Heart of the Matter

After a few days in Chicago at the meeting of the American Heart Association one cannot help but be impressed by the dimension of research and the youth and vigor of the attendees. Hardly a gray hair was seen, and coming from a “gray head” like this, it was inspirational.

This year's president, Dr. Raymond J. Gibbons of the Mayo Clinic, Rochester, Minn., called attention to the fact that in spite of our success, there are many barriers to overcome in translating our success to patients worldwide. In this country, we face the fact that almost 46 million Americans have no health insurance and are essentially excluded from preventive cardiac care and the fruits of our research. Many of our patients, both urban and rural, might just as well be in Africa as to live around the corner from a major medical center like mine.

It became apparent during the meeting that our success has made it increasingly difficult to prove new, potentially beneficial treatments. A number of randomized clinical trials were presented, testing therapy in acute myocardial infarction where the reported annual placebo mortality was 4% over a 1-year period. Although mortality has gone down, the incidence of coronary artery disease has not.

The success of our combined reperfusion and remodeling therapy for acute myocardial infarction has reduced the event rates to levels that require huge populations or therapies with efficacy that exceeds anything that we have studied to date. The problem of recruiting large populations was reemphasized by Dr. Robert Califf, newly appointed head of the Duke Translational Medicine Institute in Durham, N.C., who noted that because of the poor participation of American cardiologists, most current randomized clinical trials are being carried out in Europe and Asia. Although the diseases of the heart are ubiquitous, therapeutic interventions tested in diverse social and clinical settings may not be applicable to Americans. We are, in fact, “outsourcing” our research.

The issues relating to drug eluting stents (DES) and bare metal stents were extensively discussed. It is clear that the decrease in in-stent restenosis attributed to DES has some significant disadvantages. But the failure of the DES to endothelialize appears to lead to inflammation and thrombus formation in and around the stent and confers in those patients a lifetime risk of in-stent thrombosis and dependency on a very expensive antiplatelet therapy. What emerged from these sessions was the imperative for new types of stents.

An additional cautionary note injected into the world of percutaneous coronary intervention was provided by the report of the Occluded Artery Trial, which shocked many angiographers. The investigators examined the benefit of PCI in persistent total occlusion from 3 to 28 days after an MI and were surprised to learn that there was no benefit associated with late PCI (see p. 1).

One additional study, the Alternans Before Cardioverter Defibrillator trial, may give some hope that we can begin to define patients who will gain the most benefit from implantable cardioverter defibrillators. Using microwave T-wave alternans and electrophysiologic studies in heart failure patients with ejection fractions of less than 40%, the investigators were able to identify patients who are at low risk and may not need an ICD (see p. 8). These diagnostic techniques provide the possibility that we may be able to make better choices for ICD therapy.

As always, awards were given to distinguished scientists involved in cardiovascular research. None was more deserving than Dr. William Kannel, the creator and driving force of the Framingham Heart Study, who is professor of medicine and public health at Boston University School of Medicine. Initiated almost half a century ago, the massive study created the scientific foundation upon which we have built much of today's clinical science. It is hard to imagine where cardiovascular research would be without that center and his leadership. It was a long overdue award to a true pioneer to whom the cardiology community and the world owe a great debt. Congratulations, Bill!

After a few days in Chicago at the meeting of the American Heart Association one cannot help but be impressed by the dimension of research and the youth and vigor of the attendees. Hardly a gray hair was seen, and coming from a “gray head” like this, it was inspirational.

This year's president, Dr. Raymond J. Gibbons of the Mayo Clinic, Rochester, Minn., called attention to the fact that in spite of our success, there are many barriers to overcome in translating our success to patients worldwide. In this country, we face the fact that almost 46 million Americans have no health insurance and are essentially excluded from preventive cardiac care and the fruits of our research. Many of our patients, both urban and rural, might just as well be in Africa as to live around the corner from a major medical center like mine.

It became apparent during the meeting that our success has made it increasingly difficult to prove new, potentially beneficial treatments. A number of randomized clinical trials were presented, testing therapy in acute myocardial infarction where the reported annual placebo mortality was 4% over a 1-year period. Although mortality has gone down, the incidence of coronary artery disease has not.

