Sidney Goldstein

The forces that control health expenditure are progressively and irrevocably moving in a direction that makes Medicare administrators increasingly uneasy.

The spread between planned growth and real growth in health care costs continues to expand, leading to the need to squeeze Medicare payments to doctors and hospitals. A starry-eyed Congress passed legislation a decade ago that proposed that payments to doctors and hospitals would level off and in fact decrease over time.

Through the sustainable growth rate established in the law, the spending limits would be controlled by the rate of overall economic growth. Instead, even with the small increases in physician fees that have occurred in the last decade, the Medicare expenditures have far exceeded the proposed doctors' payments. At the same time, the development of new technology and devices has led to large increases in hospital costs.

The most recent attempts at limiting hospital expenditures proposed draconian cuts in payments to hospitals for a number of cardiac procedures, including implantation of implantable cardioverter defibrillators and coronary drug-eluting stents of 24% and 33%, respectively. But, as reported in this issue of CARDIOLOGY NEWS, (“Inpatient Cuts Far Less Severe Under Final CMS Rule,” p. 1) these cuts have been pulled back, awaiting a new payment system that will be based on hospital costs rather charges.

In the planning phase is a hospital payments system, in which the current diagnosis-related groups (DRGs) will be adjusted to patient characteristics and disease severity, rather than the current system where payments are the same regardless of severity and are based upon diagnosis alone.

This payment system may eventually make reimbursements more equitable for the general hospital and specialty hospitals, since those specialty centers appear to have more stable and less severely ill patients.

The proposed changes are not intended to decrease the $125 billion paid out by Medicare to 5,000 hospitals annually, but to redistribute those payments. The initiation of the new DRG is expected in the next year. The delay in the implementation of the programs has been a result of intense lobbying by device and hospital representatives who have a large stake in this issue. Payment schedules initiated by Medicare will have a significant influence on private insurers and Medicaid.

The other issue is the continuing battle over physician payments. The current proposal by CMS is to decrease physician fees by 5.1% (“Medicare Proposes 5.1% Physician Pay Cut in 2007,” p. 6). This, in addition to other mandated cuts, will result in an approximately 7% decrease in payments to cardiologists. Many physicians indicate that they will not accept Medicare patients in the future. Cardiologists have little choice in the matter since most of our patients are well within the Medicare age span. We will have little option in this regard.

These reimbursement changes could have a widespread effect on the availability of health care to the Medicare patients if physicians continue to limit the number of Medicare patients they treat in their practice.

In addition, the changes in hospital costs could have a major effect on the viability of many hospitals, large and small alike, and increase the competition among hospitals. The largesse of the cardiology profit center in the general hospital is spread across many other specialties that could also suffer.

Cardiology centers have also promoted growth of many community hospitals. Witness the media-advertising blitzes of many hospitals to attract cardiology patients. All of this could change if the Medicare redistribution of payments is actually carried out. The changes will face major opposition by the hospital and device industry before they can be implemented.

The forces that control health expenditure are progressively and irrevocably moving in a direction that makes Medicare administrators increasingly uneasy.

The spread between planned growth and real growth in health care costs continues to expand, leading to the need to squeeze Medicare payments to doctors and hospitals. A starry-eyed Congress passed legislation a decade ago that proposed that payments to doctors and hospitals would level off and in fact decrease over time.

Through the sustainable growth rate established in the law, the spending limits would be controlled by the rate of overall economic growth. Instead, even with the small increases in physician fees that have occurred in the last decade, the Medicare expenditures have far exceeded the proposed doctors' payments. At the same time, the development of new technology and devices has led to large increases in hospital costs.

The most recent attempts at limiting hospital expenditures proposed draconian cuts in payments to hospitals for a number of cardiac procedures, including implantation of implantable cardioverter defibrillators and coronary drug-eluting stents of 24% and 33%, respectively. But, as reported in this issue of CARDIOLOGY NEWS, (“Inpatient Cuts Far Less Severe Under Final CMS Rule,” p. 1) these cuts have been pulled back, awaiting a new payment system that will be based on hospital costs rather charges.

In the planning phase is a hospital payments system, in which the current diagnosis-related groups (DRGs) will be adjusted to patient characteristics and disease severity, rather than the current system where payments are the same regardless of severity and are based upon diagnosis alone.

This payment system may eventually make reimbursements more equitable for the general hospital and specialty hospitals, since those specialty centers appear to have more stable and less severely ill patients.

The proposed changes are not intended to decrease the $125 billion paid out by Medicare to 5,000 hospitals annually, but to redistribute those payments. The initiation of the new DRG is expected in the next year. The delay in the implementation of the programs has been a result of intense lobbying by device and hospital representatives who have a large stake in this issue. Payment schedules initiated by Medicare will have a significant influence on private insurers and Medicaid.

The other issue is the continuing battle over physician payments. The current proposal by CMS is to decrease physician fees by 5.1% (“Medicare Proposes 5.1% Physician Pay Cut in 2007,” p. 6). This, in addition to other mandated cuts, will result in an approximately 7% decrease in payments to cardiologists. Many physicians indicate that they will not accept Medicare patients in the future. Cardiologists have little choice in the matter since most of our patients are well within the Medicare age span. We will have little option in this regard.

These reimbursement changes could have a widespread effect on the availability of health care to the Medicare patients if physicians continue to limit the number of Medicare patients they treat in their practice.

In addition, the changes in hospital costs could have a major effect on the viability of many hospitals, large and small alike, and increase the competition among hospitals. The largesse of the cardiology profit center in the general hospital is spread across many other specialties that could also suffer.

Cardiology centers have also promoted growth of many community hospitals. Witness the media-advertising blitzes of many hospitals to attract cardiology patients. All of this could change if the Medicare redistribution of payments is actually carried out. The changes will face major opposition by the hospital and device industry before they can be implemented.

The forces that control health expenditure are progressively and irrevocably moving in a direction that makes Medicare administrators increasingly uneasy.

The spread between planned growth and real growth in health care costs continues to expand, leading to the need to squeeze Medicare payments to doctors and hospitals. A starry-eyed Congress passed legislation a decade ago that proposed that payments to doctors and hospitals would level off and in fact decrease over time.

Through the sustainable growth rate established in the law, the spending limits would be controlled by the rate of overall economic growth. Instead, even with the small increases in physician fees that have occurred in the last decade, the Medicare expenditures have far exceeded the proposed doctors' payments. At the same time, the development of new technology and devices has led to large increases in hospital costs.

The most recent attempts at limiting hospital expenditures proposed draconian cuts in payments to hospitals for a number of cardiac procedures, including implantation of implantable cardioverter defibrillators and coronary drug-eluting stents of 24% and 33%, respectively. But, as reported in this issue of CARDIOLOGY NEWS, (“Inpatient Cuts Far Less Severe Under Final CMS Rule,” p. 1) these cuts have been pulled back, awaiting a new payment system that will be based on hospital costs rather charges.

In the planning phase is a hospital payments system, in which the current diagnosis-related groups (DRGs) will be adjusted to patient characteristics and disease severity, rather than the current system where payments are the same regardless of severity and are based upon diagnosis alone.

This payment system may eventually make reimbursements more equitable for the general hospital and specialty hospitals, since those specialty centers appear to have more stable and less severely ill patients.

The proposed changes are not intended to decrease the $125 billion paid out by Medicare to 5,000 hospitals annually, but to redistribute those payments. The initiation of the new DRG is expected in the next year. The delay in the implementation of the programs has been a result of intense lobbying by device and hospital representatives who have a large stake in this issue. Payment schedules initiated by Medicare will have a significant influence on private insurers and Medicaid.

The other issue is the continuing battle over physician payments. The current proposal by CMS is to decrease physician fees by 5.1% (“Medicare Proposes 5.1% Physician Pay Cut in 2007,” p. 6). This, in addition to other mandated cuts, will result in an approximately 7% decrease in payments to cardiologists. Many physicians indicate that they will not accept Medicare patients in the future. Cardiologists have little choice in the matter since most of our patients are well within the Medicare age span. We will have little option in this regard.

These reimbursement changes could have a widespread effect on the availability of health care to the Medicare patients if physicians continue to limit the number of Medicare patients they treat in their practice.

In addition, the changes in hospital costs could have a major effect on the viability of many hospitals, large and small alike, and increase the competition among hospitals. The largesse of the cardiology profit center in the general hospital is spread across many other specialties that could also suffer.

Cardiology centers have also promoted growth of many community hospitals. Witness the media-advertising blitzes of many hospitals to attract cardiology patients. All of this could change if the Medicare redistribution of payments is actually carried out. The changes will face major opposition by the hospital and device industry before they can be implemented.

Those of you who have read this column over the last few years may recall that I have been spending my summers on my farm in the Hudson Valley of New York State. You also may recall that we are the custodians of a 220-year-old brick house built by my wife's ancestors just after the Revolutionary War. This place is a work in progress and has been lived in and maintained by seven previous generations. As luck would have it, it is now my turn. Well it has been an experience with a seemingly endless series of critical repairs and expensive interventions.

