem in cardiology and most certainly will increase in its incidence as our population ages and becomes more obese. The pathogenesis of the process that accelerates the deposition of cholesterol in the arterial wall in diabetes continues to elude our understanding. It is clear, however, that diabetic patients are at increased risk of atherosclerosis and coronary artery disease.

Many of the medications that have been shown to be effective in preventing the expression and progression of coronary artery disease in the general population are equally effective in diabetes patients, and are underutilized. It is estimated that fewer than 10% of diabetic patients are being treated to target for hypertension and hyperlipidemia (JAMA 2004;291:335-42). For example, ACE inhibitors were underutilized in ACCORD. And in the ADVANCE trial, fewer than 50% of the patients randomized to that study were receiving statins, and fewer than 60% were receiving aspirin. These therapies were much more widely used in ACCORD, and this increased use was associated with a lower mortality and morbidity in ACCORD than in ADVANCE.

It is possible that other targets for intervention in the diabetic patient will be developed from the further analysis of these two very important studies and subsequent research. However, it is clear from these studies that diabetic patients should be considered at high risk for the development of atherosclerosis, even if they have not expressed a clinical event. It is therefore imperative that we become more effective in instituting preventive therapies—proved effective in cardiac patients—in our diabetic patients. Even in well-organized clinical centers such as those used in these studies, these goals are difficult to achieve and are not being met.

Let's face it: Diabetes management has been off the radar screen of most cardiologists. But the recent report of two major randomized clinical trials should reenergize research in the pathogenesis of macrovascular atherosclerotic disease in diabetes and increase our efforts in the prevention of cardiovascular sequelae of this disease.

These two trials, ACCORD (Action to Control Cardiovascular Risk in Diabetes) and ADVANCE (Action in Diabetes and Vascular Disease) (N. Engl. J. Med. 2008:358;2545-72), explored the role of intensive glucose control in the development of macrovascular and microvascular disease in type 2 diabetic patients with established cardiovascular disease or additional risk factors. Since previous clinical studies showed that hyperglycemic control modulated microvascular disease in diabetics, it seemed reasonable to further modify glucose control to prevent macrovascular disease. Both studies achieved a significant decrease in blood glucose levels, although researchers used different drug protocols to achieve their targets.

In addition to more precise insulin therapy, ACCORD used the thiazolidinedione rosiglitazone as additive therapy to achieve the target, whereas ADVANCE used the sulfonylurea gliclazide in addition to perindopril and indapamide.

Both studies were negative in their unique ways. ACCORD failed to have a positive effect on the primary outcome of a composite of nonfatal myocardial infarction and stroke in addition to cardiovascular mortality. Although the study showed a significant decrease in nonfatal myocardial infarction, this decrease was associated with an increase in all-cause mortality and morbidity due to cardiovascular disease, which led to the study's premature termination.

In contrast, ADVANCE observed a nonsignificant 10% reduction in a composite of micro- and macrovascular end points. In regard to the macrovascular end points, the major emphasis of these studies, there was no benefit observed as to nonfatal myocardial infarction, stroke, or death. The failure of the intensive glucose control strategy to limit the expression of macrovascular disease emphasizes the importance of a more aggressive approach to secondary prevention.

Diabetes continues to be a growing problem in cardiology and most certainly will increase in its incidence as our population ages and becomes more obese. The pathogenesis of the process that accelerates the deposition of cholesterol in the arterial wall in diabetes continues to elude our understanding. It is clear, however, that diabetic patients are at increased risk of atherosclerosis and coronary artery disease.

Many of the medications that have been shown to be effective in preventing the expression and progression of coronary artery disease in the general population are equally effective in diabetes patients, and are underutilized. It is estimated that fewer than 10% of diabetic patients are being treated to target for hypertension and hyperlipidemia (JAMA 2004;291:335-42). For example, ACE inhibitors were underutilized in ACCORD. And in the ADVANCE trial, fewer than 50% of the patients randomized to that study were receiving statins, and fewer than 60% were receiving aspirin. These therapies were much more widely used in ACCORD, and this increased use was associated with a lower mortality and morbidity in ACCORD than in ADVANCE.

It is possible that other targets for intervention in the diabetic patient will be developed from the further analysis of these two very important studies and subsequent research. However, it is clear from these studies that diabetic patients should be considered at high risk for the development of atherosclerosis, even if they have not expressed a clinical event. It is therefore imperative that we become more effective in instituting preventive therapies—proved effective in cardiac patients—in our diabetic patients. Even in well-organized clinical centers such as those used in these studies, these goals are difficult to achieve and are not being met.

I am sure that many of you have been asked the same question that I have this summer. It typically occurred at a cocktail party, when a 50-something woman, upon learning that I am a cardiologist, sidled up and motioned toward a portly gentleman hovering over the appetizers. “That's my husband. He saw his doctor last week and was told that his blood pressure was a little high, but that he shouldn't worry. They'll check him again next year. What should he do to prevent a heart attack like Tim Russert's?”

Mr. Russert's untimely death sent shivers through millions of middle-aged men and their families. Here was a guy seemingly getting the best preventive care, yet he died from an acute myocardial infarction. Despite our efforts, sudden death remains the most common outcome of heart disease. It is estimated that at least a third of all heart attacks lead to sudden death, often the first expression of coronary heart disease. After resuscitation, patients often admit to symptoms they attributed to anything but a myocardial infarction.

Sudden death can occur as the first expression of coronary heart disease, in the setting of known coronary heart disease or in patients with advanced heart failure. Early evaluation, either by stress or by electrophysiologic testing or more sophisticated imaging with fast CT or MRI, can help in identifying patients at increased risk, but it provides little help in establishing timing of the mortality event.

It is likely that Mr. Russert's event occurred as a result of a plaque rupture and thrombus formation. The development of that plaque can be modified with statin therapy—although little is known about the effect of statins on sudden death.

Acceleration of plaque formation can occur with a variety of stimuli, including cigarette smoking, hypertension, and diabetes. The aggressive treatment of hypertension—a major step on the road to acute MI and heart failure—is critical. I am convinced that calcium entry blockers, particularly dihydropyridines, are the most effective treatment of hypertension. But since most patients with hypertension require more than one drug, β-blockers also are essential for preventing the long-term mortality and morbidity of hypertension, which include sudden death and heart failure. These drugs mitigate the adrenergic surge that occurs with an acute MI or ischemic stress. However, I admit that achieving adequate treatment of hypertension is one of the most difficult therapeutic challenges I face.

Sudden death as an expression of heart failure probably is related to a complex relation between interstitial fibrosis and increased circulating catecholamines leading to the development of micro reentry circuits that then degenerate into ventricular fibrillation. In patients with heart failure and those who have experienced a MI, β-blockers significantly decrease the risk of sudden death.