The success of our combined reperfusion and remodeling therapy for acute myocardial infarction has reduced the event rates to levels that require huge populations or therapies with efficacy that exceeds anything that we have studied to date. The problem of recruiting large populations was reemphasized by Dr. Robert Califf, newly appointed head of the Duke Translational Medicine Institute in Durham, N.C., who noted that because of the poor participation of American cardiologists, most current randomized clinical trials are being carried out in Europe and Asia. Although the diseases of the heart are ubiquitous, therapeutic interventions tested in diverse social and clinical settings may not be applicable to Americans. We are, in fact, “outsourcing” our research.

The issues relating to drug eluting stents (DES) and bare metal stents were extensively discussed. It is clear that the decrease in in-stent restenosis attributed to DES has some significant disadvantages. But the failure of the DES to endothelialize appears to lead to inflammation and thrombus formation in and around the stent and confers in those patients a lifetime risk of in-stent thrombosis and dependency on a very expensive antiplatelet therapy. What emerged from these sessions was the imperative for new types of stents.

An additional cautionary note injected into the world of percutaneous coronary intervention was provided by the report of the Occluded Artery Trial, which shocked many angiographers. The investigators examined the benefit of PCI in persistent total occlusion from 3 to 28 days after an MI and were surprised to learn that there was no benefit associated with late PCI (see p. 1).

One additional study, the Alternans Before Cardioverter Defibrillator trial, may give some hope that we can begin to define patients who will gain the most benefit from implantable cardioverter defibrillators. Using microwave T-wave alternans and electrophysiologic studies in heart failure patients with ejection fractions of less than 40%, the investigators were able to identify patients who are at low risk and may not need an ICD (see p. 8). These diagnostic techniques provide the possibility that we may be able to make better choices for ICD therapy.

As always, awards were given to distinguished scientists involved in cardiovascular research. None was more deserving than Dr. William Kannel, the creator and driving force of the Framingham Heart Study, who is professor of medicine and public health at Boston University School of Medicine. Initiated almost half a century ago, the massive study created the scientific foundation upon which we have built much of today's clinical science. It is hard to imagine where cardiovascular research would be without that center and his leadership. It was a long overdue award to a true pioneer to whom the cardiology community and the world owe a great debt. Congratulations, Bill!

After a few days in Chicago at the meeting of the American Heart Association one cannot help but be impressed by the dimension of research and the youth and vigor of the attendees. Hardly a gray hair was seen, and coming from a “gray head” like this, it was inspirational.

This year's president, Dr. Raymond J. Gibbons of the Mayo Clinic, Rochester, Minn., called attention to the fact that in spite of our success, there are many barriers to overcome in translating our success to patients worldwide. In this country, we face the fact that almost 46 million Americans have no health insurance and are essentially excluded from preventive cardiac care and the fruits of our research. Many of our patients, both urban and rural, might just as well be in Africa as to live around the corner from a major medical center like mine.

It became apparent during the meeting that our success has made it increasingly difficult to prove new, potentially beneficial treatments. A number of randomized clinical trials were presented, testing therapy in acute myocardial infarction where the reported annual placebo mortality was 4% over a 1-year period. Although mortality has gone down, the incidence of coronary artery disease has not.

The success of our combined reperfusion and remodeling therapy for acute myocardial infarction has reduced the event rates to levels that require huge populations or therapies with efficacy that exceeds anything that we have studied to date. The problem of recruiting large populations was reemphasized by Dr. Robert Califf, newly appointed head of the Duke Translational Medicine Institute in Durham, N.C., who noted that because of the poor participation of American cardiologists, most current randomized clinical trials are being carried out in Europe and Asia. Although the diseases of the heart are ubiquitous, therapeutic interventions tested in diverse social and clinical settings may not be applicable to Americans. We are, in fact, “outsourcing” our research.

The issues relating to drug eluting stents (DES) and bare metal stents were extensively discussed. It is clear that the decrease in in-stent restenosis attributed to DES has some significant disadvantages. But the failure of the DES to endothelialize appears to lead to inflammation and thrombus formation in and around the stent and confers in those patients a lifetime risk of in-stent thrombosis and dependency on a very expensive antiplatelet therapy. What emerged from these sessions was the imperative for new types of stents.

