Sidney Goldstein

The nature and distribution of the cardiology workforce has been at issue for the American College of Cardiology for more than 20 years. It impacts the college's ability to meet community requirements for quality care, and it affects the income of cardiologists.

On the basis of current projections, there will be a major shortfall of cardiologists in 2025, according to a recent Lewin Group report. To some extent, the shortage will affect interventional cardiologists, but the major impact will be felt in the ranks of general cardiologists like me, where the current shortage of 1,600 will swell to 16,000 by 2025.

Projecting the future is, at best, uncertain. These predictions are based on two measurements: first, that there are 1.8 applicants for every cardiovascular training slot, and second, that based on ACC academic, pediatric, and private practice surveys, there is “substantial excess demand for new cardiologists which cannot be met with the current number of fellows completing training annually.” The foundation of these estimates is open to some question.

Not too long ago, the size of the cardiovascular workforce was deemed adequate, with the expectation that interposition of managed care in the medical marketplace would limit patients' ability to get onto our appointment schedules. But then, managed care went up in smoke, and interventional cardiologists found vascular targets not only in the coronary bed but in the head and the legs, not to mention the aortic and mitral valves.

What the future holds for our specialty is uncertain, but if health care reform actually happens and the millions of the uninsured begin to seek medical care, one could anticipate an increase in demand for cardiology services. But in reality, most of people in need of our cardiac services are already covered by Medicare.

Also, it is worth considering that much of the increase in cardiology service demand is a “bubble.” The development of degenerative disease in the aging population speaks to increased volumes, but interventions that have been applied to younger patients may not be applicable or beneficial to the aged.

The Lewin Group report considered a number of solutions to expand the cardiology workforce and meet community needs, including more efficient use of support staff and delaying the retirement of older cardiologists.

The report does not touch on the unlikely possibility of the expansion of training programs. Currently, the number of hospital training slots is limited by the Balanced Budget Act 1997, passed at a time when there was no perceived increased need for specialists. This act fixed the number of training slots by limiting Medicare payments. Hospitals that expand their house staff beyond those limits, would do so at their own expense.

The alternative would be to take on more trainees and have the hospital pay for them. At a time when cardiology is a marketing target, this would not be at all unreasonable.

Even if more slots were provided, it is not certain how many institutions that are not already training cardiology fellows could meet the increased and more stringent quality, volume, and faculty requirements established by the Accreditation Council for General Medical Education.

One proposal, which could increase the number of clinical cardiologists in short supply, was to shorten the training programs for general cardiologists by telescoping their training into the last year of general medicine training. That proposal died a slow death at the hands of the ACGME.

Thus, it is clear that in the current political environment, an increase in cardiology workforce is unlikely.

However, much of what we see as our prime therapeutic domain—hypertension, angina, and heart failure—is treated predominately by noncardiologists. To provide the community we need, we may have to develop a more integrated and collegial relationship with the general internist and family physician. The solution for cardiologists to meet the clinical needs lies in our more efficient integration of cardiology into the general medical community.

The nature and distribution of the cardiology workforce has been at issue for the American College of Cardiology for more than 20 years. It impacts the college's ability to meet community requirements for quality care, and it affects the income of cardiologists.

On the basis of current projections, there will be a major shortfall of cardiologists in 2025, according to a recent Lewin Group report. To some extent, the shortage will affect interventional cardiologists, but the major impact will be felt in the ranks of general cardiologists like me, where the current shortage of 1,600 will swell to 16,000 by 2025.

Projecting the future is, at best, uncertain. These predictions are based on two measurements: first, that there are 1.8 applicants for every cardiovascular training slot, and second, that based on ACC academic, pediatric, and private practice surveys, there is “substantial excess demand for new cardiologists which cannot be met with the current number of fellows completing training annually.” The foundation of these estimates is open to some question.

Not too long ago, the size of the cardiovascular workforce was deemed adequate, with the expectation that interposition of managed care in the medical marketplace would limit patients' ability to get onto our appointment schedules. But then, managed care went up in smoke, and interventional cardiologists found vascular targets not only in the coronary bed but in the head and the legs, not to mention the aortic and mitral valves.

What the future holds for our specialty is uncertain, but if health care reform actually happens and the millions of the uninsured begin to seek medical care, one could anticipate an increase in demand for cardiology services. But in reality, most of people in need of our cardiac services are already covered by Medicare.

Also, it is worth considering that much of the increase in cardiology service demand is a “bubble.” The development of degenerative disease in the aging population speaks to increased volumes, but interventions that have been applied to younger patients may not be applicable or beneficial to the aged.

The Lewin Group report considered a number of solutions to expand the cardiology workforce and meet community needs, including more efficient use of support staff and delaying the retirement of older cardiologists.

The report does not touch on the unlikely possibility of the expansion of training programs. Currently, the number of hospital training slots is limited by the Balanced Budget Act 1997, passed at a time when there was no perceived increased need for specialists. This act fixed the number of training slots by limiting Medicare payments. Hospitals that expand their house staff beyond those limits, would do so at their own expense.

The alternative would be to take on more trainees and have the hospital pay for them. At a time when cardiology is a marketing target, this would not be at all unreasonable.

Even if more slots were provided, it is not certain how many institutions that are not already training cardiology fellows could meet the increased and more stringent quality, volume, and faculty requirements established by the Accreditation Council for General Medical Education.

One proposal, which could increase the number of clinical cardiologists in short supply, was to shorten the training programs for general cardiologists by telescoping their training into the last year of general medicine training. That proposal died a slow death at the hands of the ACGME.

Thus, it is clear that in the current political environment, an increase in cardiology workforce is unlikely.

However, much of what we see as our prime therapeutic domain—hypertension, angina, and heart failure—is treated predominately by noncardiologists. To provide the community we need, we may have to develop a more integrated and collegial relationship with the general internist and family physician. The solution for cardiologists to meet the clinical needs lies in our more efficient integration of cardiology into the general medical community.

The nature and distribution of the cardiology workforce has been at issue for the American College of Cardiology for more than 20 years. It impacts the college's ability to meet community requirements for quality care, and it affects the income of cardiologists.

On the basis of current projections, there will be a major shortfall of cardiologists in 2025, according to a recent Lewin Group report. To some extent, the shortage will affect interventional cardiologists, but the major impact will be felt in the ranks of general cardiologists like me, where the current shortage of 1,600 will swell to 16,000 by 2025.

Projecting the future is, at best, uncertain. These predictions are based on two measurements: first, that there are 1.8 applicants for every cardiovascular training slot, and second, that based on ACC academic, pediatric, and private practice surveys, there is “substantial excess demand for new cardiologists which cannot be met with the current number of fellows completing training annually.” The foundation of these estimates is open to some question.

Not too long ago, the size of the cardiovascular workforce was deemed adequate, with the expectation that interposition of managed care in the medical marketplace would limit patients' ability to get onto our appointment schedules. But then, managed care went up in smoke, and interventional cardiologists found vascular targets not only in the coronary bed but in the head and the legs, not to mention the aortic and mitral valves.

What the future holds for our specialty is uncertain, but if health care reform actually happens and the millions of the uninsured begin to seek medical care, one could anticipate an increase in demand for cardiology services. But in reality, most of people in need of our cardiac services are already covered by Medicare.

Also, it is worth considering that much of the increase in cardiology service demand is a “bubble.” The development of degenerative disease in the aging population speaks to increased volumes, but interventions that have been applied to younger patients may not be applicable or beneficial to the aged.

The Lewin Group report considered a number of solutions to expand the cardiology workforce and meet community needs, including more efficient use of support staff and delaying the retirement of older cardiologists.

The report does not touch on the unlikely possibility of the expansion of training programs. Currently, the number of hospital training slots is limited by the Balanced Budget Act 1997, passed at a time when there was no perceived increased need for specialists. This act fixed the number of training slots by limiting Medicare payments. Hospitals that expand their house staff beyond those limits, would do so at their own expense.

The alternative would be to take on more trainees and have the hospital pay for them. At a time when cardiology is a marketing target, this would not be at all unreasonable.

Even if more slots were provided, it is not certain how many institutions that are not already training cardiology fellows could meet the increased and more stringent quality, volume, and faculty requirements established by the Accreditation Council for General Medical Education.

One proposal, which could increase the number of clinical cardiologists in short supply, was to shorten the training programs for general cardiologists by telescoping their training into the last year of general medicine training. That proposal died a slow death at the hands of the ACGME.

Thus, it is clear that in the current political environment, an increase in cardiology workforce is unlikely.

However, much of what we see as our prime therapeutic domain—hypertension, angina, and heart failure—is treated predominately by noncardiologists. To provide the community we need, we may have to develop a more integrated and collegial relationship with the general internist and family physician. The solution for cardiologists to meet the clinical needs lies in our more efficient integration of cardiology into the general medical community.

The American Heart Association is leading a major national effort to improve and expedite treatment for ST-segment elevation myocardial infarction. With the logo Mission: Lifeline, reminiscent of TV's “Mission: Impossible,” the AHA, in collaboration with other organizations, is developing criteria and certification for members of the STEMI “treatment train,” from emergency medical services through referring hospitals to the hospital that can perform emergency percutaneous coronary intervention 24/7.

To reach the goals of fibrinolytic therapy in less than 30 minutes and PCI therapy within 90 minutes for STEMI, the nation's EMS and hospital referral system must improve. There are excellent community systems that can serve as models, but creating a uniform system is a challenge, given the wide variety of players.

Unlike the European systems, uniform in their configuration and, for the most part, federally funded and very successful at expediting care for STEMI, the U.S. system is a helter-skelter of private and voluntary players, bent on preserving their own priorities. Only 6% of American EMS systems are hospital based. The rest are provided by fire departments, volunteers, and private operators. State governments control EMS operations, which are certified for different levels of care and are variably equipped to deal with cardiac emergencies. Americans use EMS systems in less than 25% of instances to obtain emergency care for STEMI. In spite of extensive public education, Americans do not understand the need for rapid response to chest pain symptoms.

“Although the performance of primary PCI has increased from 18% to 53%” nearly 30% of patients with STEMI fail to receive either fibrinolytic therapy or PCI, said Dr. Alice Jacobs, former president of the AHA, who is leading the Mission: Lifeline effort (Circulation 2007;116:689–92). Most STEMI patients seek medical help at hospitals that are not equipped to perform primary PCI. To expand the number of PCI-approved hospitals, the requirement to have on-site cardiac surgery in such hospitals will have to be dropped. Rapid transfer to PCI hospitals can be achieved if systems are in place to expedite patient transfer or to initiate fibrinolytic therapy when primary PCI is neither feasible nor appropriate. Non-PCI hospitals within the Mission: Lifeline network would be certified as “STEMI referral hospitals” and would create pathways that expedite transfer to “STEMI receiving hospitals.” Most importantly, competency and numerical criteria have been developed for certification as a “STEMI receiving hospital.”

Mission: Lifeline registration of EMS and referring and receiving hospitals is underway. Certification of sites that meet the published criteria is soon to start. Many communities and hospital systems have the infrastructure in place, but urban and rural systems are up against major logistical and political barriers. The AHA is to be applauded for rising to the challenge of the improvement of emergency cardiac care for STEMI. But achieving the goals of Mission: Lifeline nationwide might actually be a “Mission: Impossible.”

For more information, visit www.americanheart.org/missionlifeline

The American Heart Association is leading a major national effort to improve and expedite treatment for ST-segment elevation myocardial infarction. With the logo Mission: Lifeline, reminiscent of TV's “Mission: Impossible,” the AHA, in collaboration with other organizations, is developing criteria and certification for members of the STEMI “treatment train,” from emergency medical services through referring hospitals to the hospital that can perform emergency percutaneous coronary intervention 24/7.

To reach the goals of fibrinolytic therapy in less than 30 minutes and PCI therapy within 90 minutes for STEMI, the nation's EMS and hospital referral system must improve. There are excellent community systems that can serve as models, but creating a uniform system is a challenge, given the wide variety of players.