It is therefore distressing that in studies of implantable cardioverter defibrillators in heart failure, β-blockers are underutilized. Implantable cardioverter defibrillators do play an important role in the prevention of sudden death in heart failure, but as noted in previous columns, we still do not have a good understanding of which patients are best suited for ICD use.

Lastly, a comment about aspirin. Widely used in the general population, therapy with this ubiquitous drug has a paradoxical effect, as reported in the Physicians' Health Study (N. Engl. J. Med. 1989;321:129–35), by decreasing MI mortality but increasing sudden death. Guidance for aspirin therapy for primary prevention has been based in part on Framingham risk scores (N. Engl. J. Med. 2002;346:1468–74). In my opinion, aspirin has benefit in high-risk patients with ischemic heart disease and particularly in those patients who have experienced an acute coronary syndrome. But for primary prevention, the evidence is not very supportive for its use.

This leads us to the continued quandary posed by my cocktail party questioner. Unfortunately, it is almost impossible to predict the timing of sudden death, but we have been successful in decreasing the likelihood of experiencing an event in the unknown future. Its occurrence is a little like playing Russian roulette: Sometimes, the gun is loaded.

I am sure that many of you have been asked the same question that I have this summer. It typically occurred at a cocktail party, when a 50-something woman, upon learning that I am a cardiologist, sidled up and motioned toward a portly gentleman hovering over the appetizers. “That's my husband. He saw his doctor last week and was told that his blood pressure was a little high, but that he shouldn't worry. They'll check him again next year. What should he do to prevent a heart attack like Tim Russert's?”

Mr. Russert's untimely death sent shivers through millions of middle-aged men and their families. Here was a guy seemingly getting the best preventive care, yet he died from an acute myocardial infarction. Despite our efforts, sudden death remains the most common outcome of heart disease. It is estimated that at least a third of all heart attacks lead to sudden death, often the first expression of coronary heart disease. After resuscitation, patients often admit to symptoms they attributed to anything but a myocardial infarction.

Sudden death can occur as the first expression of coronary heart disease, in the setting of known coronary heart disease or in patients with advanced heart failure. Early evaluation, either by stress or by electrophysiologic testing or more sophisticated imaging with fast CT or MRI, can help in identifying patients at increased risk, but it provides little help in establishing timing of the mortality event.

It is likely that Mr. Russert's event occurred as a result of a plaque rupture and thrombus formation. The development of that plaque can be modified with statin therapy—although little is known about the effect of statins on sudden death.

Acceleration of plaque formation can occur with a variety of stimuli, including cigarette smoking, hypertension, and diabetes. The aggressive treatment of hypertension—a major step on the road to acute MI and heart failure—is critical. I am convinced that calcium entry blockers, particularly dihydropyridines, are the most effective treatment of hypertension. But since most patients with hypertension require more than one drug, β-blockers also are essential for preventing the long-term mortality and morbidity of hypertension, which include sudden death and heart failure. These drugs mitigate the adrenergic surge that occurs with an acute MI or ischemic stress. However, I admit that achieving adequate treatment of hypertension is one of the most difficult therapeutic challenges I face.

Sudden death as an expression of heart failure probably is related to a complex relation between interstitial fibrosis and increased circulating catecholamines leading to the development of micro reentry circuits that then degenerate into ventricular fibrillation. In patients with heart failure and those who have experienced a MI, β-blockers significantly decrease the risk of sudden death.

It is therefore distressing that in studies of implantable cardioverter defibrillators in heart failure, β-blockers are underutilized. Implantable cardioverter defibrillators do play an important role in the prevention of sudden death in heart failure, but as noted in previous columns, we still do not have a good understanding of which patients are best suited for ICD use.

Lastly, a comment about aspirin. Widely used in the general population, therapy with this ubiquitous drug has a paradoxical effect, as reported in the Physicians' Health Study (N. Engl. J. Med. 1989;321:129–35), by decreasing MI mortality but increasing sudden death. Guidance for aspirin therapy for primary prevention has been based in part on Framingham risk scores (N. Engl. J. Med. 2002;346:1468–74). In my opinion, aspirin has benefit in high-risk patients with ischemic heart disease and particularly in those patients who have experienced an acute coronary syndrome. But for primary prevention, the evidence is not very supportive for its use.

This leads us to the continued quandary posed by my cocktail party questioner. Unfortunately, it is almost impossible to predict the timing of sudden death, but we have been successful in decreasing the likelihood of experiencing an event in the unknown future. Its occurrence is a little like playing Russian roulette: Sometimes, the gun is loaded.

I am sure that many of you have been asked the same question that I have this summer. It typically occurred at a cocktail party, when a 50-something woman, upon learning that I am a cardiologist, sidled up and motioned toward a portly gentleman hovering over the appetizers. “That's my husband. He saw his doctor last week and was told that his blood pressure was a little high, but that he shouldn't worry. They'll check him again next year. What should he do to prevent a heart attack like Tim Russert's?”

Mr. Russert's untimely death sent shivers through millions of middle-aged men and their families. Here was a guy seemingly getting the best preventive care, yet he died from an acute myocardial infarction. Despite our efforts, sudden death remains the most common outcome of heart disease. It is estimated that at least a third of all heart attacks lead to sudden death, often the first expression of coronary heart disease. After resuscitation, patients often admit to symptoms they attributed to anything but a myocardial infarction.

Sudden death can occur as the first expression of coronary heart disease, in the setting of known coronary heart disease or in patients with advanced heart failure. Early evaluation, either by stress or by electrophysiologic testing or more sophisticated imaging with fast CT or MRI, can help in identifying patients at increased risk, but it provides little help in establishing timing of the mortality event.

It is likely that Mr. Russert's event occurred as a result of a plaque rupture and thrombus formation. The development of that plaque can be modified with statin therapy—although little is known about the effect of statins on sudden death.

Acceleration of plaque formation can occur with a variety of stimuli, including cigarette smoking, hypertension, and diabetes. The aggressive treatment of hypertension—a major step on the road to acute MI and heart failure—is critical. I am convinced that calcium entry blockers, particularly dihydropyridines, are the most effective treatment of hypertension. But since most patients with hypertension require more than one drug, β-blockers also are essential for preventing the long-term mortality and morbidity of hypertension, which include sudden death and heart failure. These drugs mitigate the adrenergic surge that occurs with an acute MI or ischemic stress. However, I admit that achieving adequate treatment of hypertension is one of the most difficult therapeutic challenges I face.

Sudden death as an expression of heart failure probably is related to a complex relation between interstitial fibrosis and increased circulating catecholamines leading to the development of micro reentry circuits that then degenerate into ventricular fibrillation. In patients with heart failure and those who have experienced a MI, β-blockers significantly decrease the risk of sudden death.

