Sidney Goldstein, MD

The recently published PIONEER-HF study attempts to move sacubitril/valsartan (Entresto) therapy to the inpatient environment to improve patient and physician acceptance of this therapy for patients with heart failure (N Engl J Med. 2019 Feb 7;380;539-48).

When given to outpatients in the PARADIGM-HF trial, the combination was superior to enalapril for reducing the risks of death and hospitalization for heart failure (N Engl J Med 2014;371:993-1004.) Specifically, sacubitril/valsartan decreased mortality by 15% and hospitalization by 21% as an outpatient therapy for patients with systolic heart failure. Nevertheless, there has not been widespread adoption of this approach. It is well known that physicians can be slow to adopt new therapies, but one overriding factor may be the cost of the drug compared to enalapril, one of the first drugs shown to be effective in heart failure therapy (Entresto costs more than $4,000 per year; enalapril costs about $120 per year).

The investigators in the PIONEER-HF study compared Entresto to enalapril over a 2-month period in patients hospitalized with systolic heart failure. To accelerate the trial, the investigators used the proportional change in patients’ N-terminal pro-B-type natriuretic peptide (NT-proBNP) levels as the primary endpoint rather than the traditional outcome of morbidity and mortality. In the short term, no significant clinical benefits were observed, but there was a significant decrease in NT-proBNP of about 30% (P less than .001).

The investigators suggested that this finding extended the previous benefit observed with Entresto during outpatient initiation and could be used as a rationale for initiating Entresto therapy in the hospital. This earlier application of the therapy could make the drug more widely acceptable.

Considerable investigation in BNP measurement has occurred over the last few years, and although it is clear that BNP is elevated in heart failure patients, there is no evidence to confirm that the decrease in BNP is associated with improved outcome. BNP will fall with decrease in ventricular volume, which may have significant physiologic mechanisms but ventricular volume could decrease with fall in blood pressure that may have occurred in this population since hypotension tended to be more frequent with Entresto than with enalapril. The traditional measure of heart failure benefit with beta-blockers, ACE inhibitors, and aldosterone antagonists in the inpatient and early postdischarge period has depended on clinical outcomes.

Regardless of the physiologic explanation of this fall in BNP, we must pause in our assumptions when a surrogate measure is used to assess clinical benefit as inpatient therapy. The Food and Drug Administration has long given up using surrogate measures as proof of efficacy, and rightly so. Clinical medicine is replete with dubious drug benefits based on surrogate measures. Let’s not forget that only a few years ago suppression of premature ventricular contractions was considered to be a measure of the pharmacologic prevention of sudden death. We have come a long way from that and other clinical missteps to use BNP, an uncertain marker at best of clinical improvement, as a surrogate for the improvement in heart failure.

There is a substantial amount of data supporting the benefit of Entresto in the clinical management of outpatients with heart failure without using the PIONEER-HF trial results as a pretense to initiate therapy when patients are hospitalized. One might suggest that if Novartis is concerned about introducing the drug in the clinical management of heart failure, the company might consider the possibility of decreasing its price.

Dr. Goldstein is professor of medicine at Wayne State University and the division head emeritus of cardiovascular medicine at Henry Ford Hospital, both in Detroit.

The recently published PIONEER-HF study attempts to move sacubitril/valsartan (Entresto) therapy to the inpatient environment to improve patient and physician acceptance of this therapy for patients with heart failure (N Engl J Med. 2019 Feb 7;380;539-48).

When given to outpatients in the PARADIGM-HF trial, the combination was superior to enalapril for reducing the risks of death and hospitalization for heart failure (N Engl J Med 2014;371:993-1004.) Specifically, sacubitril/valsartan decreased mortality by 15% and hospitalization by 21% as an outpatient therapy for patients with systolic heart failure. Nevertheless, there has not been widespread adoption of this approach. It is well known that physicians can be slow to adopt new therapies, but one overriding factor may be the cost of the drug compared to enalapril, one of the first drugs shown to be effective in heart failure therapy (Entresto costs more than $4,000 per year; enalapril costs about $120 per year).

The investigators in the PIONEER-HF study compared Entresto to enalapril over a 2-month period in patients hospitalized with systolic heart failure. To accelerate the trial, the investigators used the proportional change in patients’ N-terminal pro-B-type natriuretic peptide (NT-proBNP) levels as the primary endpoint rather than the traditional outcome of morbidity and mortality. In the short term, no significant clinical benefits were observed, but there was a significant decrease in NT-proBNP of about 30% (P less than .001).

The investigators suggested that this finding extended the previous benefit observed with Entresto during outpatient initiation and could be used as a rationale for initiating Entresto therapy in the hospital. This earlier application of the therapy could make the drug more widely acceptable.

Considerable investigation in BNP measurement has occurred over the last few years, and although it is clear that BNP is elevated in heart failure patients, there is no evidence to confirm that the decrease in BNP is associated with improved outcome. BNP will fall with decrease in ventricular volume, which may have significant physiologic mechanisms but ventricular volume could decrease with fall in blood pressure that may have occurred in this population since hypotension tended to be more frequent with Entresto than with enalapril. The traditional measure of heart failure benefit with beta-blockers, ACE inhibitors, and aldosterone antagonists in the inpatient and early postdischarge period has depended on clinical outcomes.

Regardless of the physiologic explanation of this fall in BNP, we must pause in our assumptions when a surrogate measure is used to assess clinical benefit as inpatient therapy. The Food and Drug Administration has long given up using surrogate measures as proof of efficacy, and rightly so. Clinical medicine is replete with dubious drug benefits based on surrogate measures. Let’s not forget that only a few years ago suppression of premature ventricular contractions was considered to be a measure of the pharmacologic prevention of sudden death. We have come a long way from that and other clinical missteps to use BNP, an uncertain marker at best of clinical improvement, as a surrogate for the improvement in heart failure.

There is a substantial amount of data supporting the benefit of Entresto in the clinical management of outpatients with heart failure without using the PIONEER-HF trial results as a pretense to initiate therapy when patients are hospitalized. One might suggest that if Novartis is concerned about introducing the drug in the clinical management of heart failure, the company might consider the possibility of decreasing its price.

Dr. Goldstein is professor of medicine at Wayne State University and the division head emeritus of cardiovascular medicine at Henry Ford Hospital, both in Detroit.

The recently published PIONEER-HF study attempts to move sacubitril/valsartan (Entresto) therapy to the inpatient environment to improve patient and physician acceptance of this therapy for patients with heart failure (N Engl J Med. 2019 Feb 7;380;539-48).

When given to outpatients in the PARADIGM-HF trial, the combination was superior to enalapril for reducing the risks of death and hospitalization for heart failure (N Engl J Med 2014;371:993-1004.) Specifically, sacubitril/valsartan decreased mortality by 15% and hospitalization by 21% as an outpatient therapy for patients with systolic heart failure. Nevertheless, there has not been widespread adoption of this approach. It is well known that physicians can be slow to adopt new therapies, but one overriding factor may be the cost of the drug compared to enalapril, one of the first drugs shown to be effective in heart failure therapy (Entresto costs more than $4,000 per year; enalapril costs about $120 per year).

The investigators in the PIONEER-HF study compared Entresto to enalapril over a 2-month period in patients hospitalized with systolic heart failure. To accelerate the trial, the investigators used the proportional change in patients’ N-terminal pro-B-type natriuretic peptide (NT-proBNP) levels as the primary endpoint rather than the traditional outcome of morbidity and mortality. In the short term, no significant clinical benefits were observed, but there was a significant decrease in NT-proBNP of about 30% (P less than .001).