Unlike the European systems, uniform in their configuration and, for the most part, federally funded and very successful at expediting care for STEMI, the U.S. system is a helter-skelter of private and voluntary players, bent on preserving their own priorities. Only 6% of American EMS systems are hospital based. The rest are provided by fire departments, volunteers, and private operators. State governments control EMS operations, which are certified for different levels of care and are variably equipped to deal with cardiac emergencies. Americans use EMS systems in less than 25% of instances to obtain emergency care for STEMI. In spite of extensive public education, Americans do not understand the need for rapid response to chest pain symptoms.

“Although the performance of primary PCI has increased from 18% to 53%” nearly 30% of patients with STEMI fail to receive either fibrinolytic therapy or PCI, said Dr. Alice Jacobs, former president of the AHA, who is leading the Mission: Lifeline effort (Circulation 2007;116:689–92). Most STEMI patients seek medical help at hospitals that are not equipped to perform primary PCI. To expand the number of PCI-approved hospitals, the requirement to have on-site cardiac surgery in such hospitals will have to be dropped. Rapid transfer to PCI hospitals can be achieved if systems are in place to expedite patient transfer or to initiate fibrinolytic therapy when primary PCI is neither feasible nor appropriate. Non-PCI hospitals within the Mission: Lifeline network would be certified as “STEMI referral hospitals” and would create pathways that expedite transfer to “STEMI receiving hospitals.” Most importantly, competency and numerical criteria have been developed for certification as a “STEMI receiving hospital.”

Mission: Lifeline registration of EMS and referring and receiving hospitals is underway. Certification of sites that meet the published criteria is soon to start. Many communities and hospital systems have the infrastructure in place, but urban and rural systems are up against major logistical and political barriers. The AHA is to be applauded for rising to the challenge of the improvement of emergency cardiac care for STEMI. But achieving the goals of Mission: Lifeline nationwide might actually be a “Mission: Impossible.”

For more information, visit www.americanheart.org/missionlifeline

The American Heart Association is leading a major national effort to improve and expedite treatment for ST-segment elevation myocardial infarction. With the logo Mission: Lifeline, reminiscent of TV's “Mission: Impossible,” the AHA, in collaboration with other organizations, is developing criteria and certification for members of the STEMI “treatment train,” from emergency medical services through referring hospitals to the hospital that can perform emergency percutaneous coronary intervention 24/7.

To reach the goals of fibrinolytic therapy in less than 30 minutes and PCI therapy within 90 minutes for STEMI, the nation's EMS and hospital referral system must improve. There are excellent community systems that can serve as models, but creating a uniform system is a challenge, given the wide variety of players.

Unlike the European systems, uniform in their configuration and, for the most part, federally funded and very successful at expediting care for STEMI, the U.S. system is a helter-skelter of private and voluntary players, bent on preserving their own priorities. Only 6% of American EMS systems are hospital based. The rest are provided by fire departments, volunteers, and private operators. State governments control EMS operations, which are certified for different levels of care and are variably equipped to deal with cardiac emergencies. Americans use EMS systems in less than 25% of instances to obtain emergency care for STEMI. In spite of extensive public education, Americans do not understand the need for rapid response to chest pain symptoms.

“Although the performance of primary PCI has increased from 18% to 53%” nearly 30% of patients with STEMI fail to receive either fibrinolytic therapy or PCI, said Dr. Alice Jacobs, former president of the AHA, who is leading the Mission: Lifeline effort (Circulation 2007;116:689–92). Most STEMI patients seek medical help at hospitals that are not equipped to perform primary PCI. To expand the number of PCI-approved hospitals, the requirement to have on-site cardiac surgery in such hospitals will have to be dropped. Rapid transfer to PCI hospitals can be achieved if systems are in place to expedite patient transfer or to initiate fibrinolytic therapy when primary PCI is neither feasible nor appropriate. Non-PCI hospitals within the Mission: Lifeline network would be certified as “STEMI referral hospitals” and would create pathways that expedite transfer to “STEMI receiving hospitals.” Most importantly, competency and numerical criteria have been developed for certification as a “STEMI receiving hospital.”

Mission: Lifeline registration of EMS and referring and receiving hospitals is underway. Certification of sites that meet the published criteria is soon to start. Many communities and hospital systems have the infrastructure in place, but urban and rural systems are up against major logistical and political barriers. The AHA is to be applauded for rising to the challenge of the improvement of emergency cardiac care for STEMI. But achieving the goals of Mission: Lifeline nationwide might actually be a “Mission: Impossible.”

For more information, visit www.americanheart.org/missionlifeline

For more than half a century, physicians have been struggling with the seemingly impossible task of dosing vitamin K–dependent anticoagulants ever since they were demonstrated to be beneficial in the treatment of acute myocardial infarction.

At that time, the major risk for acute MI was the development of a pulmonary embolism occurring in the setting of weeks of prescribed absolute bed rest. Physicians, patients, and nurses have dealt with the logistical difficulties in managing the narrow dose range required to achieve maximum benefit while minimizing risk. Dose titration walks a fine line between recurrent embolic stroke and major bleed.

The slow onset of vitamin K antagonists such as warfarin associated with the variability of dose response driven by genetic polymorphism, food ingestion, and interaction with other drugs has made dosing a therapeutic nightmare. In spite of the problems, vitamin K anticoagulant therapy has remained the standard method for preventing thromboembolism in atrial fibrillation and after valve surgery. The process of dose adjustment for warfarin, the most commonly used drug of this class, requires a huge manpower effort.

Over time, attempts to find an alternative therapy have been unsuccessful. Trials comparing the combination of aspirin and clopidogrel with aspirin alone found the combination more effective than aspirin alone, but not as effective as warfarin.

The comparison of subcutaneously administered factor Xa inhibitors fondaparinux and idraparinux with warfarin resulted in fewer emboli but more bleeding. The long-term subcutaneous administration required with low-molecular-weight heparin also was unacceptable. More recently, the direct thrombin inhibitor ximelagatran was found to have a benefit similar to that of warfarin but with an unacceptable incidence of hepatotoxicity.

For the first time, an effective and safe replacement of warfarin has been developed. The direct thrombin inhibitor dabigatran, a cousin of ximelagatran, was shown to be at least as effective as warfarin and associated with fewer bleeding episodes, depending on the dosage, in the 18,000-patient RE-LY study presented in August at the European Society of Cardiology meeting (

Dabigatran, approved in Canada and Europe, is the first of this class of drugs being developed to provide an opportunity to evaluate other direct thrombin inhibitor molecules. In addition to direct thrombin inhibitors, oral factor Xa inhibitors are under intense clinic evaluation. One of these, rivaroxaban, also approved in Canada and Europe, demonstrated efficacy in prevention of venous thromboembolism following major orthopedic surgery (N. Engl. J. Med 2008;358:2776–86). Like dabigatran, it has a rapid onset of action and can be given orally in a fixed dose, comparable to warfarin with less bleeding. Both direct thrombin and factor Xa inhibitors have been tested in orthopedic patients in whom venous thrombosis can be easily identified with venography. They are yet to be tested more widely in other cardiovascular settings. A number of studies with factor Xa inhibitors are underway to evaluate their benefit in acute coronary syndromes in association with antiplatelet therapy. The clinical comparison of these two new classes of anticoagulants will require further definition.

It is clear that these drugs will change the shape of anticoagulant therapy for a variety of cardiovascular conditions. Many patients undergoing atrial fibrillation ablation may find a safe, easily taken oral medication a better alternative to electrophysiologic intervention. The safety and benefit of these new classes of anticoagulants will make it possible for more patients and physicians to adhere to published guidelines once their efficacy is proved. For now, dabigatran represents a major advance in the prevention of thromboembolism in these patients.

For more than half a century, physicians have been struggling with the seemingly impossible task of dosing vitamin K–dependent anticoagulants ever since they were demonstrated to be beneficial in the treatment of acute myocardial infarction.

At that time, the major risk for acute MI was the development of a pulmonary embolism occurring in the setting of weeks of prescribed absolute bed rest. Physicians, patients, and nurses have dealt with the logistical difficulties in managing the narrow dose range required to achieve maximum benefit while minimizing risk. Dose titration walks a fine line between recurrent embolic stroke and major bleed.

The slow onset of vitamin K antagonists such as warfarin associated with the variability of dose response driven by genetic polymorphism, food ingestion, and interaction with other drugs has made dosing a therapeutic nightmare. In spite of the problems, vitamin K anticoagulant therapy has remained the standard method for preventing thromboembolism in atrial fibrillation and after valve surgery. The process of dose adjustment for warfarin, the most commonly used drug of this class, requires a huge manpower effort.

Over time, attempts to find an alternative therapy have been unsuccessful. Trials comparing the combination of aspirin and clopidogrel with aspirin alone found the combination more effective than aspirin alone, but not as effective as warfarin.

The comparison of subcutaneously administered factor Xa inhibitors fondaparinux and idraparinux with warfarin resulted in fewer emboli but more bleeding. The long-term subcutaneous administration required with low-molecular-weight heparin also was unacceptable. More recently, the direct thrombin inhibitor ximelagatran was found to have a benefit similar to that of warfarin but with an unacceptable incidence of hepatotoxicity.

For the first time, an effective and safe replacement of warfarin has been developed. The direct thrombin inhibitor dabigatran, a cousin of ximelagatran, was shown to be at least as effective as warfarin and associated with fewer bleeding episodes, depending on the dosage, in the 18,000-patient RE-LY study presented in August at the European Society of Cardiology meeting (

Dabigatran, approved in Canada and Europe, is the first of this class of drugs being developed to provide an opportunity to evaluate other direct thrombin inhibitor molecules. In addition to direct thrombin inhibitors, oral factor Xa inhibitors are under intense clinic evaluation. One of these, rivaroxaban, also approved in Canada and Europe, demonstrated efficacy in prevention of venous thromboembolism following major orthopedic surgery (N. Engl. J. Med 2008;358:2776–86). Like dabigatran, it has a rapid onset of action and can be given orally in a fixed dose, comparable to warfarin with less bleeding. Both direct thrombin and factor Xa inhibitors have been tested in orthopedic patients in whom venous thrombosis can be easily identified with venography. They are yet to be tested more widely in other cardiovascular settings. A number of studies with factor Xa inhibitors are underway to evaluate their benefit in acute coronary syndromes in association with antiplatelet therapy. The clinical comparison of these two new classes of anticoagulants will require further definition.

It is clear that these drugs will change the shape of anticoagulant therapy for a variety of cardiovascular conditions. Many patients undergoing atrial fibrillation ablation may find a safe, easily taken oral medication a better alternative to electrophysiologic intervention. The safety and benefit of these new classes of anticoagulants will make it possible for more patients and physicians to adhere to published guidelines once their efficacy is proved. For now, dabigatran represents a major advance in the prevention of thromboembolism in these patients.

For more than half a century, physicians have been struggling with the seemingly impossible task of dosing vitamin K–dependent anticoagulants ever since they were demonstrated to be beneficial in the treatment of acute myocardial infarction.

At that time, the major risk for acute MI was the development of a pulmonary embolism occurring in the setting of weeks of prescribed absolute bed rest. Physicians, patients, and nurses have dealt with the logistical difficulties in managing the narrow dose range required to achieve maximum benefit while minimizing risk. Dose titration walks a fine line between recurrent embolic stroke and major bleed.

The slow onset of vitamin K antagonists such as warfarin associated with the variability of dose response driven by genetic polymorphism, food ingestion, and interaction with other drugs has made dosing a therapeutic nightmare. In spite of the problems, vitamin K anticoagulant therapy has remained the standard method for preventing thromboembolism in atrial fibrillation and after valve surgery. The process of dose adjustment for warfarin, the most commonly used drug of this class, requires a huge manpower effort.