An additional cautionary note injected into the world of percutaneous coronary intervention was provided by the report of the Occluded Artery Trial, which shocked many angiographers. The investigators examined the benefit of PCI in persistent total occlusion from 3 to 28 days after an MI and were surprised to learn that there was no benefit associated with late PCI (see p. 1).

One additional study, the Alternans Before Cardioverter Defibrillator trial, may give some hope that we can begin to define patients who will gain the most benefit from implantable cardioverter defibrillators. Using microwave T-wave alternans and electrophysiologic studies in heart failure patients with ejection fractions of less than 40%, the investigators were able to identify patients who are at low risk and may not need an ICD (see p. 8). These diagnostic techniques provide the possibility that we may be able to make better choices for ICD therapy.

As always, awards were given to distinguished scientists involved in cardiovascular research. None was more deserving than Dr. William Kannel, the creator and driving force of the Framingham Heart Study, who is professor of medicine and public health at Boston University School of Medicine. Initiated almost half a century ago, the massive study created the scientific foundation upon which we have built much of today's clinical science. It is hard to imagine where cardiovascular research would be without that center and his leadership. It was a long overdue award to a true pioneer to whom the cardiology community and the world owe a great debt. Congratulations, Bill!

As part of its new Recommendations From the Heart Rhythm Society Task Force on Device Performance Policies and Guidelines, the society, in conjunction with the device manufacturers, is proposing that device recalls should now be called an “advisory notice” or “safety alert.” HRS suggests that this change is meant to lessen the anxiety of patients and doctors about the implication of a recall.

The American public, and I presume much of the rest of the world, is not exactly unaccustomed to recalls. We have at least one recall a month by auto manufacturers, some by the manufacturers of the reputedly solid Japanese makes. Thanks to the watchful eyes of a variety of federal agencies, we have recalls of everything from baby food to spinach, jet airplanes to baby car seats, and Christmas toys to microwave ovens. We also have had recalls of biologic and medical items including antiarrhythmic drugs, aortic valves, and the painkiller rofecoxib (Vioxx).

Most of these recalls are taken in stride, but the recall of an electronic device implanted in your body does have some unique implications, particularly when many of the devices are there to save your life and when their removal is associated with some risk and discomfort.

The HRS is having difficulty getting this nomenclature change to come about. According to an article in this month's CARDIOLOGY NEWS (see p. 4), the Food and Drug Administration is reluctant to remove “recall” from its lexicon since it is rooted in legislation that mandates its safety responsibilities. In an uncharacteristic Washington response, the FDA is not prepared to “spin” its terminology, even when it is part of the problem.

These proposed changes are taking place in an atmosphere where the number of defibrillator devices implanted is falling short of the expectations of the physicians and manufacturers. Based on the current guidelines of the American College of Cardiology, American Heart Association, and HRS, many more of the devices should have been implanted, suggesting that quality standards are being compromised.

The concern of the HRS is that the media attention given to recalls has made both patients and physicians reluctant to follow the guidelines. It also has called attention to the risks of removing recalled devices, raising questions about which devices should be removed when they are identified as recalled. At the same, time many well-meaning physicians who treat patients at risk of sudden death are concerned about the “one size fits all” approach to the implantation guidelines and are looking for better risk stratification of the benefit that can accrue to their patients. Surely, among the millions of patients included in those guidelines, we should be able to determine in which patient individual implantation is imperative.

As a result of the flawed reporting of device failure in the past, there has been an outcry from physicians for more transparency in the reporting of malfunction of these devices. Unfortunately, increased transparency is certain to raise the level of anxiety of all those involved—patients and physicians—in the implantation of the devices. It is unlikely that the changes in nomenclature will lessen the concerns and increase the understanding of the risks and benefits of implantable devices.

As part of its new Recommendations From the Heart Rhythm Society Task Force on Device Performance Policies and Guidelines, the society, in conjunction with the device manufacturers, is proposing that device recalls should now be called an “advisory notice” or “safety alert.” HRS suggests that this change is meant to lessen the anxiety of patients and doctors about the implication of a recall.