The investigators suggested that this finding extended the previous benefit observed with Entresto during outpatient initiation and could be used as a rationale for initiating Entresto therapy in the hospital. This earlier application of the therapy could make the drug more widely acceptable.

Considerable investigation in BNP measurement has occurred over the last few years, and although it is clear that BNP is elevated in heart failure patients, there is no evidence to confirm that the decrease in BNP is associated with improved outcome. BNP will fall with decrease in ventricular volume, which may have significant physiologic mechanisms but ventricular volume could decrease with fall in blood pressure that may have occurred in this population since hypotension tended to be more frequent with Entresto than with enalapril. The traditional measure of heart failure benefit with beta-blockers, ACE inhibitors, and aldosterone antagonists in the inpatient and early postdischarge period has depended on clinical outcomes.

Regardless of the physiologic explanation of this fall in BNP, we must pause in our assumptions when a surrogate measure is used to assess clinical benefit as inpatient therapy. The Food and Drug Administration has long given up using surrogate measures as proof of efficacy, and rightly so. Clinical medicine is replete with dubious drug benefits based on surrogate measures. Let’s not forget that only a few years ago suppression of premature ventricular contractions was considered to be a measure of the pharmacologic prevention of sudden death. We have come a long way from that and other clinical missteps to use BNP, an uncertain marker at best of clinical improvement, as a surrogate for the improvement in heart failure.

There is a substantial amount of data supporting the benefit of Entresto in the clinical management of outpatients with heart failure without using the PIONEER-HF trial results as a pretense to initiate therapy when patients are hospitalized. One might suggest that if Novartis is concerned about introducing the drug in the clinical management of heart failure, the company might consider the possibility of decreasing its price.

Dr. Goldstein is professor of medicine at Wayne State University and the division head emeritus of cardiovascular medicine at Henry Ford Hospital, both in Detroit.

The recent publication of the changes and current levels of evidence for the guidelines from the American College of Cardiology, American Heart Association, and the European Society of Cardiology once again indicates that the level of high-quality scientific data supporting the decision making process is limited.

Of the thousands of recommendations among the guidelines provided, level A data – which is supported by at least two randomized, controlled trials (RCT), arguably the gold standard for the proof of benefit of a treatment program – was available in only 8.5% of ACC/AHA recommendations and in 14.2% of ESC recommendations. The recent review covering guidelines published from 2008 to 2018 has changed very little since the previous review carried out on data collected between 1999 and 2014 (JAMA. 2019 Mar 19;321[11]:1069-80). Admittedly, by the nature of their design, RCTs represent a very special subset of any disease process but they are the best we can do. The remainder of the guidelines is supported by nonrandomized data and consensus opinion of “experts.” The absence of randomized data in the rest of the guidelines creates an area of uncertainty between clinical practice and outcomes.

Guidelines have been with us for almost 30 years and have provided a near “cookbook recipe” for the treatment of almost the totality of cardiovascular care, both in the United States and Europe. There is little evidence that guideline dissemination results in a beneficial effect on cardiovascular care, instead reflecting the contemporary published research and informed opinion of our generation.

Despite the limitation of hard data based on RCTs, cardiovascular mortality has leveled off in the last few years. Although there are a number of areas that could be investigated with more focused and practical RCTs, there has been little enthusiasm by either the National Heart, Lung, and Blood Institute or the pharmaceutical or device industries to investigate existing cardiovascular drugs and/or devices to better elucidate nuanced therapy for subsets of heart disease that remain in the uncertain data areas. In fact, the current report shows that there has been little change in guidelines in the last 10 years. Most effort has been focused on new drug development and application.

Much of the advance in cardiovascular care and decrease in mortality is a result of the development of new drugs for the treatment of hypertension, management of hypercholesterolemia, and MI, together with coronary angiography and its interventional permutations of the previous 50 years. Those advances are now part of our knowledge base, our therapeutic DNA, and in the absence of some new scientific breakthrough, there is little to expect from future guideline development. Medical students and house officers are being taught as fact what we found as exciting new therapy just a few short years ago. Guidelines are now part of textbook knowledge and until new clinical outcome are reported, guidelines will probably serve a useful reference material but will not lead to much change in clinical care.

Even so, treating the patient in the clinic and in the hospital still requires the doctor to practice the “art” of medicine and to synthesize therapy based on the paucity of scientific data and quasi knowledge acquired over a generation.

The appreciation that much is unknown gives the doctor the humility required to be sensitive to patient needs and their symptoms and the aspiration for new, science-based data. This is still part of the excitement of being a doctor.

Dr. Goldstein, medical editor of Cardiology News, is professor of medicine at Wayne State University and division head emeritus of cardiovascular medicine at Henry Ford Hospital, both in Detroit. He is on data safety monitoring committees for the National Institutes of Health and several pharmaceutical companies.

The recent publication of the changes and current levels of evidence for the guidelines from the American College of Cardiology, American Heart Association, and the European Society of Cardiology once again indicates that the level of high-quality scientific data supporting the decision making process is limited.

Of the thousands of recommendations among the guidelines provided, level A data – which is supported by at least two randomized, controlled trials (RCT), arguably the gold standard for the proof of benefit of a treatment program – was available in only 8.5% of ACC/AHA recommendations and in 14.2% of ESC recommendations. The recent review covering guidelines published from 2008 to 2018 has changed very little since the previous review carried out on data collected between 1999 and 2014 (JAMA. 2019 Mar 19;321[11]:1069-80). Admittedly, by the nature of their design, RCTs represent a very special subset of any disease process but they are the best we can do. The remainder of the guidelines is supported by nonrandomized data and consensus opinion of “experts.” The absence of randomized data in the rest of the guidelines creates an area of uncertainty between clinical practice and outcomes.

Guidelines have been with us for almost 30 years and have provided a near “cookbook recipe” for the treatment of almost the totality of cardiovascular care, both in the United States and Europe. There is little evidence that guideline dissemination results in a beneficial effect on cardiovascular care, instead reflecting the contemporary published research and informed opinion of our generation.

Despite the limitation of hard data based on RCTs, cardiovascular mortality has leveled off in the last few years. Although there are a number of areas that could be investigated with more focused and practical RCTs, there has been little enthusiasm by either the National Heart, Lung, and Blood Institute or the pharmaceutical or device industries to investigate existing cardiovascular drugs and/or devices to better elucidate nuanced therapy for subsets of heart disease that remain in the uncertain data areas. In fact, the current report shows that there has been little change in guidelines in the last 10 years. Most effort has been focused on new drug development and application.

Much of the advance in cardiovascular care and decrease in mortality is a result of the development of new drugs for the treatment of hypertension, management of hypercholesterolemia, and MI, together with coronary angiography and its interventional permutations of the previous 50 years. Those advances are now part of our knowledge base, our therapeutic DNA, and in the absence of some new scientific breakthrough, there is little to expect from future guideline development. Medical students and house officers are being taught as fact what we found as exciting new therapy just a few short years ago. Guidelines are now part of textbook knowledge and until new clinical outcome are reported, guidelines will probably serve a useful reference material but will not lead to much change in clinical care.

Even so, treating the patient in the clinic and in the hospital still requires the doctor to practice the “art” of medicine and to synthesize therapy based on the paucity of scientific data and quasi knowledge acquired over a generation.

The appreciation that much is unknown gives the doctor the humility required to be sensitive to patient needs and their symptoms and the aspiration for new, science-based data. This is still part of the excitement of being a doctor.

Dr. Goldstein, medical editor of Cardiology News, is professor of medicine at Wayne State University and division head emeritus of cardiovascular medicine at Henry Ford Hospital, both in Detroit. He is on data safety monitoring committees for the National Institutes of Health and several pharmaceutical companies.