Over time, attempts to find an alternative therapy have been unsuccessful. Trials comparing the combination of aspirin and clopidogrel with aspirin alone found the combination more effective than aspirin alone, but not as effective as warfarin.

The comparison of subcutaneously administered factor Xa inhibitors fondaparinux and idraparinux with warfarin resulted in fewer emboli but more bleeding. The long-term subcutaneous administration required with low-molecular-weight heparin also was unacceptable. More recently, the direct thrombin inhibitor ximelagatran was found to have a benefit similar to that of warfarin but with an unacceptable incidence of hepatotoxicity.

For the first time, an effective and safe replacement of warfarin has been developed. The direct thrombin inhibitor dabigatran, a cousin of ximelagatran, was shown to be at least as effective as warfarin and associated with fewer bleeding episodes, depending on the dosage, in the 18,000-patient RE-LY study presented in August at the European Society of Cardiology meeting (

Dabigatran, approved in Canada and Europe, is the first of this class of drugs being developed to provide an opportunity to evaluate other direct thrombin inhibitor molecules. In addition to direct thrombin inhibitors, oral factor Xa inhibitors are under intense clinic evaluation. One of these, rivaroxaban, also approved in Canada and Europe, demonstrated efficacy in prevention of venous thromboembolism following major orthopedic surgery (N. Engl. J. Med 2008;358:2776–86). Like dabigatran, it has a rapid onset of action and can be given orally in a fixed dose, comparable to warfarin with less bleeding. Both direct thrombin and factor Xa inhibitors have been tested in orthopedic patients in whom venous thrombosis can be easily identified with venography. They are yet to be tested more widely in other cardiovascular settings. A number of studies with factor Xa inhibitors are underway to evaluate their benefit in acute coronary syndromes in association with antiplatelet therapy. The clinical comparison of these two new classes of anticoagulants will require further definition.

It is clear that these drugs will change the shape of anticoagulant therapy for a variety of cardiovascular conditions. Many patients undergoing atrial fibrillation ablation may find a safe, easily taken oral medication a better alternative to electrophysiologic intervention. The safety and benefit of these new classes of anticoagulants will make it possible for more patients and physicians to adhere to published guidelines once their efficacy is proved. For now, dabigatran represents a major advance in the prevention of thromboembolism in these patients.

The Food and Drug Administration is abdicating some of its responsibility to you and me by placing boxed warnings on its approvals for potent drugs in the face of difficult decisions regarding their risks and benefits. In the past, the approval process has been straightforward, but as we develop stronger drugs with significant risks, it has become much more complex.

Two recent approvals serve as examples. Dronedarone is a recently approved anti-arrhythmic drug developed to replace amiodarone for the maintenance of normal sinus rhythm in patients with paroxysmal atrial fibrillation. Because of the long-term effects of amiodarone on thyroid function and lung toxicity, dronedarone was developed by making structural changes in the amiodarone molecule to prevent that toxicity. Amiodarone has been effective in maintaining normal sinus rhythm, but with a trend toward increased mortality in New York Heart Association class III heart failure patients. The initial clinical trial with dronedarone, ANDROMEDA, carried out in NYHA class III-IV patients, was stopped prematurely because of the increased heart failure mortality.

ATHENA, a later short-term trial in patients with at least one episode of paroxysmal AF in the previous 3 months with dronedarone, reported a significant decrease in atrial fibrillation compared with placebo. It excluded NYHA class IV patients and those with chronic AF (N. Engl. J. Med. 2009;360:668-78). Dronedarone had a significant improvement in mortality and recurrent hospitalization (36.9% vs. 29.3%), compared with placebo. It also decreased the rehospitalization for AF from 21.8% to 14.6%. There was no ascertainment of amiodarone-like side effects because of ATHENA's short duration. Since it did not compare dronedarone with amiodarone, it is not clear which drug has a better anti-arrhythmic effect.

The FDA approval of dronedarone for the prevention of AF came with a black box warning that it “is contraindicated in patients with NYHA Class IV heart failure, or NYHA Class II-III heart failure with a recent decompensation requiring hospitalization or referral to a specialized heart failure clinic.” The FDA left it up to us to decide when to use this drug in heart failure, a moving target at best.

Shortly after this decision, the FDA approved the use of the antiplatelet agent prasugrel, for use in patients with acute coronary syndromes who were likely to undergo percutaneous coronary intervention. In the TRITON trial, comparing clopidogrel with prasugrel in ACS, prasugrel was shown to have a greater benefit for recurrent MI, cardiovascular mortality, or nonfatal stroke (12.1% vs. 9.9%), a result largely driven by “troponin-defined” non-fatal MIs. However, prasugrel was associated with an increased incidence of bleeding and thrombotic strokes about five times that of clopidogrel (6.5% vs. 1.2%), particularly in thin and elderly patients. With this information, the FDA approved prasugrel for the reduction of thrombotic cardiovascular events in ACS patients who are managed with PCI. The approval came with a black box warning that cautioned against its use in patients with a propensity to bleed and in patients aged older than 75 years, or with body weight less than 60 kg.

The current discussion of the approval process of these two drugs, whose therapeutic and safety benefits are narrow, indicates an awareness of the cautions. Over time, the black box warnings lose some of their impact and may become less important in our therapeutic decisions. It has been suggested that with the more liberal use of these warnings, they have lost some of their meaning.

There is nothing wrong with the FDA's passing on the drug-use decision process to the doctors on the front line, but it should be emphasized that many of these drugs come with a significant risk if used in the wrong patient. Doctors beware!

The Food and Drug Administration is abdicating some of its responsibility to you and me by placing boxed warnings on its approvals for potent drugs in the face of difficult decisions regarding their risks and benefits. In the past, the approval process has been straightforward, but as we develop stronger drugs with significant risks, it has become much more complex.

Two recent approvals serve as examples. Dronedarone is a recently approved anti-arrhythmic drug developed to replace amiodarone for the maintenance of normal sinus rhythm in patients with paroxysmal atrial fibrillation. Because of the long-term effects of amiodarone on thyroid function and lung toxicity, dronedarone was developed by making structural changes in the amiodarone molecule to prevent that toxicity. Amiodarone has been effective in maintaining normal sinus rhythm, but with a trend toward increased mortality in New York Heart Association class III heart failure patients. The initial clinical trial with dronedarone, ANDROMEDA, carried out in NYHA class III-IV patients, was stopped prematurely because of the increased heart failure mortality.

ATHENA, a later short-term trial in patients with at least one episode of paroxysmal AF in the previous 3 months with dronedarone, reported a significant decrease in atrial fibrillation compared with placebo. It excluded NYHA class IV patients and those with chronic AF (N. Engl. J. Med. 2009;360:668-78). Dronedarone had a significant improvement in mortality and recurrent hospitalization (36.9% vs. 29.3%), compared with placebo. It also decreased the rehospitalization for AF from 21.8% to 14.6%. There was no ascertainment of amiodarone-like side effects because of ATHENA's short duration. Since it did not compare dronedarone with amiodarone, it is not clear which drug has a better anti-arrhythmic effect.

The FDA approval of dronedarone for the prevention of AF came with a black box warning that it “is contraindicated in patients with NYHA Class IV heart failure, or NYHA Class II-III heart failure with a recent decompensation requiring hospitalization or referral to a specialized heart failure clinic.” The FDA left it up to us to decide when to use this drug in heart failure, a moving target at best.

Shortly after this decision, the FDA approved the use of the antiplatelet agent prasugrel, for use in patients with acute coronary syndromes who were likely to undergo percutaneous coronary intervention. In the TRITON trial, comparing clopidogrel with prasugrel in ACS, prasugrel was shown to have a greater benefit for recurrent MI, cardiovascular mortality, or nonfatal stroke (12.1% vs. 9.9%), a result largely driven by “troponin-defined” non-fatal MIs. However, prasugrel was associated with an increased incidence of bleeding and thrombotic strokes about five times that of clopidogrel (6.5% vs. 1.2%), particularly in thin and elderly patients. With this information, the FDA approved prasugrel for the reduction of thrombotic cardiovascular events in ACS patients who are managed with PCI. The approval came with a black box warning that cautioned against its use in patients with a propensity to bleed and in patients aged older than 75 years, or with body weight less than 60 kg.

The current discussion of the approval process of these two drugs, whose therapeutic and safety benefits are narrow, indicates an awareness of the cautions. Over time, the black box warnings lose some of their impact and may become less important in our therapeutic decisions. It has been suggested that with the more liberal use of these warnings, they have lost some of their meaning.

There is nothing wrong with the FDA's passing on the drug-use decision process to the doctors on the front line, but it should be emphasized that many of these drugs come with a significant risk if used in the wrong patient. Doctors beware!

The Food and Drug Administration is abdicating some of its responsibility to you and me by placing boxed warnings on its approvals for potent drugs in the face of difficult decisions regarding their risks and benefits. In the past, the approval process has been straightforward, but as we develop stronger drugs with significant risks, it has become much more complex.

Two recent approvals serve as examples. Dronedarone is a recently approved anti-arrhythmic drug developed to replace amiodarone for the maintenance of normal sinus rhythm in patients with paroxysmal atrial fibrillation. Because of the long-term effects of amiodarone on thyroid function and lung toxicity, dronedarone was developed by making structural changes in the amiodarone molecule to prevent that toxicity. Amiodarone has been effective in maintaining normal sinus rhythm, but with a trend toward increased mortality in New York Heart Association class III heart failure patients. The initial clinical trial with dronedarone, ANDROMEDA, carried out in NYHA class III-IV patients, was stopped prematurely because of the increased heart failure mortality.

ATHENA, a later short-term trial in patients with at least one episode of paroxysmal AF in the previous 3 months with dronedarone, reported a significant decrease in atrial fibrillation compared with placebo. It excluded NYHA class IV patients and those with chronic AF (N. Engl. J. Med. 2009;360:668-78). Dronedarone had a significant improvement in mortality and recurrent hospitalization (36.9% vs. 29.3%), compared with placebo. It also decreased the rehospitalization for AF from 21.8% to 14.6%. There was no ascertainment of amiodarone-like side effects because of ATHENA's short duration. Since it did not compare dronedarone with amiodarone, it is not clear which drug has a better anti-arrhythmic effect.

The FDA approval of dronedarone for the prevention of AF came with a black box warning that it “is contraindicated in patients with NYHA Class IV heart failure, or NYHA Class II-III heart failure with a recent decompensation requiring hospitalization or referral to a specialized heart failure clinic.” The FDA left it up to us to decide when to use this drug in heart failure, a moving target at best.

Shortly after this decision, the FDA approved the use of the antiplatelet agent prasugrel, for use in patients with acute coronary syndromes who were likely to undergo percutaneous coronary intervention. In the TRITON trial, comparing clopidogrel with prasugrel in ACS, prasugrel was shown to have a greater benefit for recurrent MI, cardiovascular mortality, or nonfatal stroke (12.1% vs. 9.9%), a result largely driven by “troponin-defined” non-fatal MIs. However, prasugrel was associated with an increased incidence of bleeding and thrombotic strokes about five times that of clopidogrel (6.5% vs. 1.2%), particularly in thin and elderly patients. With this information, the FDA approved prasugrel for the reduction of thrombotic cardiovascular events in ACS patients who are managed with PCI. The approval came with a black box warning that cautioned against its use in patients with a propensity to bleed and in patients aged older than 75 years, or with body weight less than 60 kg.

The current discussion of the approval process of these two drugs, whose therapeutic and safety benefits are narrow, indicates an awareness of the cautions. Over time, the black box warnings lose some of their impact and may become less important in our therapeutic decisions. It has been suggested that with the more liberal use of these warnings, they have lost some of their meaning.

There is nothing wrong with the FDA's passing on the drug-use decision process to the doctors on the front line, but it should be emphasized that many of these drugs come with a significant risk if used in the wrong patient. Doctors beware!