The American public, and I presume much of the rest of the world, is not exactly unaccustomed to recalls. We have at least one recall a month by auto manufacturers, some by the manufacturers of the reputedly solid Japanese makes. Thanks to the watchful eyes of a variety of federal agencies, we have recalls of everything from baby food to spinach, jet airplanes to baby car seats, and Christmas toys to microwave ovens. We also have had recalls of biologic and medical items including antiarrhythmic drugs, aortic valves, and the painkiller rofecoxib (Vioxx).

Most of these recalls are taken in stride, but the recall of an electronic device implanted in your body does have some unique implications, particularly when many of the devices are there to save your life and when their removal is associated with some risk and discomfort.

The HRS is having difficulty getting this nomenclature change to come about. According to an article in this month's CARDIOLOGY NEWS (see p. 4), the Food and Drug Administration is reluctant to remove “recall” from its lexicon since it is rooted in legislation that mandates its safety responsibilities. In an uncharacteristic Washington response, the FDA is not prepared to “spin” its terminology, even when it is part of the problem.

These proposed changes are taking place in an atmosphere where the number of defibrillator devices implanted is falling short of the expectations of the physicians and manufacturers. Based on the current guidelines of the American College of Cardiology, American Heart Association, and HRS, many more of the devices should have been implanted, suggesting that quality standards are being compromised.

The concern of the HRS is that the media attention given to recalls has made both patients and physicians reluctant to follow the guidelines. It also has called attention to the risks of removing recalled devices, raising questions about which devices should be removed when they are identified as recalled. At the same, time many well-meaning physicians who treat patients at risk of sudden death are concerned about the “one size fits all” approach to the implantation guidelines and are looking for better risk stratification of the benefit that can accrue to their patients. Surely, among the millions of patients included in those guidelines, we should be able to determine in which patient individual implantation is imperative.

As a result of the flawed reporting of device failure in the past, there has been an outcry from physicians for more transparency in the reporting of malfunction of these devices. Unfortunately, increased transparency is certain to raise the level of anxiety of all those involved—patients and physicians—in the implantation of the devices. It is unlikely that the changes in nomenclature will lessen the concerns and increase the understanding of the risks and benefits of implantable devices.

As part of its new Recommendations From the Heart Rhythm Society Task Force on Device Performance Policies and Guidelines, the society, in conjunction with the device manufacturers, is proposing that device recalls should now be called an “advisory notice” or “safety alert.” HRS suggests that this change is meant to lessen the anxiety of patients and doctors about the implication of a recall.

The American public, and I presume much of the rest of the world, is not exactly unaccustomed to recalls. We have at least one recall a month by auto manufacturers, some by the manufacturers of the reputedly solid Japanese makes. Thanks to the watchful eyes of a variety of federal agencies, we have recalls of everything from baby food to spinach, jet airplanes to baby car seats, and Christmas toys to microwave ovens. We also have had recalls of biologic and medical items including antiarrhythmic drugs, aortic valves, and the painkiller rofecoxib (Vioxx).

Most of these recalls are taken in stride, but the recall of an electronic device implanted in your body does have some unique implications, particularly when many of the devices are there to save your life and when their removal is associated with some risk and discomfort.

The HRS is having difficulty getting this nomenclature change to come about. According to an article in this month's CARDIOLOGY NEWS (see p. 4), the Food and Drug Administration is reluctant to remove “recall” from its lexicon since it is rooted in legislation that mandates its safety responsibilities. In an uncharacteristic Washington response, the FDA is not prepared to “spin” its terminology, even when it is part of the problem.

These proposed changes are taking place in an atmosphere where the number of defibrillator devices implanted is falling short of the expectations of the physicians and manufacturers. Based on the current guidelines of the American College of Cardiology, American Heart Association, and HRS, many more of the devices should have been implanted, suggesting that quality standards are being compromised.