The recent publication of the changes and current levels of evidence for the guidelines from the American College of Cardiology, American Heart Association, and the European Society of Cardiology once again indicates that the level of high-quality scientific data supporting the decision making process is limited.

Of the thousands of recommendations among the guidelines provided, level A data – which is supported by at least two randomized, controlled trials (RCT), arguably the gold standard for the proof of benefit of a treatment program – was available in only 8.5% of ACC/AHA recommendations and in 14.2% of ESC recommendations. The recent review covering guidelines published from 2008 to 2018 has changed very little since the previous review carried out on data collected between 1999 and 2014 (JAMA. 2019 Mar 19;321[11]:1069-80). Admittedly, by the nature of their design, RCTs represent a very special subset of any disease process but they are the best we can do. The remainder of the guidelines is supported by nonrandomized data and consensus opinion of “experts.” The absence of randomized data in the rest of the guidelines creates an area of uncertainty between clinical practice and outcomes.

Guidelines have been with us for almost 30 years and have provided a near “cookbook recipe” for the treatment of almost the totality of cardiovascular care, both in the United States and Europe. There is little evidence that guideline dissemination results in a beneficial effect on cardiovascular care, instead reflecting the contemporary published research and informed opinion of our generation.

Despite the limitation of hard data based on RCTs, cardiovascular mortality has leveled off in the last few years. Although there are a number of areas that could be investigated with more focused and practical RCTs, there has been little enthusiasm by either the National Heart, Lung, and Blood Institute or the pharmaceutical or device industries to investigate existing cardiovascular drugs and/or devices to better elucidate nuanced therapy for subsets of heart disease that remain in the uncertain data areas. In fact, the current report shows that there has been little change in guidelines in the last 10 years. Most effort has been focused on new drug development and application.

Much of the advance in cardiovascular care and decrease in mortality is a result of the development of new drugs for the treatment of hypertension, management of hypercholesterolemia, and MI, together with coronary angiography and its interventional permutations of the previous 50 years. Those advances are now part of our knowledge base, our therapeutic DNA, and in the absence of some new scientific breakthrough, there is little to expect from future guideline development. Medical students and house officers are being taught as fact what we found as exciting new therapy just a few short years ago. Guidelines are now part of textbook knowledge and until new clinical outcome are reported, guidelines will probably serve a useful reference material but will not lead to much change in clinical care.

Even so, treating the patient in the clinic and in the hospital still requires the doctor to practice the “art” of medicine and to synthesize therapy based on the paucity of scientific data and quasi knowledge acquired over a generation.

The appreciation that much is unknown gives the doctor the humility required to be sensitive to patient needs and their symptoms and the aspiration for new, science-based data. This is still part of the excitement of being a doctor.

Dr. Goldstein, medical editor of Cardiology News, is professor of medicine at Wayne State University and division head emeritus of cardiovascular medicine at Henry Ford Hospital, both in Detroit. He is on data safety monitoring committees for the National Institutes of Health and several pharmaceutical companies.

Determining who is responsible for the increase in health care cost in the United States has seemingly limitless possibilities. There are enough culprits to go around, but a recent analysis points a finger at hospital-based care (Health Aff. 2019 Feb;38[2]:184-9).

The authors of the paper found that, during the period from 2007 to 2014, inpatient hospital care for surgical procedures increased 42% and outpatient hospital care increased 25%. In the same period, physician care increased only 6%. Much of this increase in hospital costs was associated with hospital consolidations and mergers.

We have been led to believe that hospital mergers will cut costs by eliminating duplication of both physical and personnel overhead costs. In fact that doesn’t seem to happen. It appears that hospital mergers were associated with increased per patient costs and is a result of decrease in competition in local health care markets. This observation has been made in the past (Am Econ Rev. 2015 Jan;105:172-203), and was reiterated by the most recent report. If there were decreases in overhead observed in the mergers, they were not passed on to the patients or insurers.

There was a time when community hospitals, large and small, were run by community leaders and local doctors, often under the aegis of religious and social groups. I can remember the medical and community leadership in Utica, N.Y., where I grew up and where I worked in a hospital as a summer intern. Their goal was to provide quality health care. The financial success or failures of the hospitals were the responsibility of the local community, and the profits and losses were kept at a minimum.

Fast forward to the 21st century and health care in general, and hospital care in particular, has become a “cash cow.” Community leadership has been minimized, and where it exists, it is under constant pressure to make a profit. Hospital mergers, arranged under the guise of economy of size, are now controlled by hedge funds and large health care corporations.

The community board of trustees has been replaced by investors, whose main concern is the return on their investments regardless of quality of care or need. If those profits fail to materialize, the hospitals are taken over by another investor group. So much for quality. As the corporations grow, they buy up the competition, particularly small community hospitals leaving many, particularly in rural America, without medical support.

There seems to be little recourse to consumers or insurers to mitigate this process. Investors have a right to a return on their investment, but until we have governmental control of competition, that incentive remains. We can see similar price increases in the pharmaceutical marketplace, where Congress has limited competition to preserve the drug monopoly. Americans will be asked to pay more to maintain a system that is inherently on the road to bankruptcy and fails to provide either quality or fair drug and hospital charges.

But what do we care, we can afford it.

Dr. Goldstein is professor of medicine at Wayne State University and the division head emeritus of cardiovascular medicine at Henry Ford Hospital, both in Detroit.

Determining who is responsible for the increase in health care cost in the United States has seemingly limitless possibilities. There are enough culprits to go around, but a recent analysis points a finger at hospital-based care (Health Aff. 2019 Feb;38[2]:184-9).

The authors of the paper found that, during the period from 2007 to 2014, inpatient hospital care for surgical procedures increased 42% and outpatient hospital care increased 25%. In the same period, physician care increased only 6%. Much of this increase in hospital costs was associated with hospital consolidations and mergers.

We have been led to believe that hospital mergers will cut costs by eliminating duplication of both physical and personnel overhead costs. In fact that doesn’t seem to happen. It appears that hospital mergers were associated with increased per patient costs and is a result of decrease in competition in local health care markets. This observation has been made in the past (Am Econ Rev. 2015 Jan;105:172-203), and was reiterated by the most recent report. If there were decreases in overhead observed in the mergers, they were not passed on to the patients or insurers.

There was a time when community hospitals, large and small, were run by community leaders and local doctors, often under the aegis of religious and social groups. I can remember the medical and community leadership in Utica, N.Y., where I grew up and where I worked in a hospital as a summer intern. Their goal was to provide quality health care. The financial success or failures of the hospitals were the responsibility of the local community, and the profits and losses were kept at a minimum.

Fast forward to the 21st century and health care in general, and hospital care in particular, has become a “cash cow.” Community leadership has been minimized, and where it exists, it is under constant pressure to make a profit. Hospital mergers, arranged under the guise of economy of size, are now controlled by hedge funds and large health care corporations.

The community board of trustees has been replaced by investors, whose main concern is the return on their investments regardless of quality of care or need. If those profits fail to materialize, the hospitals are taken over by another investor group. So much for quality. As the corporations grow, they buy up the competition, particularly small community hospitals leaving many, particularly in rural America, without medical support.

There seems to be little recourse to consumers or insurers to mitigate this process. Investors have a right to a return on their investment, but until we have governmental control of competition, that incentive remains. We can see similar price increases in the pharmaceutical marketplace, where Congress has limited competition to preserve the drug monopoly. Americans will be asked to pay more to maintain a system that is inherently on the road to bankruptcy and fails to provide either quality or fair drug and hospital charges.

But what do we care, we can afford it.