As I write this column, the House of Representatives is struggling with the details of the new health care legislation, the American Affordable Health Choices Act of 2009 (H.R. 3200). By the time you read this, Congress will be in recess, having left the final form and fate of the legislation uncertain.

The goal of providing universal health insurance is ambitious, and to achieve that goal while limiting its cost is a monumental task. If achieved, it will represent a sea change in the way America pays for health coverage, just as Medicare transformed the care of the over-65 population 34 years ago. The proposed legislation will totally rewrite the rules of how Americans receive their care and how we physicians provide that care in an expanded government-controlled health care system.

The government is already heavily involved in providing health care to a third of the U.S. population. Medicare, which has been very successful in the eyes of the elderly patients if not a darling of doctors, covers more than 45 million Americans. Medicaid jointly financed by the federal and state governments covers another 60 million poor people. It would seem obvious to expand that program to include the remaining two-thirds.

For a public plan to be viable, it must include an individual mandate to participate. Everyone must be included. If not, the healthy patient by design or by personal desire will be left out and only the sickest and the most expensive will be left in the public plan. A personal mandate will require the government to subsidize the poor, just as it has in the past, but in a more organized system rather than the expensive and dysfunctional care in the emergency department.

Without a universal health plan in place, the ranks of the uninsured will continue to increase. Almost 50 million Americans are currently uninsured, representing well over 15% of our population. When Americans who are out of work in the current recession return to the workforce, the post-recession health insurance policies will not resemble the pre-recession policies. Many of the benefits will disappear and the copayments will most certainly increase. As the pool of insured patients decreases there will be increased competition among health care providers for those few insured patients. We see this already, with hospital and physicians advertising on TV and in the print media. Caught between increased cost and falling profits, insurers will have to choose between increased premiums or cutting doctors fees. The day may come when Medicare's physician fee schedule could be a welcome lifeboat for physicians' practices.

In his response to President Obama's address to the American Medical Association in June, AMA's leadership echoed the need for universal care, but indicated that a payment schedule based on Medicare rates was unacceptable. The AMA has been reluctant to articulate just what sort of universal health insurance plan is acceptable, public or private.

Nevertheless, the process of achieving a federal insurance plan has been much different than that of the Clinton plan in 1993. This time there has been a significant bargaining between Congress and the health providers. The word has been sent out by the Democratic Congress that if you want to take part in the formative process, negative advertising and publicity will lock you out. So at this point everyone is in until they are out. The pharmaceutical industry has indicated that it will provide an $80 billion savings over a 10-year period to the elderly if it limits the reduction in drug coverage to Medicare recipients trapped in the Part D “doughnut hole.” The major hospital associations pledged to save $150 billion dollars providing that the new public plan will cover the indigent. And the AMA has agreed to support HR 3200.

There is considerable concern about cost, which is now estimated at $900 million over the next 10 years. Congress hardly blinked an eye when they spent well over that in a useless war in Iraq. The social and economic necessity of a universal health plan is obvious. To achieve that, a robust universal public insurance foundation is essential. Any thing short of that will lead to further deterioration in American health care.

As I write this column, the House of Representatives is struggling with the details of the new health care legislation, the American Affordable Health Choices Act of 2009 (H.R. 3200). By the time you read this, Congress will be in recess, having left the final form and fate of the legislation uncertain.

The goal of providing universal health insurance is ambitious, and to achieve that goal while limiting its cost is a monumental task. If achieved, it will represent a sea change in the way America pays for health coverage, just as Medicare transformed the care of the over-65 population 34 years ago. The proposed legislation will totally rewrite the rules of how Americans receive their care and how we physicians provide that care in an expanded government-controlled health care system.

The government is already heavily involved in providing health care to a third of the U.S. population. Medicare, which has been very successful in the eyes of the elderly patients if not a darling of doctors, covers more than 45 million Americans. Medicaid jointly financed by the federal and state governments covers another 60 million poor people. It would seem obvious to expand that program to include the remaining two-thirds.

For a public plan to be viable, it must include an individual mandate to participate. Everyone must be included. If not, the healthy patient by design or by personal desire will be left out and only the sickest and the most expensive will be left in the public plan. A personal mandate will require the government to subsidize the poor, just as it has in the past, but in a more organized system rather than the expensive and dysfunctional care in the emergency department.

Without a universal health plan in place, the ranks of the uninsured will continue to increase. Almost 50 million Americans are currently uninsured, representing well over 15% of our population. When Americans who are out of work in the current recession return to the workforce, the post-recession health insurance policies will not resemble the pre-recession policies. Many of the benefits will disappear and the copayments will most certainly increase. As the pool of insured patients decreases there will be increased competition among health care providers for those few insured patients. We see this already, with hospital and physicians advertising on TV and in the print media. Caught between increased cost and falling profits, insurers will have to choose between increased premiums or cutting doctors fees. The day may come when Medicare's physician fee schedule could be a welcome lifeboat for physicians' practices.

In his response to President Obama's address to the American Medical Association in June, AMA's leadership echoed the need for universal care, but indicated that a payment schedule based on Medicare rates was unacceptable. The AMA has been reluctant to articulate just what sort of universal health insurance plan is acceptable, public or private.

Nevertheless, the process of achieving a federal insurance plan has been much different than that of the Clinton plan in 1993. This time there has been a significant bargaining between Congress and the health providers. The word has been sent out by the Democratic Congress that if you want to take part in the formative process, negative advertising and publicity will lock you out. So at this point everyone is in until they are out. The pharmaceutical industry has indicated that it will provide an $80 billion savings over a 10-year period to the elderly if it limits the reduction in drug coverage to Medicare recipients trapped in the Part D “doughnut hole.” The major hospital associations pledged to save $150 billion dollars providing that the new public plan will cover the indigent. And the AMA has agreed to support HR 3200.

There is considerable concern about cost, which is now estimated at $900 million over the next 10 years. Congress hardly blinked an eye when they spent well over that in a useless war in Iraq. The social and economic necessity of a universal health plan is obvious. To achieve that, a robust universal public insurance foundation is essential. Any thing short of that will lead to further deterioration in American health care.

As I write this column, the House of Representatives is struggling with the details of the new health care legislation, the American Affordable Health Choices Act of 2009 (H.R. 3200). By the time you read this, Congress will be in recess, having left the final form and fate of the legislation uncertain.

The goal of providing universal health insurance is ambitious, and to achieve that goal while limiting its cost is a monumental task. If achieved, it will represent a sea change in the way America pays for health coverage, just as Medicare transformed the care of the over-65 population 34 years ago. The proposed legislation will totally rewrite the rules of how Americans receive their care and how we physicians provide that care in an expanded government-controlled health care system.

The government is already heavily involved in providing health care to a third of the U.S. population. Medicare, which has been very successful in the eyes of the elderly patients if not a darling of doctors, covers more than 45 million Americans. Medicaid jointly financed by the federal and state governments covers another 60 million poor people. It would seem obvious to expand that program to include the remaining two-thirds.

For a public plan to be viable, it must include an individual mandate to participate. Everyone must be included. If not, the healthy patient by design or by personal desire will be left out and only the sickest and the most expensive will be left in the public plan. A personal mandate will require the government to subsidize the poor, just as it has in the past, but in a more organized system rather than the expensive and dysfunctional care in the emergency department.

Without a universal health plan in place, the ranks of the uninsured will continue to increase. Almost 50 million Americans are currently uninsured, representing well over 15% of our population. When Americans who are out of work in the current recession return to the workforce, the post-recession health insurance policies will not resemble the pre-recession policies. Many of the benefits will disappear and the copayments will most certainly increase. As the pool of insured patients decreases there will be increased competition among health care providers for those few insured patients. We see this already, with hospital and physicians advertising on TV and in the print media. Caught between increased cost and falling profits, insurers will have to choose between increased premiums or cutting doctors fees. The day may come when Medicare's physician fee schedule could be a welcome lifeboat for physicians' practices.

In his response to President Obama's address to the American Medical Association in June, AMA's leadership echoed the need for universal care, but indicated that a payment schedule based on Medicare rates was unacceptable. The AMA has been reluctant to articulate just what sort of universal health insurance plan is acceptable, public or private.

Nevertheless, the process of achieving a federal insurance plan has been much different than that of the Clinton plan in 1993. This time there has been a significant bargaining between Congress and the health providers. The word has been sent out by the Democratic Congress that if you want to take part in the formative process, negative advertising and publicity will lock you out. So at this point everyone is in until they are out. The pharmaceutical industry has indicated that it will provide an $80 billion savings over a 10-year period to the elderly if it limits the reduction in drug coverage to Medicare recipients trapped in the Part D “doughnut hole.” The major hospital associations pledged to save $150 billion dollars providing that the new public plan will cover the indigent. And the AMA has agreed to support HR 3200.

There is considerable concern about cost, which is now estimated at $900 million over the next 10 years. Congress hardly blinked an eye when they spent well over that in a useless war in Iraq. The social and economic necessity of a universal health plan is obvious. To achieve that, a robust universal public insurance foundation is essential. Any thing short of that will lead to further deterioration in American health care.

The development of the coronary care unit in the mid-1960s was a seminal event in clinical medicine. It recognized the gravity of the first few hours and days of an acute myocardial infarction and revealed a dimension of pathology previously unknown to the clinician.

These observations led to an expansion of clinical research and therapy in cardiology, which continues today. Patients with acute myocardial infarction, a clinical event first described by Dr. James Herrick in 1912, were well known. But it was not until the opening of CCUs in medical centers in the United States and England that we began to fully understand the clinical events that resulted from coronary artery thrombosis. The CCU was the launching pad from which that research evolved over the next half century.

Initially, the CCU was largely an arrhythmia-monitoring unit, but it soon became a clinical laboratory aimed at the recognition of left ventricular failure and homodynamic instability based on monitoring of cardiac function with the Swan-Ganz catheter. It became the site where we first examine the role of catecholamines and vasodilators in the treatment of hypotension and shock.

The CCU has changed significantly since then.

The spectrum of cardiac pathology has broadened with the development of biomarkers that expanded our understanding of the early expression of ischemia. These biomarker determinations identified the previously unrecognized magnitude of coronary ischemia. Cardiologists became more interested in the acute coronary syndromes and early angiographic expression of disease.

As a result, the CCU is now largely the repository of complicated ST-segment elevation myocardial infarctions, post complex percutaneous coronary intervention, and the treatment of patients with homodynamic instability and left ventricular failure.

The CCU has also blended into the hospital complex of intensive care units. In many institutions, the boundary between ICU and CCU has become blurred beyond recognition.

During a recent rounding rotation on our consult service, I was struck by the expansion of ICU beds in our institution and the role that the intensivist plays in the administration and care of patients in these units. The management of a broad spectrum of diseases, from pulmonary failure to postoperative neurosurgical problems, is no longer the responsibility of the medical discipline of origin. It is assigned instead to the domain of the generic intensivist once the patient enters the ICU.

The same pressures to provide round-the-clock care have led to the gradual invasion of the CCU by the ubiquitous intensivist. Health planners, including one of the leaders in the reinvention of health care, the Leapfrog Group, has proposed that all intensive care units, including the coronary care unit, should be under the control of a resident intensivist, who often doubles as a hospitalist. They point to studies that show an improvement in ICU mortality by up to 40% in such units (www.leapfroggroup.org/about_us/leapfrog-factsheet

The American College of Chest Physicians and the Committee on Manpower of Pulmonary and Critical Care Societies have led the expansion of the role of the intensivist. In a recent report to Congress, the groups specifically emphasized the short supply of intensivist and their important role in the care of ICU patients (Senate Report 108-81).

Generic use of intensivists in ICUs because of their round-the-clock availability in the hospital is not necessarily a step forward. There is no question that immediate physician availability is essential to the care of the critically ill patient. But the physician best equipped to render this care is the one who is trained to deal with that specialty. To fulfill our responsibility for cardiac care, we must provide more CCU experience during cardiology training. Those challenges are outlined in an excellent editorial by Dr. Jason Katz and colleagues that emphasizes the need for intensivist training in cardiology programs (J. Am. Coll. Cardiol. 2007;49:1279).

