Paul Hauptman, MD

The recent release of billing information by the Centers for Medicare & Medicaid Services was accompanied by a spurious headline on the cms.gov website: "Historic release of data gives consumers unprecedented transparency on the medical services physicians provide and how much they are paid."

Have you downloaded the Excel spreadsheets online? There are megafiles of megabytes. The data lack all context and are confusing. What does it all mean? How are patients supposed to make decisions based on the data (if at all)? Do you want a doctor with a lot of Medicare billing or very little? As a cognitive clinic "E&M"-oriented cardiologist, I perform very few procedures. So my billings are in a middle range (I guess). If one of my patients were to carry out a search and discuss with me, I think that I would be within my professional rights to quote a recent secretary of state and ask, "What difference does it make?"

©MADDRAT/thinkstockphotos.com

Perhaps that is where the government gets it wrong. Are there high-end outliers? Sure, and if the Centers for Medicare & Medicaid Services wants to carry out an audit, it can. But the publication of these data on a website does nothing to improve transparency. They may create front page headline material for newspapers, but on a day-to-day basis, patients just want to have a physician with whom they can talk, a physician who advocates for them, a physician who is skilled and thoughtful and careful. Medicare billing? Not on anyone’s Top Ten list.

Next stop by the government? The sunshine law release of information. We might as well repeat this column when that happens.

Dr. Hauptman is professor of internal medicine and assistant dean of clinical-translational research at Saint Louis University and director of heart failure at Saint Louis University Hospital. He currently serves as an associate editor for Circulation: Heart Failure and blogs while staring out his office window at the Arch.

The recent release of billing information by the Centers for Medicare & Medicaid Services was accompanied by a spurious headline on the cms.gov website: "Historic release of data gives consumers unprecedented transparency on the medical services physicians provide and how much they are paid."

Have you downloaded the Excel spreadsheets online? There are megafiles of megabytes. The data lack all context and are confusing. What does it all mean? How are patients supposed to make decisions based on the data (if at all)? Do you want a doctor with a lot of Medicare billing or very little? As a cognitive clinic "E&M"-oriented cardiologist, I perform very few procedures. So my billings are in a middle range (I guess). If one of my patients were to carry out a search and discuss with me, I think that I would be within my professional rights to quote a recent secretary of state and ask, "What difference does it make?"

©MADDRAT/thinkstockphotos.com

Perhaps that is where the government gets it wrong. Are there high-end outliers? Sure, and if the Centers for Medicare & Medicaid Services wants to carry out an audit, it can. But the publication of these data on a website does nothing to improve transparency. They may create front page headline material for newspapers, but on a day-to-day basis, patients just want to have a physician with whom they can talk, a physician who advocates for them, a physician who is skilled and thoughtful and careful. Medicare billing? Not on anyone’s Top Ten list.

Next stop by the government? The sunshine law release of information. We might as well repeat this column when that happens.

Dr. Hauptman is professor of internal medicine and assistant dean of clinical-translational research at Saint Louis University and director of heart failure at Saint Louis University Hospital. He currently serves as an associate editor for Circulation: Heart Failure and blogs while staring out his office window at the Arch.

The recent release of billing information by the Centers for Medicare & Medicaid Services was accompanied by a spurious headline on the cms.gov website: "Historic release of data gives consumers unprecedented transparency on the medical services physicians provide and how much they are paid."

Have you downloaded the Excel spreadsheets online? There are megafiles of megabytes. The data lack all context and are confusing. What does it all mean? How are patients supposed to make decisions based on the data (if at all)? Do you want a doctor with a lot of Medicare billing or very little? As a cognitive clinic "E&M"-oriented cardiologist, I perform very few procedures. So my billings are in a middle range (I guess). If one of my patients were to carry out a search and discuss with me, I think that I would be within my professional rights to quote a recent secretary of state and ask, "What difference does it make?"

©MADDRAT/thinkstockphotos.com

Perhaps that is where the government gets it wrong. Are there high-end outliers? Sure, and if the Centers for Medicare & Medicaid Services wants to carry out an audit, it can. But the publication of these data on a website does nothing to improve transparency. They may create front page headline material for newspapers, but on a day-to-day basis, patients just want to have a physician with whom they can talk, a physician who advocates for them, a physician who is skilled and thoughtful and careful. Medicare billing? Not on anyone’s Top Ten list.