Dr. Goldstein is professor of medicine at Wayne State University and the division head emeritus of cardiovascular medicine at Henry Ford Hospital, both in Detroit.

Determining who is responsible for the increase in health care cost in the United States has seemingly limitless possibilities. There are enough culprits to go around, but a recent analysis points a finger at hospital-based care (Health Aff. 2019 Feb;38[2]:184-9).

The authors of the paper found that, during the period from 2007 to 2014, inpatient hospital care for surgical procedures increased 42% and outpatient hospital care increased 25%. In the same period, physician care increased only 6%. Much of this increase in hospital costs was associated with hospital consolidations and mergers.

We have been led to believe that hospital mergers will cut costs by eliminating duplication of both physical and personnel overhead costs. In fact that doesn’t seem to happen. It appears that hospital mergers were associated with increased per patient costs and is a result of decrease in competition in local health care markets. This observation has been made in the past (Am Econ Rev. 2015 Jan;105:172-203), and was reiterated by the most recent report. If there were decreases in overhead observed in the mergers, they were not passed on to the patients or insurers.

There was a time when community hospitals, large and small, were run by community leaders and local doctors, often under the aegis of religious and social groups. I can remember the medical and community leadership in Utica, N.Y., where I grew up and where I worked in a hospital as a summer intern. Their goal was to provide quality health care. The financial success or failures of the hospitals were the responsibility of the local community, and the profits and losses were kept at a minimum.

Fast forward to the 21st century and health care in general, and hospital care in particular, has become a “cash cow.” Community leadership has been minimized, and where it exists, it is under constant pressure to make a profit. Hospital mergers, arranged under the guise of economy of size, are now controlled by hedge funds and large health care corporations.

The community board of trustees has been replaced by investors, whose main concern is the return on their investments regardless of quality of care or need. If those profits fail to materialize, the hospitals are taken over by another investor group. So much for quality. As the corporations grow, they buy up the competition, particularly small community hospitals leaving many, particularly in rural America, without medical support.

There seems to be little recourse to consumers or insurers to mitigate this process. Investors have a right to a return on their investment, but until we have governmental control of competition, that incentive remains. We can see similar price increases in the pharmaceutical marketplace, where Congress has limited competition to preserve the drug monopoly. Americans will be asked to pay more to maintain a system that is inherently on the road to bankruptcy and fails to provide either quality or fair drug and hospital charges.

But what do we care, we can afford it.

Dr. Goldstein is professor of medicine at Wayne State University and the division head emeritus of cardiovascular medicine at Henry Ford Hospital, both in Detroit.

The balance between medical research and the pharmaceutical world has always been unsettling. The recent spate of articles in the press reporting the large payments by industry to a number of highly paid medical staff of the Memorial Sloan Kettering Cancer Institute in New York has raised again the continuing issue around that relationship.

When large sums of money are paid to medical leaders for serving on advisory boards, it is reasonable to question whom are they representing: industry or medical science. These relationships are not limited to cancer hospitals and can be presumed to pertain to cardiology and other specialties. One need only look at the disclosure statements of contemporary published articles to become aware of the entanglement of science and industry.

There is little question that both industry and science need to interact to focus direct resources to appropriate targets. No one is better able to do that than well informed scientists working in their disease fields. Industry needs scientific input and scientists need the financial resources of industry. I have been able to see that relationship play out to achieve major impacts on heart disease. But corporate decisions also can be driven by market forces and not altruism. Drug and device research has been redirected or stopped as a result of decisions made by sales forces. At other times, drugs that have great potential in the laboratory have been shelved because of a lack of scientific leadership.


So where is the moral and ethical balance? Published disclosures by authors is not much more than a catharsis in the process where action is required. Medical advisory boards are critical for successful drug and device development. That exchange is crucial to move medical science forward, but the large sums of money raise appropriate questions of what is driving the discussion.

At a more grass roots level, the financial role of investigators and hospitals in clinical trials has raised some concern. Traditionally, the institution and investigators have been reimbursed for their time and expense for recruiting and following patients. Patients, of course, are not reimbursed in clinical trials but are placed at considerable risk of an uncertain result. The reimbursements for marginal expenses seem to be appropriate. More recently, payments to physicians and hospitals have been made at current fee schedules for the implantation of a variety of new devices such as pacemakers and valves. In addition, both physicians and hospitals have invested in the financial success of these clinical trials clouding over their altruistic goals. It has been an incentive for recruiting patients for trials and has been a source of considerable revenue both for the physicians and the institution, without informing the patients of their financial relationship to industry. The image of the patient being placed at risk for the success of a clinical trial of a device by doctors and hospitals seeking financial gain is more than a little disturbing.

There is a lot of money sloshing around in the health care world that has the potential to lead to ethical uncertainty. It is the physician’s responsibility to build up ethical barriers to prevent us from slipping into that morass.

Dr. Goldstein is professor of medicine at Wayne State University and the division head emeritus of cardiovascular medicine at Henry Ford Hospital, both in Detroit.

The balance between medical research and the pharmaceutical world has always been unsettling. The recent spate of articles in the press reporting the large payments by industry to a number of highly paid medical staff of the Memorial Sloan Kettering Cancer Institute in New York has raised again the continuing issue around that relationship.

When large sums of money are paid to medical leaders for serving on advisory boards, it is reasonable to question whom are they representing: industry or medical science. These relationships are not limited to cancer hospitals and can be presumed to pertain to cardiology and other specialties. One need only look at the disclosure statements of contemporary published articles to become aware of the entanglement of science and industry.

There is little question that both industry and science need to interact to focus direct resources to appropriate targets. No one is better able to do that than well informed scientists working in their disease fields. Industry needs scientific input and scientists need the financial resources of industry. I have been able to see that relationship play out to achieve major impacts on heart disease. But corporate decisions also can be driven by market forces and not altruism. Drug and device research has been redirected or stopped as a result of decisions made by sales forces. At other times, drugs that have great potential in the laboratory have been shelved because of a lack of scientific leadership.


So where is the moral and ethical balance? Published disclosures by authors is not much more than a catharsis in the process where action is required. Medical advisory boards are critical for successful drug and device development. That exchange is crucial to move medical science forward, but the large sums of money raise appropriate questions of what is driving the discussion.

At a more grass roots level, the financial role of investigators and hospitals in clinical trials has raised some concern. Traditionally, the institution and investigators have been reimbursed for their time and expense for recruiting and following patients. Patients, of course, are not reimbursed in clinical trials but are placed at considerable risk of an uncertain result. The reimbursements for marginal expenses seem to be appropriate. More recently, payments to physicians and hospitals have been made at current fee schedules for the implantation of a variety of new devices such as pacemakers and valves. In addition, both physicians and hospitals have invested in the financial success of these clinical trials clouding over their altruistic goals. It has been an incentive for recruiting patients for trials and has been a source of considerable revenue both for the physicians and the institution, without informing the patients of their financial relationship to industry. The image of the patient being placed at risk for the success of a clinical trial of a device by doctors and hospitals seeking financial gain is more than a little disturbing.

There is a lot of money sloshing around in the health care world that has the potential to lead to ethical uncertainty. It is the physician’s responsibility to build up ethical barriers to prevent us from slipping into that morass.

Dr. Goldstein is professor of medicine at Wayne State University and the division head emeritus of cardiovascular medicine at Henry Ford Hospital, both in Detroit.

The balance between medical research and the pharmaceutical world has always been unsettling. The recent spate of articles in the press reporting the large payments by industry to a number of highly paid medical staff of the Memorial Sloan Kettering Cancer Institute in New York has raised again the continuing issue around that relationship.