There is reason to be concerned that training has become subservient to the demands of technologies that are more lucrative but less than supportive of our role as cardiologists. In order for cardiologists to render quality care in the future, more CCU experience is essential in our training programs.

The CCU remains an essential clinical laboratory for the care of the cardiac patient and we must maintain our role in that environment.

The development of the coronary care unit in the mid-1960s was a seminal event in clinical medicine. It recognized the gravity of the first few hours and days of an acute myocardial infarction and revealed a dimension of pathology previously unknown to the clinician.

These observations led to an expansion of clinical research and therapy in cardiology, which continues today. Patients with acute myocardial infarction, a clinical event first described by Dr. James Herrick in 1912, were well known. But it was not until the opening of CCUs in medical centers in the United States and England that we began to fully understand the clinical events that resulted from coronary artery thrombosis. The CCU was the launching pad from which that research evolved over the next half century.

Initially, the CCU was largely an arrhythmia-monitoring unit, but it soon became a clinical laboratory aimed at the recognition of left ventricular failure and homodynamic instability based on monitoring of cardiac function with the Swan-Ganz catheter. It became the site where we first examine the role of catecholamines and vasodilators in the treatment of hypotension and shock.

The CCU has changed significantly since then.

The spectrum of cardiac pathology has broadened with the development of biomarkers that expanded our understanding of the early expression of ischemia. These biomarker determinations identified the previously unrecognized magnitude of coronary ischemia. Cardiologists became more interested in the acute coronary syndromes and early angiographic expression of disease.

As a result, the CCU is now largely the repository of complicated ST-segment elevation myocardial infarctions, post complex percutaneous coronary intervention, and the treatment of patients with homodynamic instability and left ventricular failure.

The CCU has also blended into the hospital complex of intensive care units. In many institutions, the boundary between ICU and CCU has become blurred beyond recognition.

During a recent rounding rotation on our consult service, I was struck by the expansion of ICU beds in our institution and the role that the intensivist plays in the administration and care of patients in these units. The management of a broad spectrum of diseases, from pulmonary failure to postoperative neurosurgical problems, is no longer the responsibility of the medical discipline of origin. It is assigned instead to the domain of the generic intensivist once the patient enters the ICU.

The same pressures to provide round-the-clock care have led to the gradual invasion of the CCU by the ubiquitous intensivist. Health planners, including one of the leaders in the reinvention of health care, the Leapfrog Group, has proposed that all intensive care units, including the coronary care unit, should be under the control of a resident intensivist, who often doubles as a hospitalist. They point to studies that show an improvement in ICU mortality by up to 40% in such units (www.leapfroggroup.org/about_us/leapfrog-factsheet

The American College of Chest Physicians and the Committee on Manpower of Pulmonary and Critical Care Societies have led the expansion of the role of the intensivist. In a recent report to Congress, the groups specifically emphasized the short supply of intensivist and their important role in the care of ICU patients (Senate Report 108-81).

Generic use of intensivists in ICUs because of their round-the-clock availability in the hospital is not necessarily a step forward. There is no question that immediate physician availability is essential to the care of the critically ill patient. But the physician best equipped to render this care is the one who is trained to deal with that specialty. To fulfill our responsibility for cardiac care, we must provide more CCU experience during cardiology training. Those challenges are outlined in an excellent editorial by Dr. Jason Katz and colleagues that emphasizes the need for intensivist training in cardiology programs (J. Am. Coll. Cardiol. 2007;49:1279).

There is reason to be concerned that training has become subservient to the demands of technologies that are more lucrative but less than supportive of our role as cardiologists. In order for cardiologists to render quality care in the future, more CCU experience is essential in our training programs.

The CCU remains an essential clinical laboratory for the care of the cardiac patient and we must maintain our role in that environment.

The development of the coronary care unit in the mid-1960s was a seminal event in clinical medicine. It recognized the gravity of the first few hours and days of an acute myocardial infarction and revealed a dimension of pathology previously unknown to the clinician.

These observations led to an expansion of clinical research and therapy in cardiology, which continues today. Patients with acute myocardial infarction, a clinical event first described by Dr. James Herrick in 1912, were well known. But it was not until the opening of CCUs in medical centers in the United States and England that we began to fully understand the clinical events that resulted from coronary artery thrombosis. The CCU was the launching pad from which that research evolved over the next half century.

Initially, the CCU was largely an arrhythmia-monitoring unit, but it soon became a clinical laboratory aimed at the recognition of left ventricular failure and homodynamic instability based on monitoring of cardiac function with the Swan-Ganz catheter. It became the site where we first examine the role of catecholamines and vasodilators in the treatment of hypotension and shock.

The CCU has changed significantly since then.

The spectrum of cardiac pathology has broadened with the development of biomarkers that expanded our understanding of the early expression of ischemia. These biomarker determinations identified the previously unrecognized magnitude of coronary ischemia. Cardiologists became more interested in the acute coronary syndromes and early angiographic expression of disease.

As a result, the CCU is now largely the repository of complicated ST-segment elevation myocardial infarctions, post complex percutaneous coronary intervention, and the treatment of patients with homodynamic instability and left ventricular failure.

The CCU has also blended into the hospital complex of intensive care units. In many institutions, the boundary between ICU and CCU has become blurred beyond recognition.

During a recent rounding rotation on our consult service, I was struck by the expansion of ICU beds in our institution and the role that the intensivist plays in the administration and care of patients in these units. The management of a broad spectrum of diseases, from pulmonary failure to postoperative neurosurgical problems, is no longer the responsibility of the medical discipline of origin. It is assigned instead to the domain of the generic intensivist once the patient enters the ICU.

The same pressures to provide round-the-clock care have led to the gradual invasion of the CCU by the ubiquitous intensivist. Health planners, including one of the leaders in the reinvention of health care, the Leapfrog Group, has proposed that all intensive care units, including the coronary care unit, should be under the control of a resident intensivist, who often doubles as a hospitalist. They point to studies that show an improvement in ICU mortality by up to 40% in such units (www.leapfroggroup.org/about_us/leapfrog-factsheet

The American College of Chest Physicians and the Committee on Manpower of Pulmonary and Critical Care Societies have led the expansion of the role of the intensivist. In a recent report to Congress, the groups specifically emphasized the short supply of intensivist and their important role in the care of ICU patients (Senate Report 108-81).

Generic use of intensivists in ICUs because of their round-the-clock availability in the hospital is not necessarily a step forward. There is no question that immediate physician availability is essential to the care of the critically ill patient. But the physician best equipped to render this care is the one who is trained to deal with that specialty. To fulfill our responsibility for cardiac care, we must provide more CCU experience during cardiology training. Those challenges are outlined in an excellent editorial by Dr. Jason Katz and colleagues that emphasizes the need for intensivist training in cardiology programs (J. Am. Coll. Cardiol. 2007;49:1279).

There is reason to be concerned that training has become subservient to the demands of technologies that are more lucrative but less than supportive of our role as cardiologists. In order for cardiologists to render quality care in the future, more CCU experience is essential in our training programs.

The CCU remains an essential clinical laboratory for the care of the cardiac patient and we must maintain our role in that environment.

The recent problems of Medtronic's Fidelis leads in defibrillator-pacemakers reminded me of the sea change that has occurred in medical therapeutics.

Device therapeutics has fast become a major mode of treatment in a variety of fields including cardiology, as new targets for drug therapy have become limited. In the old days, if the physician observed an adverse drug effect, the antidote was easily accomplished by stopping the medication. That is not to say that there were no long-term effects of disastrous proportion associated with oral or intravenous therapy. Drug-induced hepatitis, agranulocytosis, and shock, to name a few, still are potential adverse effects with parenteral or oral drug administration.

But with the development of device therapy, dealing with adverse events has become much more complicated. The advent of the implantable pacemaker seems to be the watershed device that changed the therapeutic landscape. I recall talking to Dr. Bill Chardack, a surgeon and coinventor with Wilson Greatbach of the implantable transvenous pacemaker in the mid 1960s about the issue of removing the right ventricular catheter should the site become infected or the catheter cease to function. His response was “that the issue was getting them in, not getting them out.” Well, a lot of catheters have been implanted since then, and many have become dysfunctional and remain in patients and can now be classified as biological “debris.”

Artificial heart valves, particularly in their early developmental stages, had to be removed as a result of thrombus formation or structural failure. Many of these valve failures required emergency surgery. Later, cracks developed in some of the aortic valve struts, which again led to both urgent and prophylactic surgery when they were identified with special x-rays. The implantation of many and varied of coronary stents, which obviously cannot be removed, created a new mechanical disease superimposed onto naturally occurring coronary artery disease. Most recently, a host of new devices has emerged that remodel the left ventricle or defibrillate it depending upon the therapeutic target. Many of these are experimental, meaning that they may or may not be of therapeutic benefit, and are implanted into the heart without any “exit strategy” should they be shown to be ineffective or hazardous.

The most troubling among them are the defibrillators. Patients have been told that without such a device they are facing imminent death. Implantation of this device has been advised on the basis of guidelines that presume that the rate of adverse events is small and the benefit is large. The benefit remains the same, but now, in the face of increased adverse events, the equation has changed. It does appear that most of the 150,000 Fidelis leads need to be disconnected (“Removing Medtronic Heart Cables is Hard Choice,” New York Times, April 7, 2009, p. B1). The easiest method is to disconnect the lead from the box and reimplant another lead. Removal of the lead is precarious and can result in rupture of the right ventricle or atrium. According to recent advisories, it should be performed only in experienced hands, if at all. Replacement with another lead may require a different vein and possibly a new defibrillator box. All of this adds up to considerable surgery in an aging population with significant left ventricular disease.

The most recent device adventure is the Watchman atrial appendage occlusive device to prevent systemic emboli in atrial fibrillation. The recently concluded PROTECT-AF study compares the device with warfarin in a small noninferiority trial. Many of the patients were not actually candidates for anticoagulant therapy; with 68% of the patients having CHADS scores of 1–2, according to the FDA's briefing document. The study demonstrated in a highly select group of patients that the device was not inferior to warfarin therapy. The Food and Drug Administration's Circulatory System Devices Panel voted in favor of approving the device by a narrow margin of 7–5. The panel historically has approved devices if they “work” and not always if they benefit patients.

The remains of old pacemakers and devices implanted for clinical research in patients may be lifesaving and may indeed relieve symptoms, but they may also end up in “human space,” not unlike old space satellites that are circling our planet. Seemingly harmless, this “debris” may become an issue in the future.

The recent problems of Medtronic's Fidelis leads in defibrillator-pacemakers reminded me of the sea change that has occurred in medical therapeutics.

Device therapeutics has fast become a major mode of treatment in a variety of fields including cardiology, as new targets for drug therapy have become limited. In the old days, if the physician observed an adverse drug effect, the antidote was easily accomplished by stopping the medication. That is not to say that there were no long-term effects of disastrous proportion associated with oral or intravenous therapy. Drug-induced hepatitis, agranulocytosis, and shock, to name a few, still are potential adverse effects with parenteral or oral drug administration.

But with the development of device therapy, dealing with adverse events has become much more complicated. The advent of the implantable pacemaker seems to be the watershed device that changed the therapeutic landscape. I recall talking to Dr. Bill Chardack, a surgeon and coinventor with Wilson Greatbach of the implantable transvenous pacemaker in the mid 1960s about the issue of removing the right ventricular catheter should the site become infected or the catheter cease to function. His response was “that the issue was getting them in, not getting them out.” Well, a lot of catheters have been implanted since then, and many have become dysfunctional and remain in patients and can now be classified as biological “debris.”