It is therefore distressing that in studies of implantable cardioverter defibrillators in heart failure, β-blockers are underutilized. Implantable cardioverter defibrillators do play an important role in the prevention of sudden death in heart failure, but as noted in previous columns, we still do not have a good understanding of which patients are best suited for ICD use.

Lastly, a comment about aspirin. Widely used in the general population, therapy with this ubiquitous drug has a paradoxical effect, as reported in the Physicians' Health Study (N. Engl. J. Med. 1989;321:129–35), by decreasing MI mortality but increasing sudden death. Guidance for aspirin therapy for primary prevention has been based in part on Framingham risk scores (N. Engl. J. Med. 2002;346:1468–74). In my opinion, aspirin has benefit in high-risk patients with ischemic heart disease and particularly in those patients who have experienced an acute coronary syndrome. But for primary prevention, the evidence is not very supportive for its use.

This leads us to the continued quandary posed by my cocktail party questioner. Unfortunately, it is almost impossible to predict the timing of sudden death, but we have been successful in decreasing the likelihood of experiencing an event in the unknown future. Its occurrence is a little like playing Russian roulette: Sometimes, the gun is loaded.

Treatment of acute coronary syndromes has come a long way since 1969, when Dr. Arthur Moss and I held a symposium at the University of Rochester titled “The Prehospital Phase of Acute Myocardial Infarction.” It was one of the first such events focused on the early pathophysiologic events and care of patients with symptoms of an acute myocardial infarction (Am. J. Card. 1969;24:609–11).

This meeting was held about 4 years after Prof. Desmond Julian in Edinburgh, Scotland, proposed the concept of a coronary care unit and a few years after Dr. Frank Partridge had organized the first mobile coronary care unit in Belfast, Northern Ireland, and Dr. Hughes Day established the first CCU in Bethany, Kan. These seminal efforts showed that patients with an acute MI were best cared for in the setting of a unit dedicated to the treatment of the pathophysiologic events associated with acute myocardial ischemia. Prior to the development of CCUs, patients with acute MIs were hospitalized in the general hospital ward without any special monitoring.

We became interested at that time in the prodromal symptoms leading up to the event and factors that lead to the decision to come to the hospital. We observed that approximately 3.5 hours elapsed from the onset of symptoms to hospital arrival (Circulation 1970;41:737–42). More than half of that time was taken up with the patient and or family making a decision to come to the hospital. It is more than likely that many patients who experienced an acute MI could have died in that time.

To deal with hospital delay, we among others urged for the first time that patients come promptly to the emergency department without consulting their physicians. This was a sharp departure from the standard of practice at that time. The rest, of course, is history. The floodgates were opened and the emergency departments (EDs) were deluged with the myriad of medical causes of chest pain, real and fancied. The emergency physicians were left to sort it all out.

Fast forward to the development of biomarkers, exercise technology, and imaging that developed from the need to define and identify the individual with an acute coronary event. Today there are approximately 8 million visits to the ED for chest pain and related symptoms. Of these, approximately 20% are defined as an acute coronary syndrome (ACS) event. Of the estimated 1.1 million myocardial infarctions annually in the United States, about half the patients survive and make it to the ED for care. Recent studies indicate that the diagnosis of acute myocardial infarction is missed in 2.1% of them (N. Engl. J. Med. 2000;342:1163–70). Similarly, 2.3% of patients seen in the ED for unstable angina are discharged and their diagnosis is missed. The risk-adjusted mortality rate in those patients in whom the diagnosis was missed is associated with an increased mortality risk.

In response to this deluge of patients coming to EDs, more than 1,500 chest pain units have been established, where patients can be monitored and evaluated outside of the hurly-burly atmosphere characteristic of EDs. These units were first established by the American College of Cardiovascular Administrators in 1991, which later merged into the Society of Chest Pain Centers and Providers (SCPCP). The organization is made up predominately of ED physicians and bridges the fields of emergency medicine, cardiology, and critical care nursing. Although often located within emergency facilities, they provide an atmosphere where patients can be evaluated using current diagnostic facilities at a cost less than that of the traditional CCU. They also expedite early therapy for patients with ACS by shortening door-to-needle time and by early administration of thrombolytic and pharmacologic therapy to minimize ischemia. The chest pain centers are now undergoing an accreditation process under the direction of the SCPCP.

To deal with this increased volume of patients coming to the ED for evaluation of chest pain, hospitals have modified facilities and procedures. The establishment of chest pain centers has provided a model of how chest pain patients can be expeditiously managed and treated in the face of increasing patient volume in an era of decreasing numbers of EDs nationwide.

Treatment of acute coronary syndromes has come a long way since 1969, when Dr. Arthur Moss and I held a symposium at the University of Rochester titled “The Prehospital Phase of Acute Myocardial Infarction.” It was one of the first such events focused on the early pathophysiologic events and care of patients with symptoms of an acute myocardial infarction (Am. J. Card. 1969;24:609–11).

This meeting was held about 4 years after Prof. Desmond Julian in Edinburgh, Scotland, proposed the concept of a coronary care unit and a few years after Dr. Frank Partridge had organized the first mobile coronary care unit in Belfast, Northern Ireland, and Dr. Hughes Day established the first CCU in Bethany, Kan. These seminal efforts showed that patients with an acute MI were best cared for in the setting of a unit dedicated to the treatment of the pathophysiologic events associated with acute myocardial ischemia. Prior to the development of CCUs, patients with acute MIs were hospitalized in the general hospital ward without any special monitoring.

We became interested at that time in the prodromal symptoms leading up to the event and factors that lead to the decision to come to the hospital. We observed that approximately 3.5 hours elapsed from the onset of symptoms to hospital arrival (Circulation 1970;41:737–42). More than half of that time was taken up with the patient and or family making a decision to come to the hospital. It is more than likely that many patients who experienced an acute MI could have died in that time.

To deal with hospital delay, we among others urged for the first time that patients come promptly to the emergency department without consulting their physicians. This was a sharp departure from the standard of practice at that time. The rest, of course, is history. The floodgates were opened and the emergency departments (EDs) were deluged with the myriad of medical causes of chest pain, real and fancied. The emergency physicians were left to sort it all out.

Fast forward to the development of biomarkers, exercise technology, and imaging that developed from the need to define and identify the individual with an acute coronary event. Today there are approximately 8 million visits to the ED for chest pain and related symptoms. Of these, approximately 20% are defined as an acute coronary syndrome (ACS) event. Of the estimated 1.1 million myocardial infarctions annually in the United States, about half the patients survive and make it to the ED for care. Recent studies indicate that the diagnosis of acute myocardial infarction is missed in 2.1% of them (N. Engl. J. Med. 2000;342:1163–70). Similarly, 2.3% of patients seen in the ED for unstable angina are discharged and their diagnosis is missed. The risk-adjusted mortality rate in those patients in whom the diagnosis was missed is associated with an increased mortality risk.