When large sums of money are paid to medical leaders for serving on advisory boards, it is reasonable to question whom are they representing: industry or medical science. These relationships are not limited to cancer hospitals and can be presumed to pertain to cardiology and other specialties. One need only look at the disclosure statements of contemporary published articles to become aware of the entanglement of science and industry.

There is little question that both industry and science need to interact to focus direct resources to appropriate targets. No one is better able to do that than well informed scientists working in their disease fields. Industry needs scientific input and scientists need the financial resources of industry. I have been able to see that relationship play out to achieve major impacts on heart disease. But corporate decisions also can be driven by market forces and not altruism. Drug and device research has been redirected or stopped as a result of decisions made by sales forces. At other times, drugs that have great potential in the laboratory have been shelved because of a lack of scientific leadership.


So where is the moral and ethical balance? Published disclosures by authors is not much more than a catharsis in the process where action is required. Medical advisory boards are critical for successful drug and device development. That exchange is crucial to move medical science forward, but the large sums of money raise appropriate questions of what is driving the discussion.

At a more grass roots level, the financial role of investigators and hospitals in clinical trials has raised some concern. Traditionally, the institution and investigators have been reimbursed for their time and expense for recruiting and following patients. Patients, of course, are not reimbursed in clinical trials but are placed at considerable risk of an uncertain result. The reimbursements for marginal expenses seem to be appropriate. More recently, payments to physicians and hospitals have been made at current fee schedules for the implantation of a variety of new devices such as pacemakers and valves. In addition, both physicians and hospitals have invested in the financial success of these clinical trials clouding over their altruistic goals. It has been an incentive for recruiting patients for trials and has been a source of considerable revenue both for the physicians and the institution, without informing the patients of their financial relationship to industry. The image of the patient being placed at risk for the success of a clinical trial of a device by doctors and hospitals seeking financial gain is more than a little disturbing.

There is a lot of money sloshing around in the health care world that has the potential to lead to ethical uncertainty. It is the physician’s responsibility to build up ethical barriers to prevent us from slipping into that morass.

Dr. Goldstein is professor of medicine at Wayne State University and the division head emeritus of cardiovascular medicine at Henry Ford Hospital, both in Detroit.

Just when I thought that all the nonsense about the benefits of aspirin for the prevention of heart attack had been obliterated with a series of reports on its danger and lack of benefit, more fake news arrived in the form of a proposal by the Centers for Disease Control and Prevention.

It proclaimed that there were “213 million opportunities to improve cardiovascular risks in America,” one of which would be to change behavior so that 9 million Americans would take a daily baby aspirin (MMWR 2018 Sep 7;67[35];983–91). Although the proposed benefits of aspirin have been around for a long time, the major contemporary emphasis resulted from the report of the Physicians’ Heart Study in healthy men in 1989 that there was a decrease in fatal and nonfatal MIs as a result of taking daily aspirin. However, listed in a separate endpoint analysis, sudden death, for some reason not considered to be a fatal event, was twice as frequent in the aspirin treated group compared to the placebo, and when included with fatal events wiped out most of the benefit of aspirin (N Engl J Med. 1989 Jul 20;321:129-35). Ask your friends like I do, if they take a baby aspirin daily and they all smile innocently and complacently and say, “Yes.”

Over the intervening years, there has been a general jousting around the benefits of aspirin with conflicting data and little convincing evidence. With the recent publications, there seems to be at least some glimmer hope that the public and medicine may come to their collective senses. In a series of articles published from the ASPREE and ASCEND trials, which included 19,114 and 15,480 healthy and diabetic patients, respectively, there is little benefit and significant risks to taking aspirin, not the least of which is severe bleeding and cancer.

In the ASPREE trial of healthy elderly men over 70, aspirin has no effect on both total all-cause mortality and cardiovascular mortality and is associated with increased major bleeding. ASPREE also reported that, in healthy elderly men, aspirin was associated with an increase in mortality because of increased cancer incidence (N Engl J Med. 2018 Oct 18;379:1499-529).

The ASCEND trial, which included in the patients with diabetes and without evidence of coronary vascular disease, aspirin use as primary prevention was associated with a decrease in cardiovascular mortality, which was erased by an increase in serious bleeding (N Engl J Med. 2018 Oct 18; 379:1529-39). In a companion review, Paul M. Ridker, MD, of Brigham and Women’s Hospital, Boston, concludes that “the best strategy for the use of aspirin in the prevention of cardiovascular disease may simply be to prescribe a statin instead” (N Engl J Med 2018 Oct. 18; 379:1572-4)

Someone needs to call the CDC.

Dr. Goldstein, medical editor of Cardiology News, is professor of medicine at Wayne State University and division head emeritus of cardiovascular medicine at Henry Ford Hospital, both in Detroit. He is on data safety monitoring committees for the National Institutes of Health and several pharmaceutical companies.

Just when I thought that all the nonsense about the benefits of aspirin for the prevention of heart attack had been obliterated with a series of reports on its danger and lack of benefit, more fake news arrived in the form of a proposal by the Centers for Disease Control and Prevention.

It proclaimed that there were “213 million opportunities to improve cardiovascular risks in America,” one of which would be to change behavior so that 9 million Americans would take a daily baby aspirin (MMWR 2018 Sep 7;67[35];983–91). Although the proposed benefits of aspirin have been around for a long time, the major contemporary emphasis resulted from the report of the Physicians’ Heart Study in healthy men in 1989 that there was a decrease in fatal and nonfatal MIs as a result of taking daily aspirin. However, listed in a separate endpoint analysis, sudden death, for some reason not considered to be a fatal event, was twice as frequent in the aspirin treated group compared to the placebo, and when included with fatal events wiped out most of the benefit of aspirin (N Engl J Med. 1989 Jul 20;321:129-35). Ask your friends like I do, if they take a baby aspirin daily and they all smile innocently and complacently and say, “Yes.”

Over the intervening years, there has been a general jousting around the benefits of aspirin with conflicting data and little convincing evidence. With the recent publications, there seems to be at least some glimmer hope that the public and medicine may come to their collective senses. In a series of articles published from the ASPREE and ASCEND trials, which included 19,114 and 15,480 healthy and diabetic patients, respectively, there is little benefit and significant risks to taking aspirin, not the least of which is severe bleeding and cancer.

In the ASPREE trial of healthy elderly men over 70, aspirin has no effect on both total all-cause mortality and cardiovascular mortality and is associated with increased major bleeding. ASPREE also reported that, in healthy elderly men, aspirin was associated with an increase in mortality because of increased cancer incidence (N Engl J Med. 2018 Oct 18;379:1499-529).

The ASCEND trial, which included in the patients with diabetes and without evidence of coronary vascular disease, aspirin use as primary prevention was associated with a decrease in cardiovascular mortality, which was erased by an increase in serious bleeding (N Engl J Med. 2018 Oct 18; 379:1529-39). In a companion review, Paul M. Ridker, MD, of Brigham and Women’s Hospital, Boston, concludes that “the best strategy for the use of aspirin in the prevention of cardiovascular disease may simply be to prescribe a statin instead” (N Engl J Med 2018 Oct. 18; 379:1572-4)

Someone needs to call the CDC.

Dr. Goldstein, medical editor of Cardiology News, is professor of medicine at Wayne State University and division head emeritus of cardiovascular medicine at Henry Ford Hospital, both in Detroit. He is on data safety monitoring committees for the National Institutes of Health and several pharmaceutical companies.

Just when I thought that all the nonsense about the benefits of aspirin for the prevention of heart attack had been obliterated with a series of reports on its danger and lack of benefit, more fake news arrived in the form of a proposal by the Centers for Disease Control and Prevention.