The most recent project was the repair of the brickwork on the house that apparently has been leaking. It never occurred to me that bricks could or would leak. This led to the first challenge to the environment. I hadn't appreciated that a number of important creatures lived in those cracks. So, with the sealing of the bricks and the rebuilding of two chimneys, the nesting place of the chimney swifts and bats were surgically removed. The chimney swifts got so disturbed that two of them flew down the chimney and out the fireplace and into the living room. I had to chase them around the living room with my grandson's butterfly net before catching them and returning them to outer space. The bats were likewise corralled when they mistakenly sought interior living. The result was that the bats and swifts disappeared in search of more hospitable living conditions and the mosquito population that had been held in check by these airborne traps gained the upper hand. We now must resort to citronella candles for survival in the evening when we sit on the porch.

The other change this summer has been the rain. Last year we lived through a drought, in fear that our well would run dry again, an experience that did not add to the hospitality afforded our overnight visitors from Detroit. This year we have had a deluge. It rained for almost 6 weeks and led to flooding to a degree short of Genesis. This year's guests were unable to leave because of the disruption in the roads and railroads, a possibility that we had never considered and found less than convenient.

The other disturbance in the equipoise relates to my friend Sam Phelps. You may remember him as my “crusty” octogenarian neighbor who refused an implantable defibrillator as prophylactic therapy for his heart failure. Sam is still doing pretty well and still turning out his weekly column for the Wallkill Valley Times.

But unfortunately, he suffered a stroke a few months ago, which left him almost blind. That has been a major disaster. He had been “trying to get out of here” ever since his wife died almost a decade ago. Now he is trying to figure out how to accelerate the process. His physical and emotional balance has been seriously impaired. He has a new dog though, Buffy, who gives him a lot of solace. She, too, has been going through some problems with equipoise. When I visited Sam last week, the dog was in “heat” and my friend had to watch over her to prevent an importunate visit from a male friend.

All of these events remind me of the critical point upon which our lives are balanced. It doesn't take much to change that balance for better or for worse.

Those of you who have read this column over the last few years may recall that I have been spending my summers on my farm in the Hudson Valley of New York State. You also may recall that we are the custodians of a 220-year-old brick house built by my wife's ancestors just after the Revolutionary War. This place is a work in progress and has been lived in and maintained by seven previous generations. As luck would have it, it is now my turn. Well it has been an experience with a seemingly endless series of critical repairs and expensive interventions.

The most recent project was the repair of the brickwork on the house that apparently has been leaking. It never occurred to me that bricks could or would leak. This led to the first challenge to the environment. I hadn't appreciated that a number of important creatures lived in those cracks. So, with the sealing of the bricks and the rebuilding of two chimneys, the nesting place of the chimney swifts and bats were surgically removed. The chimney swifts got so disturbed that two of them flew down the chimney and out the fireplace and into the living room. I had to chase them around the living room with my grandson's butterfly net before catching them and returning them to outer space. The bats were likewise corralled when they mistakenly sought interior living. The result was that the bats and swifts disappeared in search of more hospitable living conditions and the mosquito population that had been held in check by these airborne traps gained the upper hand. We now must resort to citronella candles for survival in the evening when we sit on the porch.

The other change this summer has been the rain. Last year we lived through a drought, in fear that our well would run dry again, an experience that did not add to the hospitality afforded our overnight visitors from Detroit. This year we have had a deluge. It rained for almost 6 weeks and led to flooding to a degree short of Genesis. This year's guests were unable to leave because of the disruption in the roads and railroads, a possibility that we had never considered and found less than convenient.

The other disturbance in the equipoise relates to my friend Sam Phelps. You may remember him as my “crusty” octogenarian neighbor who refused an implantable defibrillator as prophylactic therapy for his heart failure. Sam is still doing pretty well and still turning out his weekly column for the Wallkill Valley Times.

But unfortunately, he suffered a stroke a few months ago, which left him almost blind. That has been a major disaster. He had been “trying to get out of here” ever since his wife died almost a decade ago. Now he is trying to figure out how to accelerate the process. His physical and emotional balance has been seriously impaired. He has a new dog though, Buffy, who gives him a lot of solace. She, too, has been going through some problems with equipoise. When I visited Sam last week, the dog was in “heat” and my friend had to watch over her to prevent an importunate visit from a male friend.

All of these events remind me of the critical point upon which our lives are balanced. It doesn't take much to change that balance for better or for worse.

Those of you who have read this column over the last few years may recall that I have been spending my summers on my farm in the Hudson Valley of New York State. You also may recall that we are the custodians of a 220-year-old brick house built by my wife's ancestors just after the Revolutionary War. This place is a work in progress and has been lived in and maintained by seven previous generations. As luck would have it, it is now my turn. Well it has been an experience with a seemingly endless series of critical repairs and expensive interventions.

The most recent project was the repair of the brickwork on the house that apparently has been leaking. It never occurred to me that bricks could or would leak. This led to the first challenge to the environment. I hadn't appreciated that a number of important creatures lived in those cracks. So, with the sealing of the bricks and the rebuilding of two chimneys, the nesting place of the chimney swifts and bats were surgically removed. The chimney swifts got so disturbed that two of them flew down the chimney and out the fireplace and into the living room. I had to chase them around the living room with my grandson's butterfly net before catching them and returning them to outer space. The bats were likewise corralled when they mistakenly sought interior living. The result was that the bats and swifts disappeared in search of more hospitable living conditions and the mosquito population that had been held in check by these airborne traps gained the upper hand. We now must resort to citronella candles for survival in the evening when we sit on the porch.

The other change this summer has been the rain. Last year we lived through a drought, in fear that our well would run dry again, an experience that did not add to the hospitality afforded our overnight visitors from Detroit. This year we have had a deluge. It rained for almost 6 weeks and led to flooding to a degree short of Genesis. This year's guests were unable to leave because of the disruption in the roads and railroads, a possibility that we had never considered and found less than convenient.

The other disturbance in the equipoise relates to my friend Sam Phelps. You may remember him as my “crusty” octogenarian neighbor who refused an implantable defibrillator as prophylactic therapy for his heart failure. Sam is still doing pretty well and still turning out his weekly column for the Wallkill Valley Times.

But unfortunately, he suffered a stroke a few months ago, which left him almost blind. That has been a major disaster. He had been “trying to get out of here” ever since his wife died almost a decade ago. Now he is trying to figure out how to accelerate the process. His physical and emotional balance has been seriously impaired. He has a new dog though, Buffy, who gives him a lot of solace. She, too, has been going through some problems with equipoise. When I visited Sam last week, the dog was in “heat” and my friend had to watch over her to prevent an importunate visit from a male friend.

All of these events remind me of the critical point upon which our lives are balanced. It doesn't take much to change that balance for better or for worse.

In the last half-century, there have been major advances in the prevention of cardiovascular disease, and our success can be measured in the substantial decrease in mortality of myocardial infarction, stroke, and renal disease.

The decrease in the number of mortality events has occurred largely as a result of the introduction of drug therapy for hypertension. The original target of these efforts was directed at patients with severe hypertension, but over time, the target blood pressure has gradually been reduced.

In 1984, systolic hypertension was defined as blood pressure greater than 160 mm Hg. The most recent delineation by the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC 7), published in 2003, defines “normality” as a blood pressure of less than 120/80 mm Hg and pressures between 120/80 mm Hg and 140/90 mm Hg as “prehypertension.”

The introduction of the concept of prehypertension has opened up a large segment of our population for consideration for drug therapy. Although the concept has come under significant challenge, there is general agreement that, within that population, there are patients with concomitant disease such as diabetes and hypercholesterolemia who are at increased risk and who could benefit from medical therapy and lifestyle modification.

At the same time, we have become increasingly aggressive in our treatment of hypercholesterolemia. Current guidelines advise drug therapy for primary prevention in patients with fewer than two risk factors for LDL greater than 160 mg/dL and 100 mg/dL for secondary prevention in patients with established cardiovascular disease. The reality, however, is that many physicians advise primary prevention drug therapy for patients with LDL concentrations well below 160 mg/dL. There has been a significant “therapy creep” in regard to the initiation of drug therapy for primary prevention without any supporting clinic data.

The guidelines for therapy are based on randomized clinical trials in relatively high-risk patients carried out over relatively short time spans when considering the lifetime commitment to therapy that the prevention programs imply. The identification and treatment of prehypertension or hypercholesterolemia in a 20-year-old is a commitment to therapy for decades to come.

The impact of drugs on individuals exposed to lifetime therapy is unknown, and in fact, will probably never be ascertained. Attempts to extend mortality and morbidity observation beyond the temporal scope of clinical trials are still under consideration by the Food and Drug Administration.

The potential unforeseen risk of chronic therapy gained prominence with the rofecoxib (Vioxx) experience. The recent observation that therapy with ACE inhibitors for hypertension is associated with a significant increase in birth defects in children whose mothers were taking these drugs at the time of conception raises further concerns (N. Engl. J. Med. 2006;354:2443–51). Although the medical community has been aware of the potential hazard of this class of drugs in the second in third trimester of pregnancy, this information raises significant issues in young women of childbearing age. Other antihypertensive drugs appear to be safe, but with scant data to support a high degree of certainty.