In response to this deluge of patients coming to EDs, more than 1,500 chest pain units have been established, where patients can be monitored and evaluated outside of the hurly-burly atmosphere characteristic of EDs. These units were first established by the American College of Cardiovascular Administrators in 1991, which later merged into the Society of Chest Pain Centers and Providers (SCPCP). The organization is made up predominately of ED physicians and bridges the fields of emergency medicine, cardiology, and critical care nursing. Although often located within emergency facilities, they provide an atmosphere where patients can be evaluated using current diagnostic facilities at a cost less than that of the traditional CCU. They also expedite early therapy for patients with ACS by shortening door-to-needle time and by early administration of thrombolytic and pharmacologic therapy to minimize ischemia. The chest pain centers are now undergoing an accreditation process under the direction of the SCPCP.

To deal with this increased volume of patients coming to the ED for evaluation of chest pain, hospitals have modified facilities and procedures. The establishment of chest pain centers has provided a model of how chest pain patients can be expeditiously managed and treated in the face of increasing patient volume in an era of decreasing numbers of EDs nationwide.

Treatment of acute coronary syndromes has come a long way since 1969, when Dr. Arthur Moss and I held a symposium at the University of Rochester titled “The Prehospital Phase of Acute Myocardial Infarction.” It was one of the first such events focused on the early pathophysiologic events and care of patients with symptoms of an acute myocardial infarction (Am. J. Card. 1969;24:609–11).

This meeting was held about 4 years after Prof. Desmond Julian in Edinburgh, Scotland, proposed the concept of a coronary care unit and a few years after Dr. Frank Partridge had organized the first mobile coronary care unit in Belfast, Northern Ireland, and Dr. Hughes Day established the first CCU in Bethany, Kan. These seminal efforts showed that patients with an acute MI were best cared for in the setting of a unit dedicated to the treatment of the pathophysiologic events associated with acute myocardial ischemia. Prior to the development of CCUs, patients with acute MIs were hospitalized in the general hospital ward without any special monitoring.

We became interested at that time in the prodromal symptoms leading up to the event and factors that lead to the decision to come to the hospital. We observed that approximately 3.5 hours elapsed from the onset of symptoms to hospital arrival (Circulation 1970;41:737–42). More than half of that time was taken up with the patient and or family making a decision to come to the hospital. It is more than likely that many patients who experienced an acute MI could have died in that time.

To deal with hospital delay, we among others urged for the first time that patients come promptly to the emergency department without consulting their physicians. This was a sharp departure from the standard of practice at that time. The rest, of course, is history. The floodgates were opened and the emergency departments (EDs) were deluged with the myriad of medical causes of chest pain, real and fancied. The emergency physicians were left to sort it all out.

Fast forward to the development of biomarkers, exercise technology, and imaging that developed from the need to define and identify the individual with an acute coronary event. Today there are approximately 8 million visits to the ED for chest pain and related symptoms. Of these, approximately 20% are defined as an acute coronary syndrome (ACS) event. Of the estimated 1.1 million myocardial infarctions annually in the United States, about half the patients survive and make it to the ED for care. Recent studies indicate that the diagnosis of acute myocardial infarction is missed in 2.1% of them (N. Engl. J. Med. 2000;342:1163–70). Similarly, 2.3% of patients seen in the ED for unstable angina are discharged and their diagnosis is missed. The risk-adjusted mortality rate in those patients in whom the diagnosis was missed is associated with an increased mortality risk.

In response to this deluge of patients coming to EDs, more than 1,500 chest pain units have been established, where patients can be monitored and evaluated outside of the hurly-burly atmosphere characteristic of EDs. These units were first established by the American College of Cardiovascular Administrators in 1991, which later merged into the Society of Chest Pain Centers and Providers (SCPCP). The organization is made up predominately of ED physicians and bridges the fields of emergency medicine, cardiology, and critical care nursing. Although often located within emergency facilities, they provide an atmosphere where patients can be evaluated using current diagnostic facilities at a cost less than that of the traditional CCU. They also expedite early therapy for patients with ACS by shortening door-to-needle time and by early administration of thrombolytic and pharmacologic therapy to minimize ischemia. The chest pain centers are now undergoing an accreditation process under the direction of the SCPCP.

To deal with this increased volume of patients coming to the ED for evaluation of chest pain, hospitals have modified facilities and procedures. The establishment of chest pain centers has provided a model of how chest pain patients can be expeditiously managed and treated in the face of increasing patient volume in an era of decreasing numbers of EDs nationwide.

Technology continues to challenge cardiologists' ability to distinguish between clinical benefit and financial reward. For the past half-century, we have been the beneficiaries of a seemingly limitless volume of patients that can support the investment in expensive technological research. At the same time, we have a blank check authority to pay for technology, regardless of clinical value, which would never be invested in rare diseases or even a more commonplace disease. As a result, we have at our disposal a variety of new technologies such as stents, defibrillators, and artificial hearts, often provided without a clear understanding of the clinical question to which they apply.

Now we are faced with the dilemma of how to include CT angiography (CTA) into the balance between what is clinically beneficial to the patient and the economics required to support the technology and the practicing cardiologist. The dazzling image of the coronary vessels, displayed by CTA in living color and in three dimensions, can be seen with a click of the mouse on anyone visiting the New York Times Web site. Wouldn't you want to have a 3D picture of your heart, particularly if it could ensure your survival? You could even print it and hang it over your mantelpiece with a warm cozy fire to show your friends on a cold winter's night.

What does it really show us? As we moved the technology from 8 slices to 16, 32, and now 64, the pictures have become more and more elegant. But according to many experts in this technology, they will never become sensitive enough to give us the insight into the question of when and if we will have an occlusion of a specific coronary artery. And yet this is the message that is being conveyed to the general public. For the asymptomatic patient, it is being sold as a screening test. In the symptomatic and acute coronary syndromes patients, it is proposed as a noninvasive test to indicate the need for early intervention. There are few data to support either position. Nevertheless, many hospitals and physicians have invested more than a million dollars each for a scanner.

In an appropriateness study carried out by the American College of Cardiology Foundation, experts in the field found little to suggest that the CTA would provide any important information in regard to the occurrence of an acute coronary occlusion (J. Am. Coll. Cardiol. 2006;48:1475-97). In addition, it is becoming clear that there is considerable radiation risk to the patient. Some would suggest that this is not important in view of the age of the usual cardiac patient, although some physicians are suggesting annual or biannual CTA studies to evaluate “disease progression.”