Next stop by the government? The sunshine law release of information. We might as well repeat this column when that happens.

Dr. Hauptman is professor of internal medicine and assistant dean of clinical-translational research at Saint Louis University and director of heart failure at Saint Louis University Hospital. He currently serves as an associate editor for Circulation: Heart Failure and blogs while staring out his office window at the Arch.

WASHINGTON – Another annual meeting of the American College of Cardiology has drawn to a close, and aside from the seemingly endless rain (and brief snow flurries), a lot of interesting discourse took place.

In the heart failure discipline, we have to a large degree become incrementalists: Although there were no blockbusters, important data on renal denervation were released, and corridor discussions about serelaxin and ivabradine were animated. At a time of ICD-10 rollouts, electronic health record (EHR) struggles, board recertification challenges, accreditation, precertification, compliance mandates, and more, it was a delight to be a cognitive cardiologist again. For a few precious moments, we could own our profession again.

©Hoard11/Thinkstockphotos.com

We saw no hospital administrators; we did not receive any missives about the (lack of) timeliness of closing encounters in EHRs; we engaged in real peer-to-peer interactions with real peers, unlike the shadow variant we deal with during an appeal of an insurance coverage decision.

And then it was over, ironically with the sun shining. It’s now back to work, but perhaps with renewed purpose. Let’s find ways to reestablish facts on the ground: Our patients and the decisions we make about our patients come first. Research and teaching do, too. Hospital administrators? Send them to a very long annual meeting. And hope that they forget to pack umbrellas.

Dr. Hauptman is professor of internal medicine and assistant dean of clinical-translational research at Saint Louis University and director of heart failure at Saint Louis University Hospital.

WASHINGTON – Another annual meeting of the American College of Cardiology has drawn to a close, and aside from the seemingly endless rain (and brief snow flurries), a lot of interesting discourse took place.

In the heart failure discipline, we have to a large degree become incrementalists: Although there were no blockbusters, important data on renal denervation were released, and corridor discussions about serelaxin and ivabradine were animated. At a time of ICD-10 rollouts, electronic health record (EHR) struggles, board recertification challenges, accreditation, precertification, compliance mandates, and more, it was a delight to be a cognitive cardiologist again. For a few precious moments, we could own our profession again.

©Hoard11/Thinkstockphotos.com

We saw no hospital administrators; we did not receive any missives about the (lack of) timeliness of closing encounters in EHRs; we engaged in real peer-to-peer interactions with real peers, unlike the shadow variant we deal with during an appeal of an insurance coverage decision.

And then it was over, ironically with the sun shining. It’s now back to work, but perhaps with renewed purpose. Let’s find ways to reestablish facts on the ground: Our patients and the decisions we make about our patients come first. Research and teaching do, too. Hospital administrators? Send them to a very long annual meeting. And hope that they forget to pack umbrellas.

Dr. Hauptman is professor of internal medicine and assistant dean of clinical-translational research at Saint Louis University and director of heart failure at Saint Louis University Hospital.

WASHINGTON – Another annual meeting of the American College of Cardiology has drawn to a close, and aside from the seemingly endless rain (and brief snow flurries), a lot of interesting discourse took place.

In the heart failure discipline, we have to a large degree become incrementalists: Although there were no blockbusters, important data on renal denervation were released, and corridor discussions about serelaxin and ivabradine were animated. At a time of ICD-10 rollouts, electronic health record (EHR) struggles, board recertification challenges, accreditation, precertification, compliance mandates, and more, it was a delight to be a cognitive cardiologist again. For a few precious moments, we could own our profession again.

©Hoard11/Thinkstockphotos.com

We saw no hospital administrators; we did not receive any missives about the (lack of) timeliness of closing encounters in EHRs; we engaged in real peer-to-peer interactions with real peers, unlike the shadow variant we deal with during an appeal of an insurance coverage decision.

And then it was over, ironically with the sun shining. It’s now back to work, but perhaps with renewed purpose. Let’s find ways to reestablish facts on the ground: Our patients and the decisions we make about our patients come first. Research and teaching do, too. Hospital administrators? Send them to a very long annual meeting. And hope that they forget to pack umbrellas.