The benefit of lifetime therapy for primary prevention in high-risk groups is supported by strong clinical research. However, as we lower our threshold for therapy, the benefit may be illusory and the potential for risk increased. The decision to treat our high-risk patients is relatively easy, but as we become increasingly aggressive about our therapeutic target and treat lower-risk patients, claims of the risk and benefits should be considered carefully.

In the last half-century, there have been major advances in the prevention of cardiovascular disease, and our success can be measured in the substantial decrease in mortality of myocardial infarction, stroke, and renal disease.

The decrease in the number of mortality events has occurred largely as a result of the introduction of drug therapy for hypertension. The original target of these efforts was directed at patients with severe hypertension, but over time, the target blood pressure has gradually been reduced.

In 1984, systolic hypertension was defined as blood pressure greater than 160 mm Hg. The most recent delineation by the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC 7), published in 2003, defines “normality” as a blood pressure of less than 120/80 mm Hg and pressures between 120/80 mm Hg and 140/90 mm Hg as “prehypertension.”

The introduction of the concept of prehypertension has opened up a large segment of our population for consideration for drug therapy. Although the concept has come under significant challenge, there is general agreement that, within that population, there are patients with concomitant disease such as diabetes and hypercholesterolemia who are at increased risk and who could benefit from medical therapy and lifestyle modification.

At the same time, we have become increasingly aggressive in our treatment of hypercholesterolemia. Current guidelines advise drug therapy for primary prevention in patients with fewer than two risk factors for LDL greater than 160 mg/dL and 100 mg/dL for secondary prevention in patients with established cardiovascular disease. The reality, however, is that many physicians advise primary prevention drug therapy for patients with LDL concentrations well below 160 mg/dL. There has been a significant “therapy creep” in regard to the initiation of drug therapy for primary prevention without any supporting clinic data.

The guidelines for therapy are based on randomized clinical trials in relatively high-risk patients carried out over relatively short time spans when considering the lifetime commitment to therapy that the prevention programs imply. The identification and treatment of prehypertension or hypercholesterolemia in a 20-year-old is a commitment to therapy for decades to come.

The impact of drugs on individuals exposed to lifetime therapy is unknown, and in fact, will probably never be ascertained. Attempts to extend mortality and morbidity observation beyond the temporal scope of clinical trials are still under consideration by the Food and Drug Administration.

The potential unforeseen risk of chronic therapy gained prominence with the rofecoxib (Vioxx) experience. The recent observation that therapy with ACE inhibitors for hypertension is associated with a significant increase in birth defects in children whose mothers were taking these drugs at the time of conception raises further concerns (N. Engl. J. Med. 2006;354:2443–51). Although the medical community has been aware of the potential hazard of this class of drugs in the second in third trimester of pregnancy, this information raises significant issues in young women of childbearing age. Other antihypertensive drugs appear to be safe, but with scant data to support a high degree of certainty.

The benefit of lifetime therapy for primary prevention in high-risk groups is supported by strong clinical research. However, as we lower our threshold for therapy, the benefit may be illusory and the potential for risk increased. The decision to treat our high-risk patients is relatively easy, but as we become increasingly aggressive about our therapeutic target and treat lower-risk patients, claims of the risk and benefits should be considered carefully.

In the last half-century, there have been major advances in the prevention of cardiovascular disease, and our success can be measured in the substantial decrease in mortality of myocardial infarction, stroke, and renal disease.

The decrease in the number of mortality events has occurred largely as a result of the introduction of drug therapy for hypertension. The original target of these efforts was directed at patients with severe hypertension, but over time, the target blood pressure has gradually been reduced.

In 1984, systolic hypertension was defined as blood pressure greater than 160 mm Hg. The most recent delineation by the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC 7), published in 2003, defines “normality” as a blood pressure of less than 120/80 mm Hg and pressures between 120/80 mm Hg and 140/90 mm Hg as “prehypertension.”

The introduction of the concept of prehypertension has opened up a large segment of our population for consideration for drug therapy. Although the concept has come under significant challenge, there is general agreement that, within that population, there are patients with concomitant disease such as diabetes and hypercholesterolemia who are at increased risk and who could benefit from medical therapy and lifestyle modification.

At the same time, we have become increasingly aggressive in our treatment of hypercholesterolemia. Current guidelines advise drug therapy for primary prevention in patients with fewer than two risk factors for LDL greater than 160 mg/dL and 100 mg/dL for secondary prevention in patients with established cardiovascular disease. The reality, however, is that many physicians advise primary prevention drug therapy for patients with LDL concentrations well below 160 mg/dL. There has been a significant “therapy creep” in regard to the initiation of drug therapy for primary prevention without any supporting clinic data.

The guidelines for therapy are based on randomized clinical trials in relatively high-risk patients carried out over relatively short time spans when considering the lifetime commitment to therapy that the prevention programs imply. The identification and treatment of prehypertension or hypercholesterolemia in a 20-year-old is a commitment to therapy for decades to come.

The impact of drugs on individuals exposed to lifetime therapy is unknown, and in fact, will probably never be ascertained. Attempts to extend mortality and morbidity observation beyond the temporal scope of clinical trials are still under consideration by the Food and Drug Administration.

The potential unforeseen risk of chronic therapy gained prominence with the rofecoxib (Vioxx) experience. The recent observation that therapy with ACE inhibitors for hypertension is associated with a significant increase in birth defects in children whose mothers were taking these drugs at the time of conception raises further concerns (N. Engl. J. Med. 2006;354:2443–51). Although the medical community has been aware of the potential hazard of this class of drugs in the second in third trimester of pregnancy, this information raises significant issues in young women of childbearing age. Other antihypertensive drugs appear to be safe, but with scant data to support a high degree of certainty.

The benefit of lifetime therapy for primary prevention in high-risk groups is supported by strong clinical research. However, as we lower our threshold for therapy, the benefit may be illusory and the potential for risk increased. The decision to treat our high-risk patients is relatively easy, but as we become increasingly aggressive about our therapeutic target and treat lower-risk patients, claims of the risk and benefits should be considered carefully.

In 1949, Sir Henry Cohen, Lord of Birkenhead, delivered an address to the Royal College of Surgeons in London on the surgical approaches to hypoglycemia and hyperinsulinism. In that address, while discussing the advisability of total pancreatectomy for the treatment of these disorders, the chair of medicine at the University of Liverpool stated, “the feasibility of an operation is not the best indication for its performance.”

While advice like that could be applied to many clinical initiatives that have been carried out in the last half century, a recent American College of Cardiology meeting presentation on the ablation of electrical pathways in the left atrium to prevent atrial fibrillation brought this quote to mind. Although ablation therapy is a long way from becoming a certainty, the attempts to prevent atrial fibrillation with this technique are currently quite the rage among electrophysiologists.

The trench warfare being carried out in the left atrium as we attempt to prevent atrial fibrillation has captured the imagination of the electrophysiology community. It is proposed that the scarred and “debulked” left atrium will be more likely to maintain normal sinus rhythm and will be a less fertile ground for thrombi formation. Whether either of these proposals can be proved remains to be seen.

Atrial fibrillation has become a clinical problem of increasing importance as our population ages. The risks associated with atrial fibrillation lie primarily as a source of systemic emboli, particularly to the brain. Although some patients may experience cardiac symptoms as a result of chronic atrial fibrillation, most patients tolerate it very well.

The Atrial Fibrillation Follow-Up Investigation of Rhythm Management (AFFIRM) study clearly showed that there was little to be gained in regard to morbidity and mortality with the establishment of normal sinus rhythm using antiarrhythmic drugs. The major test of efficacy of therapy in atrial fibrillation is the prevention of stroke.

Many patients are driven to ablation therapy to escape the requirement of long-term anticoagulant therapy with warfarin. Although this is a burden, and is associated to some degree with adverse bleeding, help is on the way.

It is likely that in the next few years that advances in pharmacogenetics of warfarin therapy will provide better insight into which patients will benefit from this treatment. In addition, there is likelihood that oral direct thrombin and factor Xa inhibitors will become available and should make anticoagulant therapy more manageable and safer. It also is important to emphasize that ablation therapy may not exclude the left atrium as a source of cerebral embolism.

It is reasonable to continue research in the ablation in patients who are truly symptomatic as a result of chronic atrial fibrillation. However, we should be cautious in offering ablation therapy as an alternative to warfarin anticoagulation at this time.

We are long way from presuming that this form of therapy will give long-term prevention of atrial fibrillation, and even if it does, the risks of stroke may well persist as a result of the of the scarring of the left atrium that occurs with the therapy.

In 1949, Sir Henry Cohen, Lord of Birkenhead, delivered an address to the Royal College of Surgeons in London on the surgical approaches to hypoglycemia and hyperinsulinism. In that address, while discussing the advisability of total pancreatectomy for the treatment of these disorders, the chair of medicine at the University of Liverpool stated, “the feasibility of an operation is not the best indication for its performance.”

While advice like that could be applied to many clinical initiatives that have been carried out in the last half century, a recent American College of Cardiology meeting presentation on the ablation of electrical pathways in the left atrium to prevent atrial fibrillation brought this quote to mind. Although ablation therapy is a long way from becoming a certainty, the attempts to prevent atrial fibrillation with this technique are currently quite the rage among electrophysiologists.