Last December, the Centers for Medicare and Medicaid Services floated a proposal to cover CTA for acute coronary syndromes patients only if they were enrolled in a CMS trial. The intent was to gather data to understand the clinical benefit of the CTA in that clinical syndrome. The response was a storm of protests from the CTA practitioners and the ACC, whose CEO, Dr. Jack Lewin, said that this “noninvasive clinical tool … has been clinically proven to be effective in diagnosing coronary artery disease.” As a result, the CMS backed down and Medicare, as well as many private insurers, will now pay for CTA in the setting of symptomatic patients. However, the CMS will not pay for CTA in asymptomatic patients. So if you are feeling well and just want to entertain your friends, you will have to pay the $1,000 out of your own pocket.

It is not entirely clear whether the players in the battle for CTA coverage actually are interested in collecting data that would answer the clinical issue at hand. It is clear that many physicians believe in the value of this new technology. Nevertheless, the economics of CTA raise significant questions about the motivation of physicians advocating the test, which should be resolved with a clinical trial. In time, it is likely that someone will carry out a study that will confirm or negate the value of CTA. The tragedy is that with a CMS-directed trial, the data would be forthcoming much sooner, before needless radiation risks to patients had occurred, and before a lot of money was spent on a test with questionable clinical import.

Technology continues to challenge cardiologists' ability to distinguish between clinical benefit and financial reward. For the past half-century, we have been the beneficiaries of a seemingly limitless volume of patients that can support the investment in expensive technological research. At the same time, we have a blank check authority to pay for technology, regardless of clinical value, which would never be invested in rare diseases or even a more commonplace disease. As a result, we have at our disposal a variety of new technologies such as stents, defibrillators, and artificial hearts, often provided without a clear understanding of the clinical question to which they apply.

Now we are faced with the dilemma of how to include CT angiography (CTA) into the balance between what is clinically beneficial to the patient and the economics required to support the technology and the practicing cardiologist. The dazzling image of the coronary vessels, displayed by CTA in living color and in three dimensions, can be seen with a click of the mouse on anyone visiting the New York Times Web site. Wouldn't you want to have a 3D picture of your heart, particularly if it could ensure your survival? You could even print it and hang it over your mantelpiece with a warm cozy fire to show your friends on a cold winter's night.

What does it really show us? As we moved the technology from 8 slices to 16, 32, and now 64, the pictures have become more and more elegant. But according to many experts in this technology, they will never become sensitive enough to give us the insight into the question of when and if we will have an occlusion of a specific coronary artery. And yet this is the message that is being conveyed to the general public. For the asymptomatic patient, it is being sold as a screening test. In the symptomatic and acute coronary syndromes patients, it is proposed as a noninvasive test to indicate the need for early intervention. There are few data to support either position. Nevertheless, many hospitals and physicians have invested more than a million dollars each for a scanner.

In an appropriateness study carried out by the American College of Cardiology Foundation, experts in the field found little to suggest that the CTA would provide any important information in regard to the occurrence of an acute coronary occlusion (J. Am. Coll. Cardiol. 2006;48:1475-97). In addition, it is becoming clear that there is considerable radiation risk to the patient. Some would suggest that this is not important in view of the age of the usual cardiac patient, although some physicians are suggesting annual or biannual CTA studies to evaluate “disease progression.”

Last December, the Centers for Medicare and Medicaid Services floated a proposal to cover CTA for acute coronary syndromes patients only if they were enrolled in a CMS trial. The intent was to gather data to understand the clinical benefit of the CTA in that clinical syndrome. The response was a storm of protests from the CTA practitioners and the ACC, whose CEO, Dr. Jack Lewin, said that this “noninvasive clinical tool … has been clinically proven to be effective in diagnosing coronary artery disease.” As a result, the CMS backed down and Medicare, as well as many private insurers, will now pay for CTA in the setting of symptomatic patients. However, the CMS will not pay for CTA in asymptomatic patients. So if you are feeling well and just want to entertain your friends, you will have to pay the $1,000 out of your own pocket.

It is not entirely clear whether the players in the battle for CTA coverage actually are interested in collecting data that would answer the clinical issue at hand. It is clear that many physicians believe in the value of this new technology. Nevertheless, the economics of CTA raise significant questions about the motivation of physicians advocating the test, which should be resolved with a clinical trial. In time, it is likely that someone will carry out a study that will confirm or negate the value of CTA. The tragedy is that with a CMS-directed trial, the data would be forthcoming much sooner, before needless radiation risks to patients had occurred, and before a lot of money was spent on a test with questionable clinical import.

Technology continues to challenge cardiologists' ability to distinguish between clinical benefit and financial reward. For the past half-century, we have been the beneficiaries of a seemingly limitless volume of patients that can support the investment in expensive technological research. At the same time, we have a blank check authority to pay for technology, regardless of clinical value, which would never be invested in rare diseases or even a more commonplace disease. As a result, we have at our disposal a variety of new technologies such as stents, defibrillators, and artificial hearts, often provided without a clear understanding of the clinical question to which they apply.

Now we are faced with the dilemma of how to include CT angiography (CTA) into the balance between what is clinically beneficial to the patient and the economics required to support the technology and the practicing cardiologist. The dazzling image of the coronary vessels, displayed by CTA in living color and in three dimensions, can be seen with a click of the mouse on anyone visiting the New York Times Web site. Wouldn't you want to have a 3D picture of your heart, particularly if it could ensure your survival? You could even print it and hang it over your mantelpiece with a warm cozy fire to show your friends on a cold winter's night.

What does it really show us? As we moved the technology from 8 slices to 16, 32, and now 64, the pictures have become more and more elegant. But according to many experts in this technology, they will never become sensitive enough to give us the insight into the question of when and if we will have an occlusion of a specific coronary artery. And yet this is the message that is being conveyed to the general public. For the asymptomatic patient, it is being sold as a screening test. In the symptomatic and acute coronary syndromes patients, it is proposed as a noninvasive test to indicate the need for early intervention. There are few data to support either position. Nevertheless, many hospitals and physicians have invested more than a million dollars each for a scanner.

In an appropriateness study carried out by the American College of Cardiology Foundation, experts in the field found little to suggest that the CTA would provide any important information in regard to the occurrence of an acute coronary occlusion (J. Am. Coll. Cardiol. 2006;48:1475-97). In addition, it is becoming clear that there is considerable radiation risk to the patient. Some would suggest that this is not important in view of the age of the usual cardiac patient, although some physicians are suggesting annual or biannual CTA studies to evaluate “disease progression.”