Dr. Hauptman is professor of internal medicine and assistant dean of clinical-translational research at Saint Louis University and director of heart failure at Saint Louis University Hospital.

At the recent International Congress on Peer Review and Biomedical Publication, researchers at Yale University, New Haven, Conn., presented data on 18,411 original papers published in 2006 from 144 journals in the cardiovascular discipline.

They found that the median number of citations was six; 15.0% of papers were never cited; and 33.3% had only one to five citations in the following 5 years. It was no surprise that the impact factor of the journal predicted subsequent citations: That’s probably one of the reasons why those journals have high impact factors. So what do the authors conclude? They state that their data suggest "substantial waste in some combination of the funding, pursuit, publication or dissemination of cardiovascular science."

An interesting thought but flawed. Sure, the number of publications has expanded, but so what? The cardiovascular medicine community is now very large. No one presupposes that all published papers are high quality, useful, or impactful. Sometimes a paper is redundant and poorly constructed, and may not have been subjected to rigorous peer review. But "diamonds in the rough" do exist, and that is why I sometimes read journals with rather paltry impact factors. New ideas or kernels of new ideas can often be found there. The same goes for abstracts at meetings.

Rather than express concern, we should argue that our field is filled with ideas, that the way forward is often incremental and that limiting publications would potentially damage progress. If any "solution" is needed, it will come from quality peer review and economics. After all, a journal with a minuscule impact factor is not likely to sustain itself on subscriptions and advertising dollars.

So, are we really publishing too much in cardiovascular medicine? Dr. Mort Kern, chief of cardiology at the University of California, Irvine, used to say that "every paper can find a home," but the publication process can be time consuming and difficult. Let’s continue to publish and keep the conversation going.

Dr. Paul Hauptman is professor of internal medicine and assistant dean of clinical-translational research at Saint Louis University and director of heart failure at Saint Louis University Hospital. He serves as an associate editor for Circulation: Heart Failure and blogs while staring out his office window at the Arch.

At the recent International Congress on Peer Review and Biomedical Publication, researchers at Yale University, New Haven, Conn., presented data on 18,411 original papers published in 2006 from 144 journals in the cardiovascular discipline.

They found that the median number of citations was six; 15.0% of papers were never cited; and 33.3% had only one to five citations in the following 5 years. It was no surprise that the impact factor of the journal predicted subsequent citations: That’s probably one of the reasons why those journals have high impact factors. So what do the authors conclude? They state that their data suggest "substantial waste in some combination of the funding, pursuit, publication or dissemination of cardiovascular science."

An interesting thought but flawed. Sure, the number of publications has expanded, but so what? The cardiovascular medicine community is now very large. No one presupposes that all published papers are high quality, useful, or impactful. Sometimes a paper is redundant and poorly constructed, and may not have been subjected to rigorous peer review. But "diamonds in the rough" do exist, and that is why I sometimes read journals with rather paltry impact factors. New ideas or kernels of new ideas can often be found there. The same goes for abstracts at meetings.

Rather than express concern, we should argue that our field is filled with ideas, that the way forward is often incremental and that limiting publications would potentially damage progress. If any "solution" is needed, it will come from quality peer review and economics. After all, a journal with a minuscule impact factor is not likely to sustain itself on subscriptions and advertising dollars.

So, are we really publishing too much in cardiovascular medicine? Dr. Mort Kern, chief of cardiology at the University of California, Irvine, used to say that "every paper can find a home," but the publication process can be time consuming and difficult. Let’s continue to publish and keep the conversation going.

Dr. Paul Hauptman is professor of internal medicine and assistant dean of clinical-translational research at Saint Louis University and director of heart failure at Saint Louis University Hospital. He serves as an associate editor for Circulation: Heart Failure and blogs while staring out his office window at the Arch.

At the recent International Congress on Peer Review and Biomedical Publication, researchers at Yale University, New Haven, Conn., presented data on 18,411 original papers published in 2006 from 144 journals in the cardiovascular discipline.

They found that the median number of citations was six; 15.0% of papers were never cited; and 33.3% had only one to five citations in the following 5 years. It was no surprise that the impact factor of the journal predicted subsequent citations: That’s probably one of the reasons why those journals have high impact factors. So what do the authors conclude? They state that their data suggest "substantial waste in some combination of the funding, pursuit, publication or dissemination of cardiovascular science."