The trench warfare being carried out in the left atrium as we attempt to prevent atrial fibrillation has captured the imagination of the electrophysiology community. It is proposed that the scarred and “debulked” left atrium will be more likely to maintain normal sinus rhythm and will be a less fertile ground for thrombi formation. Whether either of these proposals can be proved remains to be seen.

Atrial fibrillation has become a clinical problem of increasing importance as our population ages. The risks associated with atrial fibrillation lie primarily as a source of systemic emboli, particularly to the brain. Although some patients may experience cardiac symptoms as a result of chronic atrial fibrillation, most patients tolerate it very well.

The Atrial Fibrillation Follow-Up Investigation of Rhythm Management (AFFIRM) study clearly showed that there was little to be gained in regard to morbidity and mortality with the establishment of normal sinus rhythm using antiarrhythmic drugs. The major test of efficacy of therapy in atrial fibrillation is the prevention of stroke.

Many patients are driven to ablation therapy to escape the requirement of long-term anticoagulant therapy with warfarin. Although this is a burden, and is associated to some degree with adverse bleeding, help is on the way.

It is likely that in the next few years that advances in pharmacogenetics of warfarin therapy will provide better insight into which patients will benefit from this treatment. In addition, there is likelihood that oral direct thrombin and factor Xa inhibitors will become available and should make anticoagulant therapy more manageable and safer. It also is important to emphasize that ablation therapy may not exclude the left atrium as a source of cerebral embolism.

It is reasonable to continue research in the ablation in patients who are truly symptomatic as a result of chronic atrial fibrillation. However, we should be cautious in offering ablation therapy as an alternative to warfarin anticoagulation at this time.

We are long way from presuming that this form of therapy will give long-term prevention of atrial fibrillation, and even if it does, the risks of stroke may well persist as a result of the of the scarring of the left atrium that occurs with the therapy.

In 1949, Sir Henry Cohen, Lord of Birkenhead, delivered an address to the Royal College of Surgeons in London on the surgical approaches to hypoglycemia and hyperinsulinism. In that address, while discussing the advisability of total pancreatectomy for the treatment of these disorders, the chair of medicine at the University of Liverpool stated, “the feasibility of an operation is not the best indication for its performance.”

While advice like that could be applied to many clinical initiatives that have been carried out in the last half century, a recent American College of Cardiology meeting presentation on the ablation of electrical pathways in the left atrium to prevent atrial fibrillation brought this quote to mind. Although ablation therapy is a long way from becoming a certainty, the attempts to prevent atrial fibrillation with this technique are currently quite the rage among electrophysiologists.

The trench warfare being carried out in the left atrium as we attempt to prevent atrial fibrillation has captured the imagination of the electrophysiology community. It is proposed that the scarred and “debulked” left atrium will be more likely to maintain normal sinus rhythm and will be a less fertile ground for thrombi formation. Whether either of these proposals can be proved remains to be seen.

Atrial fibrillation has become a clinical problem of increasing importance as our population ages. The risks associated with atrial fibrillation lie primarily as a source of systemic emboli, particularly to the brain. Although some patients may experience cardiac symptoms as a result of chronic atrial fibrillation, most patients tolerate it very well.

The Atrial Fibrillation Follow-Up Investigation of Rhythm Management (AFFIRM) study clearly showed that there was little to be gained in regard to morbidity and mortality with the establishment of normal sinus rhythm using antiarrhythmic drugs. The major test of efficacy of therapy in atrial fibrillation is the prevention of stroke.

Many patients are driven to ablation therapy to escape the requirement of long-term anticoagulant therapy with warfarin. Although this is a burden, and is associated to some degree with adverse bleeding, help is on the way.

It is likely that in the next few years that advances in pharmacogenetics of warfarin therapy will provide better insight into which patients will benefit from this treatment. In addition, there is likelihood that oral direct thrombin and factor Xa inhibitors will become available and should make anticoagulant therapy more manageable and safer. It also is important to emphasize that ablation therapy may not exclude the left atrium as a source of cerebral embolism.

It is reasonable to continue research in the ablation in patients who are truly symptomatic as a result of chronic atrial fibrillation. However, we should be cautious in offering ablation therapy as an alternative to warfarin anticoagulation at this time.

We are long way from presuming that this form of therapy will give long-term prevention of atrial fibrillation, and even if it does, the risks of stroke may well persist as a result of the of the scarring of the left atrium that occurs with the therapy.

The multitude of patients arriving in emergency departments with chest pain symptoms poses an almost unsolvable problem for triaging physicians. Identifying patients with bona fide ischemia, and differentiating them from patients with a pulmonary embolus or a dissecting aneurysm, is a recurring clinical dilemma.

The development of the 64-slice multidetector CT provides a new technology for the evaluation of emergency department patients with chest pain. It also may have an important role in ruling out many patients seen in the outpatient clinic with chest pain symptoms. In the emergency department, however, perplexing symptoms continue to burden staff with the need to conduct expensive and labor-intensive procedures to make certain that their patients will not be reassured, only to die in the parking lot. The need to prevent a disaster often leads to unnecessary hospitalization and can result in expensive testing and coronary angiography. Although acute coronary syndrome is in the forefront of the diagnostic possibilities facing the emergency physician, lurking in the background are the other two deadly diagnoses: pulmonary embolism and dissecting aneurysm. It may be comforting to think that with one test, we can deal with all three high-risk diagnostic possibilities.

It appears that “fast CT” goes a long way in confirming or ruling out these three entities. A number of important clinical studies are underway that compare CT with standard diagnostic techniques, including stress echocardiography, nuclear imaging, and coronary angiography. Results so far have been very encouraging, but we will need more clinical data to support these initial studies. The fast CT is relatively easy to perform, with few contraindications, although it does require dye injection and some considerable radiation. Regular sinus rhythm at a moderate heart rate is also a requirement. Currently, the cost of the procedure is in the $1,000-$1,500 range, which is comparable to costs for other cardiac tests.

The ideal candidates for CT imaging and the “triple rule-out” will be those patients with low probability of ischemic disease who have chest pain symptoms of uncertain cause. These patients may represent approximately a quarter of all patients seen in the emergency department with chest pain. Current CT technology will have marginal importance in patients with known coronary artery disease. For them, more definitive imaging will be needed to describe and evaluate anatomic abnormalities. The ability to measure definitive changes in coronary anatomy still requires further refinement in CT imaging. Future developments may overcome this limitation. Assessment of the functional importance of anatomic lesions also will depend on stress nuclear or echocardiography imaging.

CT has an important role in defining coronary anomalies, and it may provide easy access to the imaging of coronary stents and bypass grafts. However, for confirmation of the presence of noncritical coronary artery disease, pulmonary embolism, and dissecting aneurysm, fast CT may well be the diagnostic technique of choice that can provide the answer to the triple rule-out.

The multitude of patients arriving in emergency departments with chest pain symptoms poses an almost unsolvable problem for triaging physicians. Identifying patients with bona fide ischemia, and differentiating them from patients with a pulmonary embolus or a dissecting aneurysm, is a recurring clinical dilemma.

The development of the 64-slice multidetector CT provides a new technology for the evaluation of emergency department patients with chest pain. It also may have an important role in ruling out many patients seen in the outpatient clinic with chest pain symptoms. In the emergency department, however, perplexing symptoms continue to burden staff with the need to conduct expensive and labor-intensive procedures to make certain that their patients will not be reassured, only to die in the parking lot. The need to prevent a disaster often leads to unnecessary hospitalization and can result in expensive testing and coronary angiography. Although acute coronary syndrome is in the forefront of the diagnostic possibilities facing the emergency physician, lurking in the background are the other two deadly diagnoses: pulmonary embolism and dissecting aneurysm. It may be comforting to think that with one test, we can deal with all three high-risk diagnostic possibilities.

It appears that “fast CT” goes a long way in confirming or ruling out these three entities. A number of important clinical studies are underway that compare CT with standard diagnostic techniques, including stress echocardiography, nuclear imaging, and coronary angiography. Results so far have been very encouraging, but we will need more clinical data to support these initial studies. The fast CT is relatively easy to perform, with few contraindications, although it does require dye injection and some considerable radiation. Regular sinus rhythm at a moderate heart rate is also a requirement. Currently, the cost of the procedure is in the $1,000-$1,500 range, which is comparable to costs for other cardiac tests.

The ideal candidates for CT imaging and the “triple rule-out” will be those patients with low probability of ischemic disease who have chest pain symptoms of uncertain cause. These patients may represent approximately a quarter of all patients seen in the emergency department with chest pain. Current CT technology will have marginal importance in patients with known coronary artery disease. For them, more definitive imaging will be needed to describe and evaluate anatomic abnormalities. The ability to measure definitive changes in coronary anatomy still requires further refinement in CT imaging. Future developments may overcome this limitation. Assessment of the functional importance of anatomic lesions also will depend on stress nuclear or echocardiography imaging.

CT has an important role in defining coronary anomalies, and it may provide easy access to the imaging of coronary stents and bypass grafts. However, for confirmation of the presence of noncritical coronary artery disease, pulmonary embolism, and dissecting aneurysm, fast CT may well be the diagnostic technique of choice that can provide the answer to the triple rule-out.