Last December, the Centers for Medicare and Medicaid Services floated a proposal to cover CTA for acute coronary syndromes patients only if they were enrolled in a CMS trial. The intent was to gather data to understand the clinical benefit of the CTA in that clinical syndrome. The response was a storm of protests from the CTA practitioners and the ACC, whose CEO, Dr. Jack Lewin, said that this “noninvasive clinical tool … has been clinically proven to be effective in diagnosing coronary artery disease.” As a result, the CMS backed down and Medicare, as well as many private insurers, will now pay for CTA in the setting of symptomatic patients. However, the CMS will not pay for CTA in asymptomatic patients. So if you are feeling well and just want to entertain your friends, you will have to pay the $1,000 out of your own pocket.

It is not entirely clear whether the players in the battle for CTA coverage actually are interested in collecting data that would answer the clinical issue at hand. It is clear that many physicians believe in the value of this new technology. Nevertheless, the economics of CTA raise significant questions about the motivation of physicians advocating the test, which should be resolved with a clinical trial. In time, it is likely that someone will carry out a study that will confirm or negate the value of CTA. The tragedy is that with a CMS-directed trial, the data would be forthcoming much sooner, before needless radiation risks to patients had occurred, and before a lot of money was spent on a test with questionable clinical import.

The recently published Guidelines for Device-Based Therapy of Cardiac Rhythm Abnormalities do not recommend any major changes in the use of these new technologies, but do represent a watershed moment in cardiac therapy. The guidelines clearly emphasize the important role that these new devices play in cardiology therapeutics.

Implantable pacemakers are now recommended widely for the treatment of sinus bradycardia and sinus node dysfunction in proven and even suspected symptomatic bradycardia. In acquired atrioventricular block, pacemaker therapy remains the mainstay for the prevention of syncope and the treatment of cardiac failure. The technologic hurdles to achieve safe and effective pacing in a variety of clinical situations have in a large part been overcome. A new study, PACE-MI (Pacemaker and β-Blocker Therapy After Myocardial Infarction), sponsored by the National Heart, Lung, and Blood Institute, is attempting to expand the envelope of pacemaker therapy by testing the benefit of a pacemaker and β-blockers in post-MI patients who have primary or drug-induced bradycardia.

Biventricular pacing has become widely accepted for the treatment of heart failure in patients with QRS intervals more than 120 msec who remain symptomatic on standard therapy with or without an ICD. The only area of controversy is the ejection fraction threshold for defibrillator implantation in patients with an ejection fraction of 35% or 40%. Previous guidelines published in 2006 by the American College of Cardiology, the American Heart Association, and the European Society of Cardiology suggested an ejection fraction of less than 40% as the threshold, but the 2008 version by the ACC/AHA/HRS has chosen an ejection fraction of less than 35% as the threshold, on the basis of the two largest defibrillator trials (MADIT and SCD-HEFT).

Not covered in the guidelines is any concern about the safety of the defibrillators in use today. The lack of candor regarding the dangers of ICD implantation is surprising, particularly in light of the frequent occurrence of inappropriate shocks in patients receiving the device. In a recent report from the MADIT II trial (J. Am. Coll. Cardiol. 2008;51:1357) 11.5% of patients received an inappropriate shock during the 2-year follow-up period, and there was a greater than twofold increase in mortality among patients experiencing an inappropriate shock. It is not clear whether these patients are at greater risk because of the nature of their disease or that increased risk results from the inappropriate shock itself. The report indicated that patients who received an inappropriate shock had an increased frequency of atrial fibrillation; they were more commonly smokers and had a decreased use of β-blockers.

There is reason to be concerned that as ICDs become more widely used for the primary prevention of ventricular fibrillation, the number of inappropriate shocks will increase and the number of appropriate shocks will decrease. It appears that the heart rhythm doctors who write the guidelines are more intent on spreading the use of ICDs than on identifying those patients who need the device the most and in whom the device is safe.

We have not seen the end of the role of device technology in cardiology. On the drawing board and in clinical trials are devices that can potentiate myocardial contractility and remodel the molecular biology of the myocardium by providing subthreshold electrical stimulation. There are also implantable devices that stimulate the vagus nerve, which may be able to modify heart rate and blood pressure, improve myocardial function, and prevent ventricular fibrillation. Carotid sinus stimulation is also under study to lower heart rate and blood pressure in patients with heart failure. And somewhat farther afield, devices are now being tested to change and modify the shape of the dilated ventricle to improve contractility and limit ventricular remodeling.

All of these efforts are exciting and will pose important challenges to clinicians as they apply them to their patients. Unlike medical therapy, it is difficult if not impossible to stop therapy and remove the device once implanted. This raises the bar for ensuring safety before implantation.

The recently published Guidelines for Device-Based Therapy of Cardiac Rhythm Abnormalities do not recommend any major changes in the use of these new technologies, but do represent a watershed moment in cardiac therapy. The guidelines clearly emphasize the important role that these new devices play in cardiology therapeutics.

Implantable pacemakers are now recommended widely for the treatment of sinus bradycardia and sinus node dysfunction in proven and even suspected symptomatic bradycardia. In acquired atrioventricular block, pacemaker therapy remains the mainstay for the prevention of syncope and the treatment of cardiac failure. The technologic hurdles to achieve safe and effective pacing in a variety of clinical situations have in a large part been overcome. A new study, PACE-MI (Pacemaker and β-Blocker Therapy After Myocardial Infarction), sponsored by the National Heart, Lung, and Blood Institute, is attempting to expand the envelope of pacemaker therapy by testing the benefit of a pacemaker and β-blockers in post-MI patients who have primary or drug-induced bradycardia.

Biventricular pacing has become widely accepted for the treatment of heart failure in patients with QRS intervals more than 120 msec who remain symptomatic on standard therapy with or without an ICD. The only area of controversy is the ejection fraction threshold for defibrillator implantation in patients with an ejection fraction of 35% or 40%. Previous guidelines published in 2006 by the American College of Cardiology, the American Heart Association, and the European Society of Cardiology suggested an ejection fraction of less than 40% as the threshold, but the 2008 version by the ACC/AHA/HRS has chosen an ejection fraction of less than 35% as the threshold, on the basis of the two largest defibrillator trials (MADIT and SCD-HEFT).

Not covered in the guidelines is any concern about the safety of the defibrillators in use today. The lack of candor regarding the dangers of ICD implantation is surprising, particularly in light of the frequent occurrence of inappropriate shocks in patients receiving the device. In a recent report from the MADIT II trial (J. Am. Coll. Cardiol. 2008;51:1357) 11.5% of patients received an inappropriate shock during the 2-year follow-up period, and there was a greater than twofold increase in mortality among patients experiencing an inappropriate shock. It is not clear whether these patients are at greater risk because of the nature of their disease or that increased risk results from the inappropriate shock itself. The report indicated that patients who received an inappropriate shock had an increased frequency of atrial fibrillation; they were more commonly smokers and had a decreased use of β-blockers.