It proclaimed that there were “213 million opportunities to improve cardiovascular risks in America,” one of which would be to change behavior so that 9 million Americans would take a daily baby aspirin (MMWR 2018 Sep 7;67[35];983–91). Although the proposed benefits of aspirin have been around for a long time, the major contemporary emphasis resulted from the report of the Physicians’ Heart Study in healthy men in 1989 that there was a decrease in fatal and nonfatal MIs as a result of taking daily aspirin. However, listed in a separate endpoint analysis, sudden death, for some reason not considered to be a fatal event, was twice as frequent in the aspirin treated group compared to the placebo, and when included with fatal events wiped out most of the benefit of aspirin (N Engl J Med. 1989 Jul 20;321:129-35). Ask your friends like I do, if they take a baby aspirin daily and they all smile innocently and complacently and say, “Yes.”

Over the intervening years, there has been a general jousting around the benefits of aspirin with conflicting data and little convincing evidence. With the recent publications, there seems to be at least some glimmer hope that the public and medicine may come to their collective senses. In a series of articles published from the ASPREE and ASCEND trials, which included 19,114 and 15,480 healthy and diabetic patients, respectively, there is little benefit and significant risks to taking aspirin, not the least of which is severe bleeding and cancer.

In the ASPREE trial of healthy elderly men over 70, aspirin has no effect on both total all-cause mortality and cardiovascular mortality and is associated with increased major bleeding. ASPREE also reported that, in healthy elderly men, aspirin was associated with an increase in mortality because of increased cancer incidence (N Engl J Med. 2018 Oct 18;379:1499-529).

The ASCEND trial, which included in the patients with diabetes and without evidence of coronary vascular disease, aspirin use as primary prevention was associated with a decrease in cardiovascular mortality, which was erased by an increase in serious bleeding (N Engl J Med. 2018 Oct 18; 379:1529-39). In a companion review, Paul M. Ridker, MD, of Brigham and Women’s Hospital, Boston, concludes that “the best strategy for the use of aspirin in the prevention of cardiovascular disease may simply be to prescribe a statin instead” (N Engl J Med 2018 Oct. 18; 379:1572-4)

Someone needs to call the CDC.

Dr. Goldstein, medical editor of Cardiology News, is professor of medicine at Wayne State University and division head emeritus of cardiovascular medicine at Henry Ford Hospital, both in Detroit. He is on data safety monitoring committees for the National Institutes of Health and several pharmaceutical companies.

The concept that cell transplantation is the answer to the treatment of heart failure may have suffered a major setback as a result of a research scam perpetrated at Harvard University’s Brigham and Women’s Hospital in Boston.

The fraudulent cardiac research at that institution was from the lab of Piero Anversa, MD, which falsified or fabricated data. Dr. Anversa was one of the leaders in pursuing the concept that adult cardiomyocytes can not only regenerate by cell division but can also be transplanted from one animal to another, in his case a mouse.

The original reports over a decade ago caused a major stir in heart failure research. They also were met with considerable skepticism in the research field and have not been reproduced in other laboratories. Numerous small trials in humans have been unsuccessful in demonstrating the survival of autologous cells transplanted in both animal and humans. Dr. Anversa’s research has been under scrutiny by Harvard and Brigham and Women’s since 2013, ultimately resulting in the call to retract 31 published studies in mid-October. In the meantime, admission of fraud in regard to the original Anversa papers resulted in a fine of $10 million paid by the institutions to the National Institutes of Health in a 2017 settlement. Dr. Anversa left Harvard in 2015.

Nevertheless Dr. Anversa’s concepts led to the initiation of an NIH-supported multicenter trial in humans of the implantation of autologous bone marrow cells using endocardial devices to transplant cells in 144 patients with heart failure. The Combination of Autologous Bone Marrow Derived Mesenchymal and C-Kit+ Cardiac Stem Cells as Regenerative Therapy for Heart Failure (CONCERT-HF) was started in 2015 and was still recruiting until Oct. 29, when the National Heart, Lung, and Blood Institute announced that a pause in recruitment was called in order to review the fraudulent data that led to the trial’s initiation. Patients were to be followed over a 1-year period using delayed-enhanced magnetic resonance imaging (DEMRI) scans to assess scar size and left ventricular function and structure at baseline and at 6 and 12 months post study product ad-ministration. For the purpose of the endpoint analysis and safety evaluations, the investigators planned to use an intention-to-treat study population evaluating a number of clinical parameters.

Anatomists and physiologists have long been of the opinion that adult human and mammalian cardiomyocytes are terminally differentiated and do not undergo cell division. However, over time, cardiomyocytes can undergo hypertrophy as a result of increased workload. Cells can die as a result of ischemia, infarction, or stress mediated through unchecked inflammatory processes. It also has been shown that cells can die as a result of apoptosis, particularly in areas in proximity to myocardial scars. It is generally believed that these three methods of cell depletion contribute to the progression of heart failure. Dr. Anversa also proposed that there is some degree of replication of cardiomyocytes but not to a degree that can have a meaningful replacement value.

The concept of cell transplantation in medicine certainly has been in the forefront of clinical research in medicine for the last decade based in part on research by Dr. Anversa and others in cardiology and numerous investigators in other medical disciplines. With few exceptions, there has been little support for the clinical benefit of these clinical studies. We are unfortunately now faced with the release of the tainted fraudulent research that led to CONCERT-HF. Whether there is anything of scientific value to come of the trial is highly unlikely.
 

Dr. Goldstein, medical editor of Cardiology News, is professor of medicine at Wayne State University and division head emeritus of cardiovascular medicine at Henry Ford Hospital, both in Detroit. He is on data safety monitoring committees for the National Institutes of Health and several pharmaceutical companies.

This article was updated Oct. 30, 2018.

The concept that cell transplantation is the answer to the treatment of heart failure may have suffered a major setback as a result of a research scam perpetrated at Harvard University’s Brigham and Women’s Hospital in Boston.

The fraudulent cardiac research at that institution was from the lab of Piero Anversa, MD, which falsified or fabricated data. Dr. Anversa was one of the leaders in pursuing the concept that adult cardiomyocytes can not only regenerate by cell division but can also be transplanted from one animal to another, in his case a mouse.

The original reports over a decade ago caused a major stir in heart failure research. They also were met with considerable skepticism in the research field and have not been reproduced in other laboratories. Numerous small trials in humans have been unsuccessful in demonstrating the survival of autologous cells transplanted in both animal and humans. Dr. Anversa’s research has been under scrutiny by Harvard and Brigham and Women’s since 2013, ultimately resulting in the call to retract 31 published studies in mid-October. In the meantime, admission of fraud in regard to the original Anversa papers resulted in a fine of $10 million paid by the institutions to the National Institutes of Health in a 2017 settlement. Dr. Anversa left Harvard in 2015.

Nevertheless Dr. Anversa’s concepts led to the initiation of an NIH-supported multicenter trial in humans of the implantation of autologous bone marrow cells using endocardial devices to transplant cells in 144 patients with heart failure. The Combination of Autologous Bone Marrow Derived Mesenchymal and C-Kit+ Cardiac Stem Cells as Regenerative Therapy for Heart Failure (CONCERT-HF) was started in 2015 and was still recruiting until Oct. 29, when the National Heart, Lung, and Blood Institute announced that a pause in recruitment was called in order to review the fraudulent data that led to the trial’s initiation. Patients were to be followed over a 1-year period using delayed-enhanced magnetic resonance imaging (DEMRI) scans to assess scar size and left ventricular function and structure at baseline and at 6 and 12 months post study product ad-ministration. For the purpose of the endpoint analysis and safety evaluations, the investigators planned to use an intention-to-treat study population evaluating a number of clinical parameters.