The multitude of patients arriving in emergency departments with chest pain symptoms poses an almost unsolvable problem for triaging physicians. Identifying patients with bona fide ischemia, and differentiating them from patients with a pulmonary embolus or a dissecting aneurysm, is a recurring clinical dilemma.

The development of the 64-slice multidetector CT provides a new technology for the evaluation of emergency department patients with chest pain. It also may have an important role in ruling out many patients seen in the outpatient clinic with chest pain symptoms. In the emergency department, however, perplexing symptoms continue to burden staff with the need to conduct expensive and labor-intensive procedures to make certain that their patients will not be reassured, only to die in the parking lot. The need to prevent a disaster often leads to unnecessary hospitalization and can result in expensive testing and coronary angiography. Although acute coronary syndrome is in the forefront of the diagnostic possibilities facing the emergency physician, lurking in the background are the other two deadly diagnoses: pulmonary embolism and dissecting aneurysm. It may be comforting to think that with one test, we can deal with all three high-risk diagnostic possibilities.

It appears that “fast CT” goes a long way in confirming or ruling out these three entities. A number of important clinical studies are underway that compare CT with standard diagnostic techniques, including stress echocardiography, nuclear imaging, and coronary angiography. Results so far have been very encouraging, but we will need more clinical data to support these initial studies. The fast CT is relatively easy to perform, with few contraindications, although it does require dye injection and some considerable radiation. Regular sinus rhythm at a moderate heart rate is also a requirement. Currently, the cost of the procedure is in the $1,000-$1,500 range, which is comparable to costs for other cardiac tests.

The ideal candidates for CT imaging and the “triple rule-out” will be those patients with low probability of ischemic disease who have chest pain symptoms of uncertain cause. These patients may represent approximately a quarter of all patients seen in the emergency department with chest pain. Current CT technology will have marginal importance in patients with known coronary artery disease. For them, more definitive imaging will be needed to describe and evaluate anatomic abnormalities. The ability to measure definitive changes in coronary anatomy still requires further refinement in CT imaging. Future developments may overcome this limitation. Assessment of the functional importance of anatomic lesions also will depend on stress nuclear or echocardiography imaging.

CT has an important role in defining coronary anomalies, and it may provide easy access to the imaging of coronary stents and bypass grafts. However, for confirmation of the presence of noncritical coronary artery disease, pulmonary embolism, and dissecting aneurysm, fast CT may well be the diagnostic technique of choice that can provide the answer to the triple rule-out.

Recently I was told of rounding schedules in several teaching hospitals that urge physicians to shorten their patient and house-staff contact during rounds and, in some cases, to limit the time to 3–5 minutes per patient. That admonition made me look back on an era when teaching rounds were the foundation of medical education.

The presence at the bedside of the rounding physician, medical students, and house staff represented the integration and application of years of preclinical training to the patient lying before us. Our anxious presentations of the patient's history, our physical findings, and our impressions of the situation to the professor were indelible experiences.

The discussion of the patient's history and the demonstration of physical findings were the essence of that experience. All this was followed by an insightful discussion of the patient's pathophysiology and the treatment plan. It was nevertheless the apotheosis of medical teaching.

That, of course, was in a time when our therapeutic options were limited to a few now-discarded drugs. Much has changed in the interim, driven largely by economics and therapeutic advances.

There has also been the unquestionable need to modify the inhuman work hours of house officers now that we better understand that we often functioned inefficiently, out of sheer exhaustion. But then, the exigencies of care were few, and patients stayed in the hospital for weeks, in contrast to today's cost-driven admission and discharge process.

The hospital has become the center of emergent care that drives the never-ending thirst for bed access. And that drive eats up the time and energy of house officers, who struggle just to keep the assembly line moving. Admission and discharge orders are so telescoped that it is difficult to wedge a progress note into a chart. So it is no wonder that the house officers seek easy answers to complex medical questions, most of which are available on their personal digital assistants. There is a guideline for almost every disease, and if there isn't one, it will soon be written. In the end, all that is required is for house officers to take the laboratory data and plug it into the guideline, and out comes the diagnosis and treatment. If the guideline doesn't quite fit the patient, then one makes the patient fit the guideline. So why would you need any more than 3–5 minutes?

Unfortunately, the patient is eaten up in this process. It is no wonder that many seek additional support from holistic healers, who at least spend time dealing with their disease in totality. William Osler, the founder of modern day medicine, said, “The good physician treats the disease; the great physician treats the patient who has the disease.”

The issue in contemporary medical education is how to incorporate Osler's message into medical education. We cannot divorce ourselves from the daily realities of the health care pressures that we face in our hospitals and emergency wards. But we need somehow to reserve space and time for medical education to be brought back to a tradition that integrates the patients and their caregivers, and specifically, time during which the experienced teacher can impart some dimension of patient-centered wisdom to young doctors.

It will, however, take more than 3–5 minutes.

Recently I was told of rounding schedules in several teaching hospitals that urge physicians to shorten their patient and house-staff contact during rounds and, in some cases, to limit the time to 3–5 minutes per patient. That admonition made me look back on an era when teaching rounds were the foundation of medical education.

The presence at the bedside of the rounding physician, medical students, and house staff represented the integration and application of years of preclinical training to the patient lying before us. Our anxious presentations of the patient's history, our physical findings, and our impressions of the situation to the professor were indelible experiences.

The discussion of the patient's history and the demonstration of physical findings were the essence of that experience. All this was followed by an insightful discussion of the patient's pathophysiology and the treatment plan. It was nevertheless the apotheosis of medical teaching.

That, of course, was in a time when our therapeutic options were limited to a few now-discarded drugs. Much has changed in the interim, driven largely by economics and therapeutic advances.

There has also been the unquestionable need to modify the inhuman work hours of house officers now that we better understand that we often functioned inefficiently, out of sheer exhaustion. But then, the exigencies of care were few, and patients stayed in the hospital for weeks, in contrast to today's cost-driven admission and discharge process.

The hospital has become the center of emergent care that drives the never-ending thirst for bed access. And that drive eats up the time and energy of house officers, who struggle just to keep the assembly line moving. Admission and discharge orders are so telescoped that it is difficult to wedge a progress note into a chart. So it is no wonder that the house officers seek easy answers to complex medical questions, most of which are available on their personal digital assistants. There is a guideline for almost every disease, and if there isn't one, it will soon be written. In the end, all that is required is for house officers to take the laboratory data and plug it into the guideline, and out comes the diagnosis and treatment. If the guideline doesn't quite fit the patient, then one makes the patient fit the guideline. So why would you need any more than 3–5 minutes?

Unfortunately, the patient is eaten up in this process. It is no wonder that many seek additional support from holistic healers, who at least spend time dealing with their disease in totality. William Osler, the founder of modern day medicine, said, “The good physician treats the disease; the great physician treats the patient who has the disease.”

The issue in contemporary medical education is how to incorporate Osler's message into medical education. We cannot divorce ourselves from the daily realities of the health care pressures that we face in our hospitals and emergency wards. But we need somehow to reserve space and time for medical education to be brought back to a tradition that integrates the patients and their caregivers, and specifically, time during which the experienced teacher can impart some dimension of patient-centered wisdom to young doctors.

It will, however, take more than 3–5 minutes.

Recently I was told of rounding schedules in several teaching hospitals that urge physicians to shorten their patient and house-staff contact during rounds and, in some cases, to limit the time to 3–5 minutes per patient. That admonition made me look back on an era when teaching rounds were the foundation of medical education.

The presence at the bedside of the rounding physician, medical students, and house staff represented the integration and application of years of preclinical training to the patient lying before us. Our anxious presentations of the patient's history, our physical findings, and our impressions of the situation to the professor were indelible experiences.

The discussion of the patient's history and the demonstration of physical findings were the essence of that experience. All this was followed by an insightful discussion of the patient's pathophysiology and the treatment plan. It was nevertheless the apotheosis of medical teaching.

That, of course, was in a time when our therapeutic options were limited to a few now-discarded drugs. Much has changed in the interim, driven largely by economics and therapeutic advances.

There has also been the unquestionable need to modify the inhuman work hours of house officers now that we better understand that we often functioned inefficiently, out of sheer exhaustion. But then, the exigencies of care were few, and patients stayed in the hospital for weeks, in contrast to today's cost-driven admission and discharge process.

The hospital has become the center of emergent care that drives the never-ending thirst for bed access. And that drive eats up the time and energy of house officers, who struggle just to keep the assembly line moving. Admission and discharge orders are so telescoped that it is difficult to wedge a progress note into a chart. So it is no wonder that the house officers seek easy answers to complex medical questions, most of which are available on their personal digital assistants. There is a guideline for almost every disease, and if there isn't one, it will soon be written. In the end, all that is required is for house officers to take the laboratory data and plug it into the guideline, and out comes the diagnosis and treatment. If the guideline doesn't quite fit the patient, then one makes the patient fit the guideline. So why would you need any more than 3–5 minutes?

Unfortunately, the patient is eaten up in this process. It is no wonder that many seek additional support from holistic healers, who at least spend time dealing with their disease in totality. William Osler, the founder of modern day medicine, said, “The good physician treats the disease; the great physician treats the patient who has the disease.”