There is reason to be concerned that as ICDs become more widely used for the primary prevention of ventricular fibrillation, the number of inappropriate shocks will increase and the number of appropriate shocks will decrease. It appears that the heart rhythm doctors who write the guidelines are more intent on spreading the use of ICDs than on identifying those patients who need the device the most and in whom the device is safe.

We have not seen the end of the role of device technology in cardiology. On the drawing board and in clinical trials are devices that can potentiate myocardial contractility and remodel the molecular biology of the myocardium by providing subthreshold electrical stimulation. There are also implantable devices that stimulate the vagus nerve, which may be able to modify heart rate and blood pressure, improve myocardial function, and prevent ventricular fibrillation. Carotid sinus stimulation is also under study to lower heart rate and blood pressure in patients with heart failure. And somewhat farther afield, devices are now being tested to change and modify the shape of the dilated ventricle to improve contractility and limit ventricular remodeling.

All of these efforts are exciting and will pose important challenges to clinicians as they apply them to their patients. Unlike medical therapy, it is difficult if not impossible to stop therapy and remove the device once implanted. This raises the bar for ensuring safety before implantation.

The recently published Guidelines for Device-Based Therapy of Cardiac Rhythm Abnormalities do not recommend any major changes in the use of these new technologies, but do represent a watershed moment in cardiac therapy. The guidelines clearly emphasize the important role that these new devices play in cardiology therapeutics.

Implantable pacemakers are now recommended widely for the treatment of sinus bradycardia and sinus node dysfunction in proven and even suspected symptomatic bradycardia. In acquired atrioventricular block, pacemaker therapy remains the mainstay for the prevention of syncope and the treatment of cardiac failure. The technologic hurdles to achieve safe and effective pacing in a variety of clinical situations have in a large part been overcome. A new study, PACE-MI (Pacemaker and β-Blocker Therapy After Myocardial Infarction), sponsored by the National Heart, Lung, and Blood Institute, is attempting to expand the envelope of pacemaker therapy by testing the benefit of a pacemaker and β-blockers in post-MI patients who have primary or drug-induced bradycardia.

Biventricular pacing has become widely accepted for the treatment of heart failure in patients with QRS intervals more than 120 msec who remain symptomatic on standard therapy with or without an ICD. The only area of controversy is the ejection fraction threshold for defibrillator implantation in patients with an ejection fraction of 35% or 40%. Previous guidelines published in 2006 by the American College of Cardiology, the American Heart Association, and the European Society of Cardiology suggested an ejection fraction of less than 40% as the threshold, but the 2008 version by the ACC/AHA/HRS has chosen an ejection fraction of less than 35% as the threshold, on the basis of the two largest defibrillator trials (MADIT and SCD-HEFT).

Not covered in the guidelines is any concern about the safety of the defibrillators in use today. The lack of candor regarding the dangers of ICD implantation is surprising, particularly in light of the frequent occurrence of inappropriate shocks in patients receiving the device. In a recent report from the MADIT II trial (J. Am. Coll. Cardiol. 2008;51:1357) 11.5% of patients received an inappropriate shock during the 2-year follow-up period, and there was a greater than twofold increase in mortality among patients experiencing an inappropriate shock. It is not clear whether these patients are at greater risk because of the nature of their disease or that increased risk results from the inappropriate shock itself. The report indicated that patients who received an inappropriate shock had an increased frequency of atrial fibrillation; they were more commonly smokers and had a decreased use of β-blockers.

There is reason to be concerned that as ICDs become more widely used for the primary prevention of ventricular fibrillation, the number of inappropriate shocks will increase and the number of appropriate shocks will decrease. It appears that the heart rhythm doctors who write the guidelines are more intent on spreading the use of ICDs than on identifying those patients who need the device the most and in whom the device is safe.

We have not seen the end of the role of device technology in cardiology. On the drawing board and in clinical trials are devices that can potentiate myocardial contractility and remodel the molecular biology of the myocardium by providing subthreshold electrical stimulation. There are also implantable devices that stimulate the vagus nerve, which may be able to modify heart rate and blood pressure, improve myocardial function, and prevent ventricular fibrillation. Carotid sinus stimulation is also under study to lower heart rate and blood pressure in patients with heart failure. And somewhat farther afield, devices are now being tested to change and modify the shape of the dilated ventricle to improve contractility and limit ventricular remodeling.

All of these efforts are exciting and will pose important challenges to clinicians as they apply them to their patients. Unlike medical therapy, it is difficult if not impossible to stop therapy and remove the device once implanted. This raises the bar for ensuring safety before implantation.

The National Heart Institute was created in 1948 by President Harry Truman and was funded by Congress in 1951 with an authorization of $16 million dollars. It subsequently became part of the National Institutes of Health (NIH) and was later integrated into the National Heart, Lung, and Blood Institute (NHLBI) in 1972. Since its inception, it has experienced considerable growth. In 2006, its budget was slightly less than $3 billion dollars, with approximately $2.5 billion going to research and most of the remainder to training grants. Of this total, about $1.6 billion supports heart and vascular disease research. The expenditure for medical research by Congress at the NIH and the NHLBI far exceeds that of any other nation and in a large part explains the leadership that the United States has shown in the last half century.

Much of the research carried out in our medical schools and research institutions depends upon NIH support. During the later part of the 20th century, the funding increased greatly. Between 1998 and 2003, support for the NHLBI doubled, resulting in a number of important initiatives including the human genome project, development of a variety of new diagnostic techniques directed toward our understanding of pharmacogenetics, and the development of personalized medical therapeutics. Since then, however, there has been a budgetary plateau resulting in little or no increase in federal funding for medical research in general and cardiac research in particular.

This plateau has had profound effects on the ability of the NIH to respond to new research requests and to continue to support ongoing research. The current budget proposed by the president for the NIH and the NHLBI reflects a continuation of this plateau research support. When taken in the context of continued inflation during the last 5 years, it represents a significant actual decrease in funding. There has been no lack of research proposals and requests, however. Although there has been a continuing increase in research applications (more than 3,500 in 2007), the number of approved research projects has decreased from a high of more than 35% in 2001 to approximately 27% in 2005. The “pay line” for research projects, which reflects the percentage of approved grants that are actually funded, which was as high as 35% in 2001, fell to less than 20% in 2005 and has continued to fall since then. This year, it is projected to be 14% for previous investigators and 19% for first-time investigators. The most profound effect will be on new investigators. Although given a slight preference over continuing grant requests, they will be facing even greater difficulty in obtaining support. This is certain to discourage young physicians from continuing research careers. The failure to rejuvenate our investigator pool will have far-ranging effects on future research productivity.