The concern of the HRS is that the media attention given to recalls has made both patients and physicians reluctant to follow the guidelines. It also has called attention to the risks of removing recalled devices, raising questions about which devices should be removed when they are identified as recalled. At the same, time many well-meaning physicians who treat patients at risk of sudden death are concerned about the “one size fits all” approach to the implantation guidelines and are looking for better risk stratification of the benefit that can accrue to their patients. Surely, among the millions of patients included in those guidelines, we should be able to determine in which patient individual implantation is imperative.

As a result of the flawed reporting of device failure in the past, there has been an outcry from physicians for more transparency in the reporting of malfunction of these devices. Unfortunately, increased transparency is certain to raise the level of anxiety of all those involved—patients and physicians—in the implantation of the devices. It is unlikely that the changes in nomenclature will lessen the concerns and increase the understanding of the risks and benefits of implantable devices.

There are few if any medical therapies that are without any risks. No matter what the treatment, there have always been some risks associated with therapeutic intervention.

Drug-eluting stents (DES) appeared to be an exception to the rule once they were shown to have excellent short-term patency, compared with the bare-metal stents (BMS). DES are now widely used for the treatment of stenotic coronary arteries even in conditions for which there are few data to support a clinical benefit. In the last few years the indication for implantation of stents, and particularly DES, has slipped to a state where clinical judgment has given way to an unfettered response to the “oculostenotic reflex” of the angiographer.

The fact is that the only proven clinical benefit of percutaneous coronary intervention for chronic coronary artery disease is to improve the symptoms of angina. There is nothing to support a mortality or morbidity benefit for the treatment of angina pectoris with PCI. There is also abundant information to indicate that the next acute coronary event usually involves a site in the coronary artery that has little or no preexisting disease. Despite this, PCI with stenting, particularly with the seemingly safe DES, is applied to many asymptomatic patients with anatomic abnormalities alone, to prevent future acute ischemic events.

It now appears that drug-eluting stents, like many previous therapeutic interventions, are not quite as safe as it may seem. Recent press reports indicate that Boston Scientific recently appraised the Food and Drug Administration of its concerns about the long-term morbidity and mortality of the paclitaxel-eluting (Taxus) stent when compared with BMS in regard to the development of thromboses. This follows the reports at the recent meeting of the European Society of Cardiology that Swiss investigators found a significant increase in myocardial infarctions and death in patients receiving DES compared with the BMS in patients followed out to 3 years (see p. 1). In that study, adverse events occurred to a greater degree in the sirolimus-eluting (Sirius) stent than in the Taxus stent.

A proposed mechanism for this late thrombosis is the lack of endothelialization in the DES and the inconsistent use of chronic antiplatelet agents. It was also noted that there was a unique increase in noncardiac deaths, including cancer and infection, suggesting that the antimitotic drug coating of the stents could lead to adverse systemic effects.

All of these reports are preliminary and require further examination. However, if true it could have far reaching effects on the millions of patients who have received DES. It is an even greater paradox for the many asymptomatic patients who received these stents to prevent the morbidity and mortality of coronary artery disease. They now have developed a new disease, the nature and duration of which is uncertain.

Unfortunately, we do not have adequate monitoring systems to fully understand the magnitude of events following implantation of DES. Nevertheless, these very preliminary observations should infuse into the interventional cardiology world caution before implanting DES into asymptomatic patients and in symptomatic patients only after failure with drug therapy.

There are few if any medical therapies that are without any risks. No matter what the treatment, there have always been some risks associated with therapeutic intervention.

Drug-eluting stents (DES) appeared to be an exception to the rule once they were shown to have excellent short-term patency, compared with the bare-metal stents (BMS). DES are now widely used for the treatment of stenotic coronary arteries even in conditions for which there are few data to support a clinical benefit. In the last few years the indication for implantation of stents, and particularly DES, has slipped to a state where clinical judgment has given way to an unfettered response to the “oculostenotic reflex” of the angiographer.

The fact is that the only proven clinical benefit of percutaneous coronary intervention for chronic coronary artery disease is to improve the symptoms of angina. There is nothing to support a mortality or morbidity benefit for the treatment of angina pectoris with PCI. There is also abundant information to indicate that the next acute coronary event usually involves a site in the coronary artery that has little or no preexisting disease. Despite this, PCI with stenting, particularly with the seemingly safe DES, is applied to many asymptomatic patients with anatomic abnormalities alone, to prevent future acute ischemic events.