Anatomists and physiologists have long been of the opinion that adult human and mammalian cardiomyocytes are terminally differentiated and do not undergo cell division. However, over time, cardiomyocytes can undergo hypertrophy as a result of increased workload. Cells can die as a result of ischemia, infarction, or stress mediated through unchecked inflammatory processes. It also has been shown that cells can die as a result of apoptosis, particularly in areas in proximity to myocardial scars. It is generally believed that these three methods of cell depletion contribute to the progression of heart failure. Dr. Anversa also proposed that there is some degree of replication of cardiomyocytes but not to a degree that can have a meaningful replacement value.

The concept of cell transplantation in medicine certainly has been in the forefront of clinical research in medicine for the last decade based in part on research by Dr. Anversa and others in cardiology and numerous investigators in other medical disciplines. With few exceptions, there has been little support for the clinical benefit of these clinical studies. We are unfortunately now faced with the release of the tainted fraudulent research that led to CONCERT-HF. Whether there is anything of scientific value to come of the trial is highly unlikely.
 

Dr. Goldstein, medical editor of Cardiology News, is professor of medicine at Wayne State University and division head emeritus of cardiovascular medicine at Henry Ford Hospital, both in Detroit. He is on data safety monitoring committees for the National Institutes of Health and several pharmaceutical companies.

This article was updated Oct. 30, 2018.

The concept that cell transplantation is the answer to the treatment of heart failure may have suffered a major setback as a result of a research scam perpetrated at Harvard University’s Brigham and Women’s Hospital in Boston.

The fraudulent cardiac research at that institution was from the lab of Piero Anversa, MD, which falsified or fabricated data. Dr. Anversa was one of the leaders in pursuing the concept that adult cardiomyocytes can not only regenerate by cell division but can also be transplanted from one animal to another, in his case a mouse.

The original reports over a decade ago caused a major stir in heart failure research. They also were met with considerable skepticism in the research field and have not been reproduced in other laboratories. Numerous small trials in humans have been unsuccessful in demonstrating the survival of autologous cells transplanted in both animal and humans. Dr. Anversa’s research has been under scrutiny by Harvard and Brigham and Women’s since 2013, ultimately resulting in the call to retract 31 published studies in mid-October. In the meantime, admission of fraud in regard to the original Anversa papers resulted in a fine of $10 million paid by the institutions to the National Institutes of Health in a 2017 settlement. Dr. Anversa left Harvard in 2015.

Nevertheless Dr. Anversa’s concepts led to the initiation of an NIH-supported multicenter trial in humans of the implantation of autologous bone marrow cells using endocardial devices to transplant cells in 144 patients with heart failure. The Combination of Autologous Bone Marrow Derived Mesenchymal and C-Kit+ Cardiac Stem Cells as Regenerative Therapy for Heart Failure (CONCERT-HF) was started in 2015 and was still recruiting until Oct. 29, when the National Heart, Lung, and Blood Institute announced that a pause in recruitment was called in order to review the fraudulent data that led to the trial’s initiation. Patients were to be followed over a 1-year period using delayed-enhanced magnetic resonance imaging (DEMRI) scans to assess scar size and left ventricular function and structure at baseline and at 6 and 12 months post study product ad-ministration. For the purpose of the endpoint analysis and safety evaluations, the investigators planned to use an intention-to-treat study population evaluating a number of clinical parameters.

Anatomists and physiologists have long been of the opinion that adult human and mammalian cardiomyocytes are terminally differentiated and do not undergo cell division. However, over time, cardiomyocytes can undergo hypertrophy as a result of increased workload. Cells can die as a result of ischemia, infarction, or stress mediated through unchecked inflammatory processes. It also has been shown that cells can die as a result of apoptosis, particularly in areas in proximity to myocardial scars. It is generally believed that these three methods of cell depletion contribute to the progression of heart failure. Dr. Anversa also proposed that there is some degree of replication of cardiomyocytes but not to a degree that can have a meaningful replacement value.

The concept of cell transplantation in medicine certainly has been in the forefront of clinical research in medicine for the last decade based in part on research by Dr. Anversa and others in cardiology and numerous investigators in other medical disciplines. With few exceptions, there has been little support for the clinical benefit of these clinical studies. We are unfortunately now faced with the release of the tainted fraudulent research that led to CONCERT-HF. Whether there is anything of scientific value to come of the trial is highly unlikely.
 

Dr. Goldstein, medical editor of Cardiology News, is professor of medicine at Wayne State University and division head emeritus of cardiovascular medicine at Henry Ford Hospital, both in Detroit. He is on data safety monitoring committees for the National Institutes of Health and several pharmaceutical companies.

This article was updated Oct. 30, 2018.

I am not sure when it occurred. I don’t know how it happened. I don’t think anyone took a vote on it. It happened gradually over the last decade. I think it happened when the administrative staff became larger than the medical staff. In order to include everyone under the same umbrella, everyone became a provider.

The title of doctor, nurse, technician all disappeared, and we all became providers. All those patients in our waiting room suddenly became consumers or clients. My grandfather ran a grocery store and had a lot of customers, and my father was a lawyer and had a lot of clients. None of those customers or clients would come to see me as their doctor with their illnesses today if I were a provider. The use of the terminology of “providers” and “customers” lowers all health care staff to the lowest common denominator and demeans the concerns of my patients.

I am not sure when it occurred. I don’t know how it happened. I don’t think anyone took a vote on it. It happened gradually over the last decade. I think it happened when the administrative staff became larger than the medical staff. In order to include everyone under the same umbrella, everyone became a provider.

The title of doctor, nurse, technician all disappeared, and we all became providers. All those patients in our waiting room suddenly became consumers or clients. My grandfather ran a grocery store and had a lot of customers, and my father was a lawyer and had a lot of clients. None of those customers or clients would come to see me as their doctor with their illnesses today if I were a provider. The use of the terminology of “providers” and “customers” lowers all health care staff to the lowest common denominator and demeans the concerns of my patients.

I am not sure when it occurred. I don’t know how it happened. I don’t think anyone took a vote on it. It happened gradually over the last decade. I think it happened when the administrative staff became larger than the medical staff. In order to include everyone under the same umbrella, everyone became a provider.

The title of doctor, nurse, technician all disappeared, and we all became providers. All those patients in our waiting room suddenly became consumers or clients. My grandfather ran a grocery store and had a lot of customers, and my father was a lawyer and had a lot of clients. None of those customers or clients would come to see me as their doctor with their illnesses today if I were a provider. The use of the terminology of “providers” and “customers” lowers all health care staff to the lowest common denominator and demeans the concerns of my patients.

I recently received a letter from a former fellow who completed his training almost 25 years ago, thanking me for guiding him through his education and to his successful medical career. It’s one of those letters that we all have received and that makes us feel that it is all worth it. When he went through his requisite 2 years of training, it seemed to me that my responsibility was to provide a model of how to provide excellent care at the bedside and clinic with expertise and compassion.

Dr. Goldstein, medical editor of Cardiology News, is professor of medicine at Wayne State University and division head emeritus of cardiovascular medicine at Henry Ford Hospital, both in Detroit. He is on data safety monitoring committees for the National Institutes of Health and several pharmaceutical companies.
 

I recently received a letter from a former fellow who completed his training almost 25 years ago, thanking me for guiding him through his education and to his successful medical career. It’s one of those letters that we all have received and that makes us feel that it is all worth it. When he went through his requisite 2 years of training, it seemed to me that my responsibility was to provide a model of how to provide excellent care at the bedside and clinic with expertise and compassion.