Artificial heart valves, particularly in their early developmental stages, had to be removed as a result of thrombus formation or structural failure. Many of these valve failures required emergency surgery. Later, cracks developed in some of the aortic valve struts, which again led to both urgent and prophylactic surgery when they were identified with special x-rays. The implantation of many and varied of coronary stents, which obviously cannot be removed, created a new mechanical disease superimposed onto naturally occurring coronary artery disease. Most recently, a host of new devices has emerged that remodel the left ventricle or defibrillate it depending upon the therapeutic target. Many of these are experimental, meaning that they may or may not be of therapeutic benefit, and are implanted into the heart without any “exit strategy” should they be shown to be ineffective or hazardous.

The most troubling among them are the defibrillators. Patients have been told that without such a device they are facing imminent death. Implantation of this device has been advised on the basis of guidelines that presume that the rate of adverse events is small and the benefit is large. The benefit remains the same, but now, in the face of increased adverse events, the equation has changed. It does appear that most of the 150,000 Fidelis leads need to be disconnected (“Removing Medtronic Heart Cables is Hard Choice,” New York Times, April 7, 2009, p. B1). The easiest method is to disconnect the lead from the box and reimplant another lead. Removal of the lead is precarious and can result in rupture of the right ventricle or atrium. According to recent advisories, it should be performed only in experienced hands, if at all. Replacement with another lead may require a different vein and possibly a new defibrillator box. All of this adds up to considerable surgery in an aging population with significant left ventricular disease.

The most recent device adventure is the Watchman atrial appendage occlusive device to prevent systemic emboli in atrial fibrillation. The recently concluded PROTECT-AF study compares the device with warfarin in a small noninferiority trial. Many of the patients were not actually candidates for anticoagulant therapy; with 68% of the patients having CHADS scores of 1–2, according to the FDA's briefing document. The study demonstrated in a highly select group of patients that the device was not inferior to warfarin therapy. The Food and Drug Administration's Circulatory System Devices Panel voted in favor of approving the device by a narrow margin of 7–5. The panel historically has approved devices if they “work” and not always if they benefit patients.

The remains of old pacemakers and devices implanted for clinical research in patients may be lifesaving and may indeed relieve symptoms, but they may also end up in “human space,” not unlike old space satellites that are circling our planet. Seemingly harmless, this “debris” may become an issue in the future.

The recent problems of Medtronic's Fidelis leads in defibrillator-pacemakers reminded me of the sea change that has occurred in medical therapeutics.

Device therapeutics has fast become a major mode of treatment in a variety of fields including cardiology, as new targets for drug therapy have become limited. In the old days, if the physician observed an adverse drug effect, the antidote was easily accomplished by stopping the medication. That is not to say that there were no long-term effects of disastrous proportion associated with oral or intravenous therapy. Drug-induced hepatitis, agranulocytosis, and shock, to name a few, still are potential adverse effects with parenteral or oral drug administration.

But with the development of device therapy, dealing with adverse events has become much more complicated. The advent of the implantable pacemaker seems to be the watershed device that changed the therapeutic landscape. I recall talking to Dr. Bill Chardack, a surgeon and coinventor with Wilson Greatbach of the implantable transvenous pacemaker in the mid 1960s about the issue of removing the right ventricular catheter should the site become infected or the catheter cease to function. His response was “that the issue was getting them in, not getting them out.” Well, a lot of catheters have been implanted since then, and many have become dysfunctional and remain in patients and can now be classified as biological “debris.”

Artificial heart valves, particularly in their early developmental stages, had to be removed as a result of thrombus formation or structural failure. Many of these valve failures required emergency surgery. Later, cracks developed in some of the aortic valve struts, which again led to both urgent and prophylactic surgery when they were identified with special x-rays. The implantation of many and varied of coronary stents, which obviously cannot be removed, created a new mechanical disease superimposed onto naturally occurring coronary artery disease. Most recently, a host of new devices has emerged that remodel the left ventricle or defibrillate it depending upon the therapeutic target. Many of these are experimental, meaning that they may or may not be of therapeutic benefit, and are implanted into the heart without any “exit strategy” should they be shown to be ineffective or hazardous.

The most troubling among them are the defibrillators. Patients have been told that without such a device they are facing imminent death. Implantation of this device has been advised on the basis of guidelines that presume that the rate of adverse events is small and the benefit is large. The benefit remains the same, but now, in the face of increased adverse events, the equation has changed. It does appear that most of the 150,000 Fidelis leads need to be disconnected (“Removing Medtronic Heart Cables is Hard Choice,” New York Times, April 7, 2009, p. B1). The easiest method is to disconnect the lead from the box and reimplant another lead. Removal of the lead is precarious and can result in rupture of the right ventricle or atrium. According to recent advisories, it should be performed only in experienced hands, if at all. Replacement with another lead may require a different vein and possibly a new defibrillator box. All of this adds up to considerable surgery in an aging population with significant left ventricular disease.

The most recent device adventure is the Watchman atrial appendage occlusive device to prevent systemic emboli in atrial fibrillation. The recently concluded PROTECT-AF study compares the device with warfarin in a small noninferiority trial. Many of the patients were not actually candidates for anticoagulant therapy; with 68% of the patients having CHADS scores of 1–2, according to the FDA's briefing document. The study demonstrated in a highly select group of patients that the device was not inferior to warfarin therapy. The Food and Drug Administration's Circulatory System Devices Panel voted in favor of approving the device by a narrow margin of 7–5. The panel historically has approved devices if they “work” and not always if they benefit patients.

The remains of old pacemakers and devices implanted for clinical research in patients may be lifesaving and may indeed relieve symptoms, but they may also end up in “human space,” not unlike old space satellites that are circling our planet. Seemingly harmless, this “debris” may become an issue in the future.

There is mounting frustration for both clinical trialists and the pharmaceutical industry with the difficulty of moving clinical trial results to patient care. Over the past 10 years, there has been a paucity of new cardiac drugs approved by the Food and Drug Administration. This drought follows a flood of drugs that came into clinical care in the previous 2 decades.

The increasing difficulty and expense of carrying out clinical trials in the United States has led to reliance on patient recruitment in Eastern Europe and Asia.

As a result, a number of the large pharmaceutical companies have withdrawn from the development of new cardiac drugs and have moved to other more fertile disease systems. At the same time, because of the current economic environment, it has been difficult to obtain venture capital funding to initiate studies of new drugs.

Nevertheless, some areas that remain “hot” targets of cardiovascular disease are receiving continued interest and support by Big Pharma. This has been particularly true in acute coronary syndromes: Although long-term mortality rates have changed dramatically, new interventional procedures and change in diagnostic criteria have provided a ready supply of patients available for recruitment.

The area of heart failure, where the 60-day mortality rate for hospitalized patients exceeds 25% in spite of advances with ACE inhibitors and beta-blockers, has also been an appealing target of research.

Although the interest in these areas is welcome, it raises some interesting issues for the clinician when interpreting the results of intervention.

In acute coronary syndromes, for which a decrease in mortality had been the major therapeutic target, mortality now represents less than 25% of all combined events in some clinical trials. As mortality became a smaller part of the end point measurement, troponin-defined reinfarction increased in both statistical and clinical significance. As we all know, reinfarction is subject to significant variation and interpretation as more sensitive biomarkers reflect smaller degrees of infarction which may be of questionable clinical importance.

The clinical relevance of reinfarction has come into special prominence as we develop more potent antithrombotic and antiplatelet agents that are associated with an increased potential for major bleeding. The benefit of achieving this combined end point, dominated by myocardial infarction determined using a biomarker, weighed against the potential of increased bleeding risk, is less obvious.

The investigation of new drugs for the treatment of heart failure, particularly in an aging population, has resulted in a search for relevant measures that truly impact a patient's life. In addition to mortality, rehospitalization is the most commonly-used measure of therapeutic success, reflecting both the clinical and economic burdens of the disease.

In young heart failure patients, subsequent hospitalization could result from a cardiac event. But as our population ages and we apply new therapies to older patients, total hospitalization has become much more heterogeneous. Rehospitalization in octogenarians, who increasingly dominate our heart failure population, may have different implications. The readmissions may be a result of noncardiac concerns such as cancer, pulmonary disease, trauma, or debilitating neurologic events.

In addition, the increasing reliance on patients from Eastern Europe and Asia to participate in clinical trials, because of economic and legal restrictions, has made the use of rehospitalization a less certain end point when applying trial results to Western Europe and North America.

The increased reliance upon these patients in both heart failure and ACS trials has become a necessity for sufficient recruitment. A recent analysis of the EVEREST (Efficacy of Vasopressin Antagonism in Heart Failure: Outcome Study with Tolvaptan) trial revealed considerable baseline and mortality differences between patients randomized in Eastern Europe and those participants from the United States and Western Europe (J. Am. Coll. Cardiol. 2008;52:1640-8).

All of these issues have challenged designers of clinical trials to create a study that is relevant to local societal requirements. The world has not become so flat that studies in India and China can have complete relevancy to Americans when we stray from hard core end points such as mortality.

There is mounting frustration for both clinical trialists and the pharmaceutical industry with the difficulty of moving clinical trial results to patient care. Over the past 10 years, there has been a paucity of new cardiac drugs approved by the Food and Drug Administration. This drought follows a flood of drugs that came into clinical care in the previous 2 decades.

The increasing difficulty and expense of carrying out clinical trials in the United States has led to reliance on patient recruitment in Eastern Europe and Asia.

As a result, a number of the large pharmaceutical companies have withdrawn from the development of new cardiac drugs and have moved to other more fertile disease systems. At the same time, because of the current economic environment, it has been difficult to obtain venture capital funding to initiate studies of new drugs.

Nevertheless, some areas that remain “hot” targets of cardiovascular disease are receiving continued interest and support by Big Pharma. This has been particularly true in acute coronary syndromes: Although long-term mortality rates have changed dramatically, new interventional procedures and change in diagnostic criteria have provided a ready supply of patients available for recruitment.

The area of heart failure, where the 60-day mortality rate for hospitalized patients exceeds 25% in spite of advances with ACE inhibitors and beta-blockers, has also been an appealing target of research.

Although the interest in these areas is welcome, it raises some interesting issues for the clinician when interpreting the results of intervention.

In acute coronary syndromes, for which a decrease in mortality had been the major therapeutic target, mortality now represents less than 25% of all combined events in some clinical trials. As mortality became a smaller part of the end point measurement, troponin-defined reinfarction increased in both statistical and clinical significance. As we all know, reinfarction is subject to significant variation and interpretation as more sensitive biomarkers reflect smaller degrees of infarction which may be of questionable clinical importance.

The clinical relevance of reinfarction has come into special prominence as we develop more potent antithrombotic and antiplatelet agents that are associated with an increased potential for major bleeding. The benefit of achieving this combined end point, dominated by myocardial infarction determined using a biomarker, weighed against the potential of increased bleeding risk, is less obvious.

The investigation of new drugs for the treatment of heart failure, particularly in an aging population, has resulted in a search for relevant measures that truly impact a patient's life. In addition to mortality, rehospitalization is the most commonly-used measure of therapeutic success, reflecting both the clinical and economic burdens of the disease.

In young heart failure patients, subsequent hospitalization could result from a cardiac event. But as our population ages and we apply new therapies to older patients, total hospitalization has become much more heterogeneous. Rehospitalization in octogenarians, who increasingly dominate our heart failure population, may have different implications. The readmissions may be a result of noncardiac concerns such as cancer, pulmonary disease, trauma, or debilitating neurologic events.

In addition, the increasing reliance on patients from Eastern Europe and Asia to participate in clinical trials, because of economic and legal restrictions, has made the use of rehospitalization a less certain end point when applying trial results to Western Europe and North America.

The increased reliance upon these patients in both heart failure and ACS trials has become a necessity for sufficient recruitment. A recent analysis of the EVEREST (Efficacy of Vasopressin Antagonism in Heart Failure: Outcome Study with Tolvaptan) trial revealed considerable baseline and mortality differences between patients randomized in Eastern Europe and those participants from the United States and Western Europe (J. Am. Coll. Cardiol. 2008;52:1640-8).