The issue in contemporary medical education is how to incorporate Osler's message into medical education. We cannot divorce ourselves from the daily realities of the health care pressures that we face in our hospitals and emergency wards. But we need somehow to reserve space and time for medical education to be brought back to a tradition that integrates the patients and their caregivers, and specifically, time during which the experienced teacher can impart some dimension of patient-centered wisdom to young doctors.

It will, however, take more than 3–5 minutes.

In the beginning, continuing medical education was the province of medical schools, supported in part by federal funds.

In the 1980s the pharmaceutical industry, later joined by the device industry, developed a series of blockbuster drugs and devices that had the potential to benefit large numbers of patients with cardiovascular diseases. In order to educate physicians about these new advances, CME programs appeared to be a natural vehicle. The federal government had long given up on its support of outreach programs, and academic medical centers saw industry support as a way to expand both postgraduate and house staff educational programs.

The pharmaceutical and device industries saw CME as a method for marketing their products to physicians in the hospital setting, while providing an educational service to the medical profession. There was a clear need to educate physicians in the use of new and effective drugs that were developed to treat hypertension, angina, and postmyocardial infarction patients. Drug and device manufacturers could use academics and investigators who had participated in clinical trials to carry the message of the trials to the physician. This proved to be a very effective way of translating the results of clinical trials to the bedside, and it led eventually to evidence-based medicine and clinical guidelines.

By wrapping their product information inside a bona fide, disease-centered scientific program, drug and device manufacturers could advance both the principles of good medicine and the use of their products. Using academic medical centers, industry could achieve legitimacy, and by carefully selecting members of “speakers' bureaus,” it could make sure that doctors, both familiar and sympathetic to its products, articulated its message.

The pharmaceutical and device industries now support almost the entire spectrum of CME, from house staff lunches to the conventions of our national medical organizations. Without their support, postgraduate medical education would collapse. Medical educators have not been naive to the mixed motives of industry. In the last decade, industry has established a variety of guidelines by which medical education programs are monitored and conducted. Many of the excesses have been largely corrected.

To some, the intimacy of industry with medical education is still uncomfortable, and to others it is considered unethical. Proposals in editorials (JAMA 2006;295:429) and reported in this newspaper have suggested several changes in the relationship of industry to CME. These include the nonparticipation of academic faculty in speakers' bureaus and the construction of educational pools funded by industry and administered by academic medical centers in which industry input would be barred.

It remains to be seen how far academia and industry will be willing to participate in these changes. There is little question of the tremendous need for CME in our rapidly changing medical world. There is clearly a lack of funds from any other source. It is also apparent that industry depends on an educated medical profession to sell its products. Everyone can benefit by creating an educational environment focused on science and free of marketing bias.

In the beginning, continuing medical education was the province of medical schools, supported in part by federal funds.

In the 1980s the pharmaceutical industry, later joined by the device industry, developed a series of blockbuster drugs and devices that had the potential to benefit large numbers of patients with cardiovascular diseases. In order to educate physicians about these new advances, CME programs appeared to be a natural vehicle. The federal government had long given up on its support of outreach programs, and academic medical centers saw industry support as a way to expand both postgraduate and house staff educational programs.

The pharmaceutical and device industries saw CME as a method for marketing their products to physicians in the hospital setting, while providing an educational service to the medical profession. There was a clear need to educate physicians in the use of new and effective drugs that were developed to treat hypertension, angina, and postmyocardial infarction patients. Drug and device manufacturers could use academics and investigators who had participated in clinical trials to carry the message of the trials to the physician. This proved to be a very effective way of translating the results of clinical trials to the bedside, and it led eventually to evidence-based medicine and clinical guidelines.

By wrapping their product information inside a bona fide, disease-centered scientific program, drug and device manufacturers could advance both the principles of good medicine and the use of their products. Using academic medical centers, industry could achieve legitimacy, and by carefully selecting members of “speakers' bureaus,” it could make sure that doctors, both familiar and sympathetic to its products, articulated its message.

The pharmaceutical and device industries now support almost the entire spectrum of CME, from house staff lunches to the conventions of our national medical organizations. Without their support, postgraduate medical education would collapse. Medical educators have not been naive to the mixed motives of industry. In the last decade, industry has established a variety of guidelines by which medical education programs are monitored and conducted. Many of the excesses have been largely corrected.

To some, the intimacy of industry with medical education is still uncomfortable, and to others it is considered unethical. Proposals in editorials (JAMA 2006;295:429) and reported in this newspaper have suggested several changes in the relationship of industry to CME. These include the nonparticipation of academic faculty in speakers' bureaus and the construction of educational pools funded by industry and administered by academic medical centers in which industry input would be barred.

It remains to be seen how far academia and industry will be willing to participate in these changes. There is little question of the tremendous need for CME in our rapidly changing medical world. There is clearly a lack of funds from any other source. It is also apparent that industry depends on an educated medical profession to sell its products. Everyone can benefit by creating an educational environment focused on science and free of marketing bias.

In the beginning, continuing medical education was the province of medical schools, supported in part by federal funds.

In the 1980s the pharmaceutical industry, later joined by the device industry, developed a series of blockbuster drugs and devices that had the potential to benefit large numbers of patients with cardiovascular diseases. In order to educate physicians about these new advances, CME programs appeared to be a natural vehicle. The federal government had long given up on its support of outreach programs, and academic medical centers saw industry support as a way to expand both postgraduate and house staff educational programs.

The pharmaceutical and device industries saw CME as a method for marketing their products to physicians in the hospital setting, while providing an educational service to the medical profession. There was a clear need to educate physicians in the use of new and effective drugs that were developed to treat hypertension, angina, and postmyocardial infarction patients. Drug and device manufacturers could use academics and investigators who had participated in clinical trials to carry the message of the trials to the physician. This proved to be a very effective way of translating the results of clinical trials to the bedside, and it led eventually to evidence-based medicine and clinical guidelines.

By wrapping their product information inside a bona fide, disease-centered scientific program, drug and device manufacturers could advance both the principles of good medicine and the use of their products. Using academic medical centers, industry could achieve legitimacy, and by carefully selecting members of “speakers' bureaus,” it could make sure that doctors, both familiar and sympathetic to its products, articulated its message.

The pharmaceutical and device industries now support almost the entire spectrum of CME, from house staff lunches to the conventions of our national medical organizations. Without their support, postgraduate medical education would collapse. Medical educators have not been naive to the mixed motives of industry. In the last decade, industry has established a variety of guidelines by which medical education programs are monitored and conducted. Many of the excesses have been largely corrected.

To some, the intimacy of industry with medical education is still uncomfortable, and to others it is considered unethical. Proposals in editorials (JAMA 2006;295:429) and reported in this newspaper have suggested several changes in the relationship of industry to CME. These include the nonparticipation of academic faculty in speakers' bureaus and the construction of educational pools funded by industry and administered by academic medical centers in which industry input would be barred.

It remains to be seen how far academia and industry will be willing to participate in these changes. There is little question of the tremendous need for CME in our rapidly changing medical world. There is clearly a lack of funds from any other source. It is also apparent that industry depends on an educated medical profession to sell its products. Everyone can benefit by creating an educational environment focused on science and free of marketing bias.

In the past 25 years, there has been an explosion of investment by the pharmaceutical and medical-device industries in basic and applied medical research, from $2 billion in 1980 to $39 billion in 2004.

This support has had a profound influence on academia. It has changed the atmosphere in academic research from one of altruism to one with an entrepreneurial edge, as evidenced by the burgeoning numbers of invention disclosures and new patent applications from academic institutions. It has resulted in a significant increase in commercialization of academic medical centers and their faculties. It has also led to a natural desire for a greater ownership of concepts and profits by both the physician investigator and the sponsoring institution. In clinical trials, the boundary between the patient and the physician as an investigator and the physician as an inventor and entrepreneur has become more complex—particularly when they are the same person or the same institution.

There has been a recent spate of publicity about the financial relationships between physicians, academic research institutions, and companies developing new drugs and devices. Charges and countercharges have been made suggesting inappropriate involvement by physicians and medical institutions in devices or drugs that could result in significant financial return to them.

What is involved here is not obvious unethical behavior but the appearance that such behavior is taking place. It is not unusual that a clinical investigator would seek external high-risk financial support in order to carry an idea forward. The investigator who has invested in the research project would like to profit from that investment should the project become successful. Medical institutions, knowledgeable about new concepts, wish to invest in their development.

The patient who is asked to participate in a clinical trial knows nothing about the financial strings attached to the research project he or she is enrolled in. The patient is told there is a reasonable possibility, but no certainty, that the study could benefit them. The contract that the patient and physician sign, articulated in the consent form, indicates that scientific equipoise exists between active therapy and conventional therapy. The patient is motivated by the possibility of personally benefiting from the new therapy or at least the belief that it might benefit future patients. It is a contract founded on personal benefit and altruism. The injection of a profit motive by either the physician or the institution has the potential to contaminate the entire consent process.

The high road is one in which the inventor or institution has no patient contact in a research project from which either might profit financially. Physician scientists who wish to have their ideas tested should delegate the study and the analysis to more objective researchers. Likewise, institutions that have invested in the product should not participate in the investigation, to avoid the possibility of influencing staff participation in the trial and recruitment of patients. Anything short of this opens the investigator and institution to criticism of bias.