It now appears that drug-eluting stents, like many previous therapeutic interventions, are not quite as safe as it may seem. Recent press reports indicate that Boston Scientific recently appraised the Food and Drug Administration of its concerns about the long-term morbidity and mortality of the paclitaxel-eluting (Taxus) stent when compared with BMS in regard to the development of thromboses. This follows the reports at the recent meeting of the European Society of Cardiology that Swiss investigators found a significant increase in myocardial infarctions and death in patients receiving DES compared with the BMS in patients followed out to 3 years (see p. 1). In that study, adverse events occurred to a greater degree in the sirolimus-eluting (Sirius) stent than in the Taxus stent.

A proposed mechanism for this late thrombosis is the lack of endothelialization in the DES and the inconsistent use of chronic antiplatelet agents. It was also noted that there was a unique increase in noncardiac deaths, including cancer and infection, suggesting that the antimitotic drug coating of the stents could lead to adverse systemic effects.

All of these reports are preliminary and require further examination. However, if true it could have far reaching effects on the millions of patients who have received DES. It is an even greater paradox for the many asymptomatic patients who received these stents to prevent the morbidity and mortality of coronary artery disease. They now have developed a new disease, the nature and duration of which is uncertain.

Unfortunately, we do not have adequate monitoring systems to fully understand the magnitude of events following implantation of DES. Nevertheless, these very preliminary observations should infuse into the interventional cardiology world caution before implanting DES into asymptomatic patients and in symptomatic patients only after failure with drug therapy.

There are few if any medical therapies that are without any risks. No matter what the treatment, there have always been some risks associated with therapeutic intervention.

Drug-eluting stents (DES) appeared to be an exception to the rule once they were shown to have excellent short-term patency, compared with the bare-metal stents (BMS). DES are now widely used for the treatment of stenotic coronary arteries even in conditions for which there are few data to support a clinical benefit. In the last few years the indication for implantation of stents, and particularly DES, has slipped to a state where clinical judgment has given way to an unfettered response to the “oculostenotic reflex” of the angiographer.

The fact is that the only proven clinical benefit of percutaneous coronary intervention for chronic coronary artery disease is to improve the symptoms of angina. There is nothing to support a mortality or morbidity benefit for the treatment of angina pectoris with PCI. There is also abundant information to indicate that the next acute coronary event usually involves a site in the coronary artery that has little or no preexisting disease. Despite this, PCI with stenting, particularly with the seemingly safe DES, is applied to many asymptomatic patients with anatomic abnormalities alone, to prevent future acute ischemic events.

It now appears that drug-eluting stents, like many previous therapeutic interventions, are not quite as safe as it may seem. Recent press reports indicate that Boston Scientific recently appraised the Food and Drug Administration of its concerns about the long-term morbidity and mortality of the paclitaxel-eluting (Taxus) stent when compared with BMS in regard to the development of thromboses. This follows the reports at the recent meeting of the European Society of Cardiology that Swiss investigators found a significant increase in myocardial infarctions and death in patients receiving DES compared with the BMS in patients followed out to 3 years (see p. 1). In that study, adverse events occurred to a greater degree in the sirolimus-eluting (Sirius) stent than in the Taxus stent.

A proposed mechanism for this late thrombosis is the lack of endothelialization in the DES and the inconsistent use of chronic antiplatelet agents. It was also noted that there was a unique increase in noncardiac deaths, including cancer and infection, suggesting that the antimitotic drug coating of the stents could lead to adverse systemic effects.

All of these reports are preliminary and require further examination. However, if true it could have far reaching effects on the millions of patients who have received DES. It is an even greater paradox for the many asymptomatic patients who received these stents to prevent the morbidity and mortality of coronary artery disease. They now have developed a new disease, the nature and duration of which is uncertain.

Unfortunately, we do not have adequate monitoring systems to fully understand the magnitude of events following implantation of DES. Nevertheless, these very preliminary observations should infuse into the interventional cardiology world caution before implanting DES into asymptomatic patients and in symptomatic patients only after failure with drug therapy.

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.