All of these issues have challenged designers of clinical trials to create a study that is relevant to local societal requirements. The world has not become so flat that studies in India and China can have complete relevancy to Americans when we stray from hard core end points such as mortality.

There is mounting frustration for both clinical trialists and the pharmaceutical industry with the difficulty of moving clinical trial results to patient care. Over the past 10 years, there has been a paucity of new cardiac drugs approved by the Food and Drug Administration. This drought follows a flood of drugs that came into clinical care in the previous 2 decades.

The increasing difficulty and expense of carrying out clinical trials in the United States has led to reliance on patient recruitment in Eastern Europe and Asia.

As a result, a number of the large pharmaceutical companies have withdrawn from the development of new cardiac drugs and have moved to other more fertile disease systems. At the same time, because of the current economic environment, it has been difficult to obtain venture capital funding to initiate studies of new drugs.

Nevertheless, some areas that remain “hot” targets of cardiovascular disease are receiving continued interest and support by Big Pharma. This has been particularly true in acute coronary syndromes: Although long-term mortality rates have changed dramatically, new interventional procedures and change in diagnostic criteria have provided a ready supply of patients available for recruitment.

The area of heart failure, where the 60-day mortality rate for hospitalized patients exceeds 25% in spite of advances with ACE inhibitors and beta-blockers, has also been an appealing target of research.

Although the interest in these areas is welcome, it raises some interesting issues for the clinician when interpreting the results of intervention.

In acute coronary syndromes, for which a decrease in mortality had been the major therapeutic target, mortality now represents less than 25% of all combined events in some clinical trials. As mortality became a smaller part of the end point measurement, troponin-defined reinfarction increased in both statistical and clinical significance. As we all know, reinfarction is subject to significant variation and interpretation as more sensitive biomarkers reflect smaller degrees of infarction which may be of questionable clinical importance.

The clinical relevance of reinfarction has come into special prominence as we develop more potent antithrombotic and antiplatelet agents that are associated with an increased potential for major bleeding. The benefit of achieving this combined end point, dominated by myocardial infarction determined using a biomarker, weighed against the potential of increased bleeding risk, is less obvious.

The investigation of new drugs for the treatment of heart failure, particularly in an aging population, has resulted in a search for relevant measures that truly impact a patient's life. In addition to mortality, rehospitalization is the most commonly-used measure of therapeutic success, reflecting both the clinical and economic burdens of the disease.

In young heart failure patients, subsequent hospitalization could result from a cardiac event. But as our population ages and we apply new therapies to older patients, total hospitalization has become much more heterogeneous. Rehospitalization in octogenarians, who increasingly dominate our heart failure population, may have different implications. The readmissions may be a result of noncardiac concerns such as cancer, pulmonary disease, trauma, or debilitating neurologic events.

In addition, the increasing reliance on patients from Eastern Europe and Asia to participate in clinical trials, because of economic and legal restrictions, has made the use of rehospitalization a less certain end point when applying trial results to Western Europe and North America.

The increased reliance upon these patients in both heart failure and ACS trials has become a necessity for sufficient recruitment. A recent analysis of the EVEREST (Efficacy of Vasopressin Antagonism in Heart Failure: Outcome Study with Tolvaptan) trial revealed considerable baseline and mortality differences between patients randomized in Eastern Europe and those participants from the United States and Western Europe (J. Am. Coll. Cardiol. 2008;52:1640-8).

All of these issues have challenged designers of clinical trials to create a study that is relevant to local societal requirements. The world has not become so flat that studies in India and China can have complete relevancy to Americans when we stray from hard core end points such as mortality.

This column has in the past commented on the shortcomings of guidelines in a number of clinical situations, including the expanded use of coronary interventional procedures and the implantation of automatic defibrillators in heart failure.

Guidelines designed as advisory to clinicians have achieved almost biblical, or, if you will, Koranic, status in the care of patients.

As a result, many physicians young and old have developed a state of mental paralysis, unable to make clinical decisions based on pathophysiology, pharmacology, or social status of the patient. They go through a maze of decision trees that often lead to a clinical judgment without fully considering the patient's status.

The process is reminiscent of the Yogi Berra aphorism, “When you come to a fork in the road, take it.”

The recent analysis by the Duke Clinical Research Institute of the ACC/AHA Clinical Practice Guidelines process over the last 25 years provides an incisive examination of the weakness of this otherwise well meaning process (JAMA 2009;301:831-41).

Guidelines were created largely to incorporate the results of randomized clinical trials (RCTs) into clinical care. Such trials, designed to prove the efficacy of new drugs and devices, represent major investments by pharmaceutical companies, which are focused on testing their products in the most advantageous environment. As a result, many patients with comorbid illnesses are excluded to provide a clear message about the drugs' specificity in a given illness.

Those of us who straddle the clinical research world and clinical practice know very well patients included in trials bear little resemblance to those we treat at the bedside or in the clinic. Most Medicare beneficiaries have multiple comorbidities that affect both therapy and outcome. Nevertheless, the guidelines have used RCT results when available.

Unfortunately, RCTs cover only a small fraction of clinical practice. In lieu of RCT data, “expert opinion and standard of care” were used to fill the gaps in evidence, which comprise most of the clinical decision process.

This reliance on expert opinion in guideline committees also has been challenged as a potential source of bias. Industry has had such profound impact on clinical research and trials that it is almost impossible to find physicians with expertise who do not have some potential bias as a result of research support, advisory committees, speakers' bureaus, and consulting fees. Many of these experts included in guideline panels have honest scientific investment in therapeutic concepts, which also have the potential to cloud their judgment.

Unfortunately, there is a paucity of guidelines that are even supported by RCTs. According to the Duke analysis, with a class I recommendation, defined as when “there is evidence and/or general agreement that a given procedure is useful and effective” only 19% had a class A level of evidence, defined as being supported with RCT data. In 36% of the class I recommendations, “expert opinion, case studies or standard of care” —class C evidence level—was the support. The analysis further suggested that as guidelines expanded over time, the use of class II recommendations, where there is “conflicting evidence and/or a diversion of opinion” has increased.

To put this in the context of current clinical practice, the report cited data from the ACC National Registry showing that 30% of all the percutaneous coronary interventions and 39% of those performed after an acute MI fell under class II indications. This represented 115,000 and 45,000 procedures, respectively.

The development of standards for medical therapy is important for the care of our patients, and RCTs are crucial to understanding the safety and benefit of new therapies. Much of the success in reducing the mortality in heart disease has been the result of the incorporation of RCT results into bedside care.

Nevertheless, our current process needs to be improved. We need to develop a mechanism for testing therapy in the real world dominated by an increasingly aging patient population with myriad comorbid diseases.

The current attempts by the Centers for Medicare and Medicaid Services to assess the efficacy and safety of new therapies have been inadequate. The development of registries such as the ACC's ICD Registry, has not met the full potential of this process.

We need randomized trial data of real patients as a new therapy is introduced in clinical care. In the absence of that, the collection of registry data must be strengthened and the analyses made available to the medical community as soon as possible.

This column has in the past commented on the shortcomings of guidelines in a number of clinical situations, including the expanded use of coronary interventional procedures and the implantation of automatic defibrillators in heart failure.

Guidelines designed as advisory to clinicians have achieved almost biblical, or, if you will, Koranic, status in the care of patients.

As a result, many physicians young and old have developed a state of mental paralysis, unable to make clinical decisions based on pathophysiology, pharmacology, or social status of the patient. They go through a maze of decision trees that often lead to a clinical judgment without fully considering the patient's status.

The process is reminiscent of the Yogi Berra aphorism, “When you come to a fork in the road, take it.”

The recent analysis by the Duke Clinical Research Institute of the ACC/AHA Clinical Practice Guidelines process over the last 25 years provides an incisive examination of the weakness of this otherwise well meaning process (JAMA 2009;301:831-41).

Guidelines were created largely to incorporate the results of randomized clinical trials (RCTs) into clinical care. Such trials, designed to prove the efficacy of new drugs and devices, represent major investments by pharmaceutical companies, which are focused on testing their products in the most advantageous environment. As a result, many patients with comorbid illnesses are excluded to provide a clear message about the drugs' specificity in a given illness.

Those of us who straddle the clinical research world and clinical practice know very well patients included in trials bear little resemblance to those we treat at the bedside or in the clinic. Most Medicare beneficiaries have multiple comorbidities that affect both therapy and outcome. Nevertheless, the guidelines have used RCT results when available.

Unfortunately, RCTs cover only a small fraction of clinical practice. In lieu of RCT data, “expert opinion and standard of care” were used to fill the gaps in evidence, which comprise most of the clinical decision process.

This reliance on expert opinion in guideline committees also has been challenged as a potential source of bias. Industry has had such profound impact on clinical research and trials that it is almost impossible to find physicians with expertise who do not have some potential bias as a result of research support, advisory committees, speakers' bureaus, and consulting fees. Many of these experts included in guideline panels have honest scientific investment in therapeutic concepts, which also have the potential to cloud their judgment.

Unfortunately, there is a paucity of guidelines that are even supported by RCTs. According to the Duke analysis, with a class I recommendation, defined as when “there is evidence and/or general agreement that a given procedure is useful and effective” only 19% had a class A level of evidence, defined as being supported with RCT data. In 36% of the class I recommendations, “expert opinion, case studies or standard of care” —class C evidence level—was the support. The analysis further suggested that as guidelines expanded over time, the use of class II recommendations, where there is “conflicting evidence and/or a diversion of opinion” has increased.

To put this in the context of current clinical practice, the report cited data from the ACC National Registry showing that 30% of all the percutaneous coronary interventions and 39% of those performed after an acute MI fell under class II indications. This represented 115,000 and 45,000 procedures, respectively.

The development of standards for medical therapy is important for the care of our patients, and RCTs are crucial to understanding the safety and benefit of new therapies. Much of the success in reducing the mortality in heart disease has been the result of the incorporation of RCT results into bedside care.

Nevertheless, our current process needs to be improved. We need to develop a mechanism for testing therapy in the real world dominated by an increasingly aging patient population with myriad comorbid diseases.

The current attempts by the Centers for Medicare and Medicaid Services to assess the efficacy and safety of new therapies have been inadequate. The development of registries such as the ACC's ICD Registry, has not met the full potential of this process.

We need randomized trial data of real patients as a new therapy is introduced in clinical care. In the absence of that, the collection of registry data must be strengthened and the analyses made available to the medical community as soon as possible.

This column has in the past commented on the shortcomings of guidelines in a number of clinical situations, including the expanded use of coronary interventional procedures and the implantation of automatic defibrillators in heart failure.

Guidelines designed as advisory to clinicians have achieved almost biblical, or, if you will, Koranic, status in the care of patients.

As a result, many physicians young and old have developed a state of mental paralysis, unable to make clinical decisions based on pathophysiology, pharmacology, or social status of the patient. They go through a maze of decision trees that often lead to a clinical judgment without fully considering the patient's status.

The process is reminiscent of the Yogi Berra aphorism, “When you come to a fork in the road, take it.”

The recent analysis by the Duke Clinical Research Institute of the ACC/AHA Clinical Practice Guidelines process over the last 25 years provides an incisive examination of the weakness of this otherwise well meaning process (JAMA 2009;301:831-41).

Guidelines were created largely to incorporate the results of randomized clinical trials (RCTs) into clinical care. Such trials, designed to prove the efficacy of new drugs and devices, represent major investments by pharmaceutical companies, which are focused on testing their products in the most advantageous environment. As a result, many patients with comorbid illnesses are excluded to provide a clear message about the drugs' specificity in a given illness.

Those of us who straddle the clinical research world and clinical practice know very well patients included in trials bear little resemblance to those we treat at the bedside or in the clinic. Most Medicare beneficiaries have multiple comorbidities that affect both therapy and outcome. Nevertheless, the guidelines have used RCT results when available.