Dr. Goldstein, medical editor of Cardiology News, is professor of medicine at Wayne State University and division head emeritus of cardiovascular medicine at Henry Ford Hospital, both in Detroit. He is on data safety monitoring committees for the National Institutes of Health and several pharmaceutical companies.
 

I recently received a letter from a former fellow who completed his training almost 25 years ago, thanking me for guiding him through his education and to his successful medical career. It’s one of those letters that we all have received and that makes us feel that it is all worth it. When he went through his requisite 2 years of training, it seemed to me that my responsibility was to provide a model of how to provide excellent care at the bedside and clinic with expertise and compassion.

Dr. Goldstein, medical editor of Cardiology News, is professor of medicine at Wayne State University and division head emeritus of cardiovascular medicine at Henry Ford Hospital, both in Detroit. He is on data safety monitoring committees for the National Institutes of Health and several pharmaceutical companies.
 

This is the mantra that the world hears when they call most, if not all, hospitals and medical clinics for the symptomatic relief of a myriad of health care complaints. Exactly what is the definition of an emergency is uncertain. We all could include severe chest pain, shortness of breath or sudden collapse or loss of consciousness.

To a patient, an emergency might just include the pressing need to speak to their doctor about the occurrence of symptoms and or anxieties that suddenly have occurred. In the past, before the telephone was invented, a friend or family member was sent by horseback or a Ford V8 to find the local doctor. With the advent of the telephone, doctors actually listed their number in a phone directory to facilitate contact with their patient.

Dr. Goldstein, medical editor of Cardiology News, is professor of medicine at Wayne State University and division head emeritus of cardiovascular medicine at Henry Ford Hospital, both in Detroit. He is on data safety monitoring committees for the National Institutes of Health and several pharmaceutical companies.

This is the mantra that the world hears when they call most, if not all, hospitals and medical clinics for the symptomatic relief of a myriad of health care complaints. Exactly what is the definition of an emergency is uncertain. We all could include severe chest pain, shortness of breath or sudden collapse or loss of consciousness.

To a patient, an emergency might just include the pressing need to speak to their doctor about the occurrence of symptoms and or anxieties that suddenly have occurred. In the past, before the telephone was invented, a friend or family member was sent by horseback or a Ford V8 to find the local doctor. With the advent of the telephone, doctors actually listed their number in a phone directory to facilitate contact with their patient.

Dr. Goldstein, medical editor of Cardiology News, is professor of medicine at Wayne State University and division head emeritus of cardiovascular medicine at Henry Ford Hospital, both in Detroit. He is on data safety monitoring committees for the National Institutes of Health and several pharmaceutical companies.

This is the mantra that the world hears when they call most, if not all, hospitals and medical clinics for the symptomatic relief of a myriad of health care complaints. Exactly what is the definition of an emergency is uncertain. We all could include severe chest pain, shortness of breath or sudden collapse or loss of consciousness.

To a patient, an emergency might just include the pressing need to speak to their doctor about the occurrence of symptoms and or anxieties that suddenly have occurred. In the past, before the telephone was invented, a friend or family member was sent by horseback or a Ford V8 to find the local doctor. With the advent of the telephone, doctors actually listed their number in a phone directory to facilitate contact with their patient.

Dr. Goldstein, medical editor of Cardiology News, is professor of medicine at Wayne State University and division head emeritus of cardiovascular medicine at Henry Ford Hospital, both in Detroit. He is on data safety monitoring committees for the National Institutes of Health and several pharmaceutical companies.

A lot has changed in acute myocardial infarction management in the 36 years since investigators for the Beta-Blocker Heart Attack Trial (BHAT) reported that the treatment of AMI in patients with propranolol, the beta-blocker of the day, reduced mortality by over 25% over 3 years (JAMA. 1981 Nov 6;246[18]:2073-4), and a European trial of timolol confirmed those findings.

New medications have been developed, including ACE inhibitors, statins, and a variety of drugs that modify the thrombotic process that occurs with the event. In addition, endovascular procedures have modified the obstructive coronary vascular anatomy that precipitated the event. At the same time, the definition of an AMI has changed dramatically, now depending in many instances on transitory elevation of the highly sensitive troponins. The BHAT definition depended largely on electrocardiographic changes associated with the event, which were ST-segment elevations in 79% of the occurrences, or significant ST-segment changes associated often with elevation of the insensitive enzyme, serum glutamic transaminase, and significant symptoms. The characteristics of the BHAT patient only faintly resemble the patients who we now classify with AMIs, and its definition expanded well beyond the BHAT patients. And yet beta-blocker therapy is still part of the class I or II recommendations for the treatment of an AMI.

Dr. Goldstein, medical editor of Cardiology News, is professor of medicine at Wayne State University and division head emeritus of cardiovascular medicine at Henry Ford Hospital, both in Detroit. He is on data safety monitoring committees for the National Institutes of Health and several pharmaceutical companies.

A lot has changed in acute myocardial infarction management in the 36 years since investigators for the Beta-Blocker Heart Attack Trial (BHAT) reported that the treatment of AMI in patients with propranolol, the beta-blocker of the day, reduced mortality by over 25% over 3 years (JAMA. 1981 Nov 6;246[18]:2073-4), and a European trial of timolol confirmed those findings.

New medications have been developed, including ACE inhibitors, statins, and a variety of drugs that modify the thrombotic process that occurs with the event. In addition, endovascular procedures have modified the obstructive coronary vascular anatomy that precipitated the event. At the same time, the definition of an AMI has changed dramatically, now depending in many instances on transitory elevation of the highly sensitive troponins. The BHAT definition depended largely on electrocardiographic changes associated with the event, which were ST-segment elevations in 79% of the occurrences, or significant ST-segment changes associated often with elevation of the insensitive enzyme, serum glutamic transaminase, and significant symptoms. The characteristics of the BHAT patient only faintly resemble the patients who we now classify with AMIs, and its definition expanded well beyond the BHAT patients. And yet beta-blocker therapy is still part of the class I or II recommendations for the treatment of an AMI.

Dr. Goldstein, medical editor of Cardiology News, is professor of medicine at Wayne State University and division head emeritus of cardiovascular medicine at Henry Ford Hospital, both in Detroit. He is on data safety monitoring committees for the National Institutes of Health and several pharmaceutical companies.

A lot has changed in acute myocardial infarction management in the 36 years since investigators for the Beta-Blocker Heart Attack Trial (BHAT) reported that the treatment of AMI in patients with propranolol, the beta-blocker of the day, reduced mortality by over 25% over 3 years (JAMA. 1981 Nov 6;246[18]:2073-4), and a European trial of timolol confirmed those findings.

New medications have been developed, including ACE inhibitors, statins, and a variety of drugs that modify the thrombotic process that occurs with the event. In addition, endovascular procedures have modified the obstructive coronary vascular anatomy that precipitated the event. At the same time, the definition of an AMI has changed dramatically, now depending in many instances on transitory elevation of the highly sensitive troponins. The BHAT definition depended largely on electrocardiographic changes associated with the event, which were ST-segment elevations in 79% of the occurrences, or significant ST-segment changes associated often with elevation of the insensitive enzyme, serum glutamic transaminase, and significant symptoms. The characteristics of the BHAT patient only faintly resemble the patients who we now classify with AMIs, and its definition expanded well beyond the BHAT patients. And yet beta-blocker therapy is still part of the class I or II recommendations for the treatment of an AMI.

Dr. Goldstein, medical editor of Cardiology News, is professor of medicine at Wayne State University and division head emeritus of cardiovascular medicine at Henry Ford Hospital, both in Detroit. He is on data safety monitoring committees for the National Institutes of Health and several pharmaceutical companies.