In the past 25 years, there has been an explosion of investment by the pharmaceutical and medical-device industries in basic and applied medical research, from $2 billion in 1980 to $39 billion in 2004.

This support has had a profound influence on academia. It has changed the atmosphere in academic research from one of altruism to one with an entrepreneurial edge, as evidenced by the burgeoning numbers of invention disclosures and new patent applications from academic institutions. It has resulted in a significant increase in commercialization of academic medical centers and their faculties. It has also led to a natural desire for a greater ownership of concepts and profits by both the physician investigator and the sponsoring institution. In clinical trials, the boundary between the patient and the physician as an investigator and the physician as an inventor and entrepreneur has become more complex—particularly when they are the same person or the same institution.

There has been a recent spate of publicity about the financial relationships between physicians, academic research institutions, and companies developing new drugs and devices. Charges and countercharges have been made suggesting inappropriate involvement by physicians and medical institutions in devices or drugs that could result in significant financial return to them.

What is involved here is not obvious unethical behavior but the appearance that such behavior is taking place. It is not unusual that a clinical investigator would seek external high-risk financial support in order to carry an idea forward. The investigator who has invested in the research project would like to profit from that investment should the project become successful. Medical institutions, knowledgeable about new concepts, wish to invest in their development.

The patient who is asked to participate in a clinical trial knows nothing about the financial strings attached to the research project he or she is enrolled in. The patient is told there is a reasonable possibility, but no certainty, that the study could benefit them. The contract that the patient and physician sign, articulated in the consent form, indicates that scientific equipoise exists between active therapy and conventional therapy. The patient is motivated by the possibility of personally benefiting from the new therapy or at least the belief that it might benefit future patients. It is a contract founded on personal benefit and altruism. The injection of a profit motive by either the physician or the institution has the potential to contaminate the entire consent process.

The high road is one in which the inventor or institution has no patient contact in a research project from which either might profit financially. Physician scientists who wish to have their ideas tested should delegate the study and the analysis to more objective researchers. Likewise, institutions that have invested in the product should not participate in the investigation, to avoid the possibility of influencing staff participation in the trial and recruitment of patients. Anything short of this opens the investigator and institution to criticism of bias.

In the past 25 years, there has been an explosion of investment by the pharmaceutical and medical-device industries in basic and applied medical research, from $2 billion in 1980 to $39 billion in 2004.

This support has had a profound influence on academia. It has changed the atmosphere in academic research from one of altruism to one with an entrepreneurial edge, as evidenced by the burgeoning numbers of invention disclosures and new patent applications from academic institutions. It has resulted in a significant increase in commercialization of academic medical centers and their faculties. It has also led to a natural desire for a greater ownership of concepts and profits by both the physician investigator and the sponsoring institution. In clinical trials, the boundary between the patient and the physician as an investigator and the physician as an inventor and entrepreneur has become more complex—particularly when they are the same person or the same institution.

There has been a recent spate of publicity about the financial relationships between physicians, academic research institutions, and companies developing new drugs and devices. Charges and countercharges have been made suggesting inappropriate involvement by physicians and medical institutions in devices or drugs that could result in significant financial return to them.

What is involved here is not obvious unethical behavior but the appearance that such behavior is taking place. It is not unusual that a clinical investigator would seek external high-risk financial support in order to carry an idea forward. The investigator who has invested in the research project would like to profit from that investment should the project become successful. Medical institutions, knowledgeable about new concepts, wish to invest in their development.

The patient who is asked to participate in a clinical trial knows nothing about the financial strings attached to the research project he or she is enrolled in. The patient is told there is a reasonable possibility, but no certainty, that the study could benefit them. The contract that the patient and physician sign, articulated in the consent form, indicates that scientific equipoise exists between active therapy and conventional therapy. The patient is motivated by the possibility of personally benefiting from the new therapy or at least the belief that it might benefit future patients. It is a contract founded on personal benefit and altruism. The injection of a profit motive by either the physician or the institution has the potential to contaminate the entire consent process.

The high road is one in which the inventor or institution has no patient contact in a research project from which either might profit financially. Physician scientists who wish to have their ideas tested should delegate the study and the analysis to more objective researchers. Likewise, institutions that have invested in the product should not participate in the investigation, to avoid the possibility of influencing staff participation in the trial and recruitment of patients. Anything short of this opens the investigator and institution to criticism of bias.

America is facing a major shortage of nurses and doctors, with no real solution in sight. For more than a half a century, we have depended on the foreign health professionals to satisfy our domestic requirements. U.S. medical and nursing schools have failed to respond to this need.

According to data from the 2004 U.S. Physician Masterfile, more than 200,000 physicians, or 25% of those practicing in the United States, were trained outside this country. More than 60% of those were trained in low-income countries such as India, the Philippines, and Pakistan (N. Engl. J. Med. 2005;353:1810–8). Another 25,000 were U.S. citizens who received their medical training abroad.

Not until this year has there been any significant change in the number of students entering U.S. medical schools. Between 1971 and 1985, American medical school graduates increased from approximately 10,000 to 16,000 per year. Since 1985, the number of medical graduates has been flat.

Over the past 20 years, there has been a significant change in the makeup of medical school classes as the number of female graduates has increased and the number of male graduates has decreased. In 2004, there were just 1,000 fewer female graduates than male graduates. During the same period, there has been a gradual increase in both African American and Hispanic students.

According to a recent report from the Association of American Medical Colleges, this year, for the first time in almost two decades, there has been an increase of 2.1% in medical school enrollees, to more than 17,000 first-year medical students.

Even with this overall increase in enrollments, demand far outstrips supply. By failing to train enough American doctors for our needs, we are siphoning off foreign-trained doctors from developing countries, thus contributing to the lowering of public health standards in those countries.

As economics and immigration policies change, both here and around the world, we may not be able to rely on a continuing supply of doctors from abroad, especially considering that a shortfall of more than 200,000 doctors is projected by 2020.

The outlook for nursing is even worse. We continue to meet much of our need for nurses by recruiting from underdeveloped countries. However, this is an international problem. Recent legislation passed by Congress has made it easier for foreign-trained nurses to work in this country, which, as with the doctors, has aggravated the shortfall of nurses in their countries of origin. The number of nurses working in the United States has remained relatively flat over the last few years, at about 2 million, but there is a projected 50% increase over the next decade in the demand for nurses. As the nurse-patient ratios decrease by legislation, as they have in California, this short supply will be exacerbated. In addition, as our population ages, so will more nurses retire, placing further pressure on the shortage.

The Association of American Medical Colleges and the American Nurses Association should play a role in solving to these manpower issues, but there has been little evidence of their leadership at the national level. Practicing physicians have little recourse other than wringing their hands and wishing for help.

America is facing a major shortage of nurses and doctors, with no real solution in sight. For more than a half a century, we have depended on the foreign health professionals to satisfy our domestic requirements. U.S. medical and nursing schools have failed to respond to this need.

According to data from the 2004 U.S. Physician Masterfile, more than 200,000 physicians, or 25% of those practicing in the United States, were trained outside this country. More than 60% of those were trained in low-income countries such as India, the Philippines, and Pakistan (N. Engl. J. Med. 2005;353:1810–8). Another 25,000 were U.S. citizens who received their medical training abroad.

Not until this year has there been any significant change in the number of students entering U.S. medical schools. Between 1971 and 1985, American medical school graduates increased from approximately 10,000 to 16,000 per year. Since 1985, the number of medical graduates has been flat.

Over the past 20 years, there has been a significant change in the makeup of medical school classes as the number of female graduates has increased and the number of male graduates has decreased. In 2004, there were just 1,000 fewer female graduates than male graduates. During the same period, there has been a gradual increase in both African American and Hispanic students.

According to a recent report from the Association of American Medical Colleges, this year, for the first time in almost two decades, there has been an increase of 2.1% in medical school enrollees, to more than 17,000 first-year medical students.

Even with this overall increase in enrollments, demand far outstrips supply. By failing to train enough American doctors for our needs, we are siphoning off foreign-trained doctors from developing countries, thus contributing to the lowering of public health standards in those countries.

As economics and immigration policies change, both here and around the world, we may not be able to rely on a continuing supply of doctors from abroad, especially considering that a shortfall of more than 200,000 doctors is projected by 2020.

The outlook for nursing is even worse. We continue to meet much of our need for nurses by recruiting from underdeveloped countries. However, this is an international problem. Recent legislation passed by Congress has made it easier for foreign-trained nurses to work in this country, which, as with the doctors, has aggravated the shortfall of nurses in their countries of origin. The number of nurses working in the United States has remained relatively flat over the last few years, at about 2 million, but there is a projected 50% increase over the next decade in the demand for nurses. As the nurse-patient ratios decrease by legislation, as they have in California, this short supply will be exacerbated. In addition, as our population ages, so will more nurses retire, placing further pressure on the shortage.

The Association of American Medical Colleges and the American Nurses Association should play a role in solving to these manpower issues, but there has been little evidence of their leadership at the national level. Practicing physicians have little recourse other than wringing their hands and wishing for help.

America is facing a major shortage of nurses and doctors, with no real solution in sight. For more than a half a century, we have depended on the foreign health professionals to satisfy our domestic requirements. U.S. medical and nursing schools have failed to respond to this need.