Over the last half century, much of industry-supported research has been built on research emanating from the basic laboratories in medical schools and research institutions largely supported by the NIH. This basic research has been the platform upon which new drugs and devices have been created. The knowledge gained from this research and its translation to the bedside has had a profound effect on the mortality of cardiac patients both in this country and around the world.

These budgetary issues may appear to have little relevance to the practicing cardiologists who are busy trying to balance their own books, but they represent important issues facing cardiology in the future. We have benefited immensely from the research productivity during the last half century. It has provided the impetus and support of much of what we do in our day-to-day clinical activities and has been translated into the standard of everyday care of our patients. The impact that this has had on our patients' health cannot be underestimated. It is essential that we continue to maintain our research efforts into the future. The underfunding of cardiovascular research at the national level represents a major barrier to the continuation of our success and places future generations at risk of experiencing heart disease.

The National Heart Institute was created in 1948 by President Harry Truman and was funded by Congress in 1951 with an authorization of $16 million dollars. It subsequently became part of the National Institutes of Health (NIH) and was later integrated into the National Heart, Lung, and Blood Institute (NHLBI) in 1972. Since its inception, it has experienced considerable growth. In 2006, its budget was slightly less than $3 billion dollars, with approximately $2.5 billion going to research and most of the remainder to training grants. Of this total, about $1.6 billion supports heart and vascular disease research. The expenditure for medical research by Congress at the NIH and the NHLBI far exceeds that of any other nation and in a large part explains the leadership that the United States has shown in the last half century.

Much of the research carried out in our medical schools and research institutions depends upon NIH support. During the later part of the 20th century, the funding increased greatly. Between 1998 and 2003, support for the NHLBI doubled, resulting in a number of important initiatives including the human genome project, development of a variety of new diagnostic techniques directed toward our understanding of pharmacogenetics, and the development of personalized medical therapeutics. Since then, however, there has been a budgetary plateau resulting in little or no increase in federal funding for medical research in general and cardiac research in particular.

This plateau has had profound effects on the ability of the NIH to respond to new research requests and to continue to support ongoing research. The current budget proposed by the president for the NIH and the NHLBI reflects a continuation of this plateau research support. When taken in the context of continued inflation during the last 5 years, it represents a significant actual decrease in funding. There has been no lack of research proposals and requests, however. Although there has been a continuing increase in research applications (more than 3,500 in 2007), the number of approved research projects has decreased from a high of more than 35% in 2001 to approximately 27% in 2005. The “pay line” for research projects, which reflects the percentage of approved grants that are actually funded, which was as high as 35% in 2001, fell to less than 20% in 2005 and has continued to fall since then. This year, it is projected to be 14% for previous investigators and 19% for first-time investigators. The most profound effect will be on new investigators. Although given a slight preference over continuing grant requests, they will be facing even greater difficulty in obtaining support. This is certain to discourage young physicians from continuing research careers. The failure to rejuvenate our investigator pool will have far-ranging effects on future research productivity.

Over the last half century, much of industry-supported research has been built on research emanating from the basic laboratories in medical schools and research institutions largely supported by the NIH. This basic research has been the platform upon which new drugs and devices have been created. The knowledge gained from this research and its translation to the bedside has had a profound effect on the mortality of cardiac patients both in this country and around the world.

These budgetary issues may appear to have little relevance to the practicing cardiologists who are busy trying to balance their own books, but they represent important issues facing cardiology in the future. We have benefited immensely from the research productivity during the last half century. It has provided the impetus and support of much of what we do in our day-to-day clinical activities and has been translated into the standard of everyday care of our patients. The impact that this has had on our patients' health cannot be underestimated. It is essential that we continue to maintain our research efforts into the future. The underfunding of cardiovascular research at the national level represents a major barrier to the continuation of our success and places future generations at risk of experiencing heart disease.

The National Heart Institute was created in 1948 by President Harry Truman and was funded by Congress in 1951 with an authorization of $16 million dollars. It subsequently became part of the National Institutes of Health (NIH) and was later integrated into the National Heart, Lung, and Blood Institute (NHLBI) in 1972. Since its inception, it has experienced considerable growth. In 2006, its budget was slightly less than $3 billion dollars, with approximately $2.5 billion going to research and most of the remainder to training grants. Of this total, about $1.6 billion supports heart and vascular disease research. The expenditure for medical research by Congress at the NIH and the NHLBI far exceeds that of any other nation and in a large part explains the leadership that the United States has shown in the last half century.

Much of the research carried out in our medical schools and research institutions depends upon NIH support. During the later part of the 20th century, the funding increased greatly. Between 1998 and 2003, support for the NHLBI doubled, resulting in a number of important initiatives including the human genome project, development of a variety of new diagnostic techniques directed toward our understanding of pharmacogenetics, and the development of personalized medical therapeutics. Since then, however, there has been a budgetary plateau resulting in little or no increase in federal funding for medical research in general and cardiac research in particular.

This plateau has had profound effects on the ability of the NIH to respond to new research requests and to continue to support ongoing research. The current budget proposed by the president for the NIH and the NHLBI reflects a continuation of this plateau research support. When taken in the context of continued inflation during the last 5 years, it represents a significant actual decrease in funding. There has been no lack of research proposals and requests, however. Although there has been a continuing increase in research applications (more than 3,500 in 2007), the number of approved research projects has decreased from a high of more than 35% in 2001 to approximately 27% in 2005. The “pay line” for research projects, which reflects the percentage of approved grants that are actually funded, which was as high as 35% in 2001, fell to less than 20% in 2005 and has continued to fall since then. This year, it is projected to be 14% for previous investigators and 19% for first-time investigators. The most profound effect will be on new investigators. Although given a slight preference over continuing grant requests, they will be facing even greater difficulty in obtaining support. This is certain to discourage young physicians from continuing research careers. The failure to rejuvenate our investigator pool will have far-ranging effects on future research productivity.

Over the last half century, much of industry-supported research has been built on research emanating from the basic laboratories in medical schools and research institutions largely supported by the NIH. This basic research has been the platform upon which new drugs and devices have been created. The knowledge gained from this research and its translation to the bedside has had a profound effect on the mortality of cardiac patients both in this country and around the world.

These budgetary issues may appear to have little relevance to the practicing cardiologists who are busy trying to balance their own books, but they represent important issues facing cardiology in the future. We have benefited immensely from the research productivity during the last half century. It has provided the impetus and support of much of what we do in our day-to-day clinical activities and has been translated into the standard of everyday care of our patients. The impact that this has had on our patients' health cannot be underestimated. It is essential that we continue to maintain our research efforts into the future. The underfunding of cardiovascular research at the national level represents a major barrier to the continuation of our success and places future generations at risk of experiencing heart disease.