Unfortunately, RCTs cover only a small fraction of clinical practice. In lieu of RCT data, “expert opinion and standard of care” were used to fill the gaps in evidence, which comprise most of the clinical decision process.

This reliance on expert opinion in guideline committees also has been challenged as a potential source of bias. Industry has had such profound impact on clinical research and trials that it is almost impossible to find physicians with expertise who do not have some potential bias as a result of research support, advisory committees, speakers' bureaus, and consulting fees. Many of these experts included in guideline panels have honest scientific investment in therapeutic concepts, which also have the potential to cloud their judgment.

Unfortunately, there is a paucity of guidelines that are even supported by RCTs. According to the Duke analysis, with a class I recommendation, defined as when “there is evidence and/or general agreement that a given procedure is useful and effective” only 19% had a class A level of evidence, defined as being supported with RCT data. In 36% of the class I recommendations, “expert opinion, case studies or standard of care” —class C evidence level—was the support. The analysis further suggested that as guidelines expanded over time, the use of class II recommendations, where there is “conflicting evidence and/or a diversion of opinion” has increased.

To put this in the context of current clinical practice, the report cited data from the ACC National Registry showing that 30% of all the percutaneous coronary interventions and 39% of those performed after an acute MI fell under class II indications. This represented 115,000 and 45,000 procedures, respectively.

The development of standards for medical therapy is important for the care of our patients, and RCTs are crucial to understanding the safety and benefit of new therapies. Much of the success in reducing the mortality in heart disease has been the result of the incorporation of RCT results into bedside care.

Nevertheless, our current process needs to be improved. We need to develop a mechanism for testing therapy in the real world dominated by an increasingly aging patient population with myriad comorbid diseases.

The current attempts by the Centers for Medicare and Medicaid Services to assess the efficacy and safety of new therapies have been inadequate. The development of registries such as the ACC's ICD Registry, has not met the full potential of this process.

We need randomized trial data of real patients as a new therapy is introduced in clinical care. In the absence of that, the collection of registry data must be strengthened and the analyses made available to the medical community as soon as possible.

Vast changes are about to occur in health insurance in America. Some will occur as a result of economic necessities, others by political action. The election of President Barack Obama signaled at least the willingness of Americans to look for change.

Whether the new president can negotiate through the minefield of doctors, insurers, labor unions, and industry to find an amicable solution is, to say the least, uncertain. He has framed the issue of health insurance no longer as an American's right but more importantly as an economic necessity. Health insurance is a way to get Americans back to work.

Glenn Beck of CNN has likened the solution of the economic problems facing Social Security, Medicare, and Medicaid to the cost of stopping an asteroid aimed at this country, due to strike in 2019, at a cost of $53 trillion. According to the Social Security and Medicare trustees, only a 122% increase in Medicare tax and a 26% increase in Social Security tax can avert it. In 2007, health care expenditures increased by 6.1% to $2.2 trillion, or $7,421 per person. Total private and federally funded health costs represent 16.2% of the gross domestic product, compared with 16% in 2006 (Health Affairs 2009;28;246–61). Well, those are issues for the next generation. Forget about them for now and let's just consider some of the issues facing health care tomorrow.

To provide the universality of health insurance, major changes will occur in how we pay, what we pay, and who does the paying. As physicians and hospitals are squeezed in the current economic environment, it might be a chance to look at what is going on in the health insurance world. Private insurers are coming under significant pressure as unemployment and health costs increase (AMNews, Nov. 24, 2008). Insurers are having increasing difficulty providing dividends to their stockholders without raising premiums. This is an issue as membership falls and the burden is placed on fewer subscribers. At the same time, investment income that had been used to support services has taken a beating in the stock market.

In Michigan, where many current and former auto workers are losing some or all of their health insurance coverage, Blue Cross and Blue Shield of Michigan is talking of increasing premiums for single contracts and Medicare supplemental coverage up to 55% (Detroit Free Press, Jan. 17, 2009). Such a hike will be sure to force even more people to join the ranks of the uninsured.

President Obama's proposal during the run-up to the election called for supplementing private job-based health plans with a federal plan. Faced with increasing unemployment, employer-based health insurance may not provide much of a support and may not be depended on for long. It is possible that in this economic environment, the public may be more interested in moving more fully to a government-funded program. Before withdrawing his nomination for Secretary of Health and Human Services, Tom Daschle had been talking about starting a federal insurance plan fashioned after Medicare and running it in competition with the private insurers. Congress already is enlarging federally supported health plans by expanding the SCHIP program by adding 4 million children under age 18 at an upgraded poverty level. The Massachusetts health insurance plan, which mandates a combination of industry- and state-funded health insurance plans, is being held up as a potential model. It has decreased the percentage of uninsured in Massachusetts to the single-digit level.

Regardless of the plan chosen, it is certain that impact on the total cost of health care will not be achieved without physicians giving up part of or the entire traditional fee-for-service payment system. That system has resulted in excess use of procedures and specialists. Historically, as fees were decreased, the volume of services increased to compensate.

The quality care guidelines of the American College of Cardiology and the American Heart Association have had no measurable effect on the utilization and cost of health care. How fee-for-service payment will be modified is uncertain, but it will likely lead to something more than just decreasing fees.

Some suggest that the current economic environment will not permit major changes; other suggest that the mounting need to provide health insurance to the uninsured will force congressional action. Stay tuned.

Vast changes are about to occur in health insurance in America. Some will occur as a result of economic necessities, others by political action. The election of President Barack Obama signaled at least the willingness of Americans to look for change.

Whether the new president can negotiate through the minefield of doctors, insurers, labor unions, and industry to find an amicable solution is, to say the least, uncertain. He has framed the issue of health insurance no longer as an American's right but more importantly as an economic necessity. Health insurance is a way to get Americans back to work.

Glenn Beck of CNN has likened the solution of the economic problems facing Social Security, Medicare, and Medicaid to the cost of stopping an asteroid aimed at this country, due to strike in 2019, at a cost of $53 trillion. According to the Social Security and Medicare trustees, only a 122% increase in Medicare tax and a 26% increase in Social Security tax can avert it. In 2007, health care expenditures increased by 6.1% to $2.2 trillion, or $7,421 per person. Total private and federally funded health costs represent 16.2% of the gross domestic product, compared with 16% in 2006 (Health Affairs 2009;28;246–61). Well, those are issues for the next generation. Forget about them for now and let's just consider some of the issues facing health care tomorrow.

To provide the universality of health insurance, major changes will occur in how we pay, what we pay, and who does the paying. As physicians and hospitals are squeezed in the current economic environment, it might be a chance to look at what is going on in the health insurance world. Private insurers are coming under significant pressure as unemployment and health costs increase (AMNews, Nov. 24, 2008). Insurers are having increasing difficulty providing dividends to their stockholders without raising premiums. This is an issue as membership falls and the burden is placed on fewer subscribers. At the same time, investment income that had been used to support services has taken a beating in the stock market.

In Michigan, where many current and former auto workers are losing some or all of their health insurance coverage, Blue Cross and Blue Shield of Michigan is talking of increasing premiums for single contracts and Medicare supplemental coverage up to 55% (Detroit Free Press, Jan. 17, 2009). Such a hike will be sure to force even more people to join the ranks of the uninsured.

President Obama's proposal during the run-up to the election called for supplementing private job-based health plans with a federal plan. Faced with increasing unemployment, employer-based health insurance may not provide much of a support and may not be depended on for long. It is possible that in this economic environment, the public may be more interested in moving more fully to a government-funded program. Before withdrawing his nomination for Secretary of Health and Human Services, Tom Daschle had been talking about starting a federal insurance plan fashioned after Medicare and running it in competition with the private insurers. Congress already is enlarging federally supported health plans by expanding the SCHIP program by adding 4 million children under age 18 at an upgraded poverty level. The Massachusetts health insurance plan, which mandates a combination of industry- and state-funded health insurance plans, is being held up as a potential model. It has decreased the percentage of uninsured in Massachusetts to the single-digit level.

Regardless of the plan chosen, it is certain that impact on the total cost of health care will not be achieved without physicians giving up part of or the entire traditional fee-for-service payment system. That system has resulted in excess use of procedures and specialists. Historically, as fees were decreased, the volume of services increased to compensate.

The quality care guidelines of the American College of Cardiology and the American Heart Association have had no measurable effect on the utilization and cost of health care. How fee-for-service payment will be modified is uncertain, but it will likely lead to something more than just decreasing fees.

Some suggest that the current economic environment will not permit major changes; other suggest that the mounting need to provide health insurance to the uninsured will force congressional action. Stay tuned.

Vast changes are about to occur in health insurance in America. Some will occur as a result of economic necessities, others by political action. The election of President Barack Obama signaled at least the willingness of Americans to look for change.

Whether the new president can negotiate through the minefield of doctors, insurers, labor unions, and industry to find an amicable solution is, to say the least, uncertain. He has framed the issue of health insurance no longer as an American's right but more importantly as an economic necessity. Health insurance is a way to get Americans back to work.

Glenn Beck of CNN has likened the solution of the economic problems facing Social Security, Medicare, and Medicaid to the cost of stopping an asteroid aimed at this country, due to strike in 2019, at a cost of $53 trillion. According to the Social Security and Medicare trustees, only a 122% increase in Medicare tax and a 26% increase in Social Security tax can avert it. In 2007, health care expenditures increased by 6.1% to $2.2 trillion, or $7,421 per person. Total private and federally funded health costs represent 16.2% of the gross domestic product, compared with 16% in 2006 (Health Affairs 2009;28;246–61). Well, those are issues for the next generation. Forget about them for now and let's just consider some of the issues facing health care tomorrow.

To provide the universality of health insurance, major changes will occur in how we pay, what we pay, and who does the paying. As physicians and hospitals are squeezed in the current economic environment, it might be a chance to look at what is going on in the health insurance world. Private insurers are coming under significant pressure as unemployment and health costs increase (AMNews, Nov. 24, 2008). Insurers are having increasing difficulty providing dividends to their stockholders without raising premiums. This is an issue as membership falls and the burden is placed on fewer subscribers. At the same time, investment income that had been used to support services has taken a beating in the stock market.

In Michigan, where many current and former auto workers are losing some or all of their health insurance coverage, Blue Cross and Blue Shield of Michigan is talking of increasing premiums for single contracts and Medicare supplemental coverage up to 55% (Detroit Free Press, Jan. 17, 2009). Such a hike will be sure to force even more people to join the ranks of the uninsured.

President Obama's proposal during the run-up to the election called for supplementing private job-based health plans with a federal plan. Faced with increasing unemployment, employer-based health insurance may not provide much of a support and may not be depended on for long. It is possible that in this economic environment, the public may be more interested in moving more fully to a government-funded program. Before withdrawing his nomination for Secretary of Health and Human Services, Tom Daschle had been talking about starting a federal insurance plan fashioned after Medicare and running it in competition with the private insurers. Congress already is enlarging federally supported health plans by expanding the SCHIP program by adding 4 million children under age 18 at an upgraded poverty level. The Massachusetts health insurance plan, which mandates a combination of industry- and state-funded health insurance plans, is being held up as a potential model. It has decreased the percentage of uninsured in Massachusetts to the single-digit level.

Regardless of the plan chosen, it is certain that impact on the total cost of health care will not be achieved without physicians giving up part of or the entire traditional fee-for-service payment system. That system has resulted in excess use of procedures and specialists. Historically, as fees were decreased, the volume of services increased to compensate.

The quality care guidelines of the American College of Cardiology and the American Heart Association have had no measurable effect on the utilization and cost of health care. How fee-for-service payment will be modified is uncertain, but it will likely lead to something more than just decreasing fees.

Some suggest that the current economic environment will not permit major changes; other suggest that the mounting need to provide health insurance to the uninsured will force congressional action. Stay tuned.