According to data from the 2004 U.S. Physician Masterfile, more than 200,000 physicians, or 25% of those practicing in the United States, were trained outside this country. More than 60% of those were trained in low-income countries such as India, the Philippines, and Pakistan (N. Engl. J. Med. 2005;353:1810–8). Another 25,000 were U.S. citizens who received their medical training abroad.

Not until this year has there been any significant change in the number of students entering U.S. medical schools. Between 1971 and 1985, American medical school graduates increased from approximately 10,000 to 16,000 per year. Since 1985, the number of medical graduates has been flat.

Over the past 20 years, there has been a significant change in the makeup of medical school classes as the number of female graduates has increased and the number of male graduates has decreased. In 2004, there were just 1,000 fewer female graduates than male graduates. During the same period, there has been a gradual increase in both African American and Hispanic students.

According to a recent report from the Association of American Medical Colleges, this year, for the first time in almost two decades, there has been an increase of 2.1% in medical school enrollees, to more than 17,000 first-year medical students.

Even with this overall increase in enrollments, demand far outstrips supply. By failing to train enough American doctors for our needs, we are siphoning off foreign-trained doctors from developing countries, thus contributing to the lowering of public health standards in those countries.

As economics and immigration policies change, both here and around the world, we may not be able to rely on a continuing supply of doctors from abroad, especially considering that a shortfall of more than 200,000 doctors is projected by 2020.

The outlook for nursing is even worse. We continue to meet much of our need for nurses by recruiting from underdeveloped countries. However, this is an international problem. Recent legislation passed by Congress has made it easier for foreign-trained nurses to work in this country, which, as with the doctors, has aggravated the shortfall of nurses in their countries of origin. The number of nurses working in the United States has remained relatively flat over the last few years, at about 2 million, but there is a projected 50% increase over the next decade in the demand for nurses. As the nurse-patient ratios decrease by legislation, as they have in California, this short supply will be exacerbated. In addition, as our population ages, so will more nurses retire, placing further pressure on the shortage.

The Association of American Medical Colleges and the American Nurses Association should play a role in solving to these manpower issues, but there has been little evidence of their leadership at the national level. Practicing physicians have little recourse other than wringing their hands and wishing for help.

By all appearances, we have reached a plateau in our attack on heart disease, and the recent meeting of the American Heart Association in Dallas provided ample evidence of this.

Numerous presentations and clinical trials were reported at the meeting, and some are included in this issue of CARDIOLOGY NEWS. But the findings reported have not moved us very far forward. Clinical trials spanning a variety of targets failed to show any significant benefits. Much of what was reported compared one drug or device with another, with an eye to safety rather than showing any improvement in mortality or morbidity.

In many cases, investigators examined new stents and antithrombotic drugs, but provided no reason to deviate from current practice. Some studies suggested that one stent might be better than another, but were often conducted in differing patient populations, which modulated most of the observed benefits and negated the differences.

In the device area, a variety of new techniques directed at improving the marginal benefits of ablation therapy for atrial fibrillation were reported. Several studies focused on trying to identify those patients who benefit the most from biventricular pacing.

More surprisingly, the results of the Multicenter Automatic Defibrillator Implantation Trial II (MADIT II) indicated that heart failure mortality increased significantly after a single discharge of the defibrillator. These observations suggested that the MADIT II patients were trading sudden death for progressive heart failure. There was no ready explanation for these observations, which generated considerable discussion among attendees about the trade-off.

The results of two clinical trials with levosimendan, a calcium-sensitizing drug for heart failure that is available in Europe but not approved in the United States, were also reported. Although patients seemed to experience improvement in symptoms acutely, morbidity and mortality were not significantly improved. It seems that current heart failure therapy with intravenous inotropic drugs supports patients through the acute episode, only to expose them to repeat and progressive failure. The cost of this support is further myocardial damage. It is becoming clear that there is a need for drugs that will improve cardiac function without causing cell damage in the setting of acute heart failure, a syndrome that is drawing increasing interest from investigators.

In the area of lipid therapy, fenofibrate was studied in patients with type 2 diabetes. There was a significant decrease in nonfatal MIs, but also a nonsignificant increase in total mortality.

With some certainty, our major therapeutic tools have stood the test of examination during the last year, but they have not provided a window to any new therapies. It seems that we have lowered cardiac mortality to a level that might make it difficult to demonstrate drug benefit.

Perhaps these observations will become more pertinent to the future of cardiology as costs and reimbursements begin to play an even greater role in our decision making. It is possible that we may be pricing ourselves out of the market as the numbers in our uninsured population burgeon.

By all appearances, we have reached a plateau in our attack on heart disease, and the recent meeting of the American Heart Association in Dallas provided ample evidence of this.

Numerous presentations and clinical trials were reported at the meeting, and some are included in this issue of CARDIOLOGY NEWS. But the findings reported have not moved us very far forward. Clinical trials spanning a variety of targets failed to show any significant benefits. Much of what was reported compared one drug or device with another, with an eye to safety rather than showing any improvement in mortality or morbidity.

In many cases, investigators examined new stents and antithrombotic drugs, but provided no reason to deviate from current practice. Some studies suggested that one stent might be better than another, but were often conducted in differing patient populations, which modulated most of the observed benefits and negated the differences.

In the device area, a variety of new techniques directed at improving the marginal benefits of ablation therapy for atrial fibrillation were reported. Several studies focused on trying to identify those patients who benefit the most from biventricular pacing.

More surprisingly, the results of the Multicenter Automatic Defibrillator Implantation Trial II (MADIT II) indicated that heart failure mortality increased significantly after a single discharge of the defibrillator. These observations suggested that the MADIT II patients were trading sudden death for progressive heart failure. There was no ready explanation for these observations, which generated considerable discussion among attendees about the trade-off.

The results of two clinical trials with levosimendan, a calcium-sensitizing drug for heart failure that is available in Europe but not approved in the United States, were also reported. Although patients seemed to experience improvement in symptoms acutely, morbidity and mortality were not significantly improved. It seems that current heart failure therapy with intravenous inotropic drugs supports patients through the acute episode, only to expose them to repeat and progressive failure. The cost of this support is further myocardial damage. It is becoming clear that there is a need for drugs that will improve cardiac function without causing cell damage in the setting of acute heart failure, a syndrome that is drawing increasing interest from investigators.

In the area of lipid therapy, fenofibrate was studied in patients with type 2 diabetes. There was a significant decrease in nonfatal MIs, but also a nonsignificant increase in total mortality.

With some certainty, our major therapeutic tools have stood the test of examination during the last year, but they have not provided a window to any new therapies. It seems that we have lowered cardiac mortality to a level that might make it difficult to demonstrate drug benefit.

Perhaps these observations will become more pertinent to the future of cardiology as costs and reimbursements begin to play an even greater role in our decision making. It is possible that we may be pricing ourselves out of the market as the numbers in our uninsured population burgeon.

By all appearances, we have reached a plateau in our attack on heart disease, and the recent meeting of the American Heart Association in Dallas provided ample evidence of this.

Numerous presentations and clinical trials were reported at the meeting, and some are included in this issue of CARDIOLOGY NEWS. But the findings reported have not moved us very far forward. Clinical trials spanning a variety of targets failed to show any significant benefits. Much of what was reported compared one drug or device with another, with an eye to safety rather than showing any improvement in mortality or morbidity.

In many cases, investigators examined new stents and antithrombotic drugs, but provided no reason to deviate from current practice. Some studies suggested that one stent might be better than another, but were often conducted in differing patient populations, which modulated most of the observed benefits and negated the differences.

In the device area, a variety of new techniques directed at improving the marginal benefits of ablation therapy for atrial fibrillation were reported. Several studies focused on trying to identify those patients who benefit the most from biventricular pacing.

More surprisingly, the results of the Multicenter Automatic Defibrillator Implantation Trial II (MADIT II) indicated that heart failure mortality increased significantly after a single discharge of the defibrillator. These observations suggested that the MADIT II patients were trading sudden death for progressive heart failure. There was no ready explanation for these observations, which generated considerable discussion among attendees about the trade-off.

The results of two clinical trials with levosimendan, a calcium-sensitizing drug for heart failure that is available in Europe but not approved in the United States, were also reported. Although patients seemed to experience improvement in symptoms acutely, morbidity and mortality were not significantly improved. It seems that current heart failure therapy with intravenous inotropic drugs supports patients through the acute episode, only to expose them to repeat and progressive failure. The cost of this support is further myocardial damage. It is becoming clear that there is a need for drugs that will improve cardiac function without causing cell damage in the setting of acute heart failure, a syndrome that is drawing increasing interest from investigators.

In the area of lipid therapy, fenofibrate was studied in patients with type 2 diabetes. There was a significant decrease in nonfatal MIs, but also a nonsignificant increase in total mortality.

With some certainty, our major therapeutic tools have stood the test of examination during the last year, but they have not provided a window to any new therapies. It seems that we have lowered cardiac mortality to a level that might make it difficult to demonstrate drug benefit.

Perhaps these observations will become more pertinent to the future of cardiology as costs and reimbursements begin to play an even greater role in our decision making. It is possible that we may be pricing ourselves out of the market as the numbers in our uninsured population burgeon.