An interesting thought but flawed. Sure, the number of publications has expanded, but so what? The cardiovascular medicine community is now very large. No one presupposes that all published papers are high quality, useful, or impactful. Sometimes a paper is redundant and poorly constructed, and may not have been subjected to rigorous peer review. But "diamonds in the rough" do exist, and that is why I sometimes read journals with rather paltry impact factors. New ideas or kernels of new ideas can often be found there. The same goes for abstracts at meetings.

Rather than express concern, we should argue that our field is filled with ideas, that the way forward is often incremental and that limiting publications would potentially damage progress. If any "solution" is needed, it will come from quality peer review and economics. After all, a journal with a minuscule impact factor is not likely to sustain itself on subscriptions and advertising dollars.

So, are we really publishing too much in cardiovascular medicine? Dr. Mort Kern, chief of cardiology at the University of California, Irvine, used to say that "every paper can find a home," but the publication process can be time consuming and difficult. Let’s continue to publish and keep the conversation going.

Dr. Paul Hauptman is professor of internal medicine and assistant dean of clinical-translational research at Saint Louis University and director of heart failure at Saint Louis University Hospital. He serves as an associate editor for Circulation: Heart Failure and blogs while staring out his office window at the Arch.

Just as spring training has begun, the National Institutes of Health has withdrawn funding for an important clinical trial, "Phosphodiesterase Type 5 Inhibition With Tadalafil Changes Outcomes in Heart Failure," or PITCH.

The role of PDE-5 inhibition in heart failure should be fully explored; the fact that the trial will not move forward now is a blow to the heart failure community and most importantly, patients. Although the details are not fully known, it appears that enrollment was slower than anticipated, a common phenomenon when clinical trials are initiated. (Full disclosure: I was in the process of submission of the regulatory paperwork and contracting to participate as a local principal investigator in PITCH when the trial was terminated.)

© Brocreative/Fotolia.com

PITCH is an example of translational medicine on steroids. A wealth of basic and preclinical data suggested that nitric oxide–induced vasodilation may impact outcomes in human heart failure. A lot of effort, much of it supported by the National Heart, Lung, and Blood Institute, was expended over the last two decades in this area. Indeed, just ask the Nobel Prize winners of 1998.

Is there any way for the investigators to get back "on the mound" to test the hypothesis? With patents expiring, don’t expect industry support to materialize. This leaves us with an important unanswered question. Quite unfortunate, when you think about how much we have examined inhibition of the renin-angiotensin system from every conceivable angle. PITCH needs a reliever. Who will it be?

Dr. Paul Hauptman is professor of internal medicine and assistant dean of clinical-translational research at Saint Louis University, and director of heart failure at Saint Louis University Hospital. He serves as an associate editor for Circulation: Heart Failure and blogs while staring out his office window at the Arch.

Just as spring training has begun, the National Institutes of Health has withdrawn funding for an important clinical trial, "Phosphodiesterase Type 5 Inhibition With Tadalafil Changes Outcomes in Heart Failure," or PITCH.

The role of PDE-5 inhibition in heart failure should be fully explored; the fact that the trial will not move forward now is a blow to the heart failure community and most importantly, patients. Although the details are not fully known, it appears that enrollment was slower than anticipated, a common phenomenon when clinical trials are initiated. (Full disclosure: I was in the process of submission of the regulatory paperwork and contracting to participate as a local principal investigator in PITCH when the trial was terminated.)

© Brocreative/Fotolia.com

PITCH is an example of translational medicine on steroids. A wealth of basic and preclinical data suggested that nitric oxide–induced vasodilation may impact outcomes in human heart failure. A lot of effort, much of it supported by the National Heart, Lung, and Blood Institute, was expended over the last two decades in this area. Indeed, just ask the Nobel Prize winners of 1998.

Is there any way for the investigators to get back "on the mound" to test the hypothesis? With patents expiring, don’t expect industry support to materialize. This leaves us with an important unanswered question. Quite unfortunate, when you think about how much we have examined inhibition of the renin-angiotensin system from every conceivable angle. PITCH needs a reliever. Who will it be?

Dr. Paul Hauptman is professor of internal medicine and assistant dean of clinical-translational research at Saint Louis University, and director of heart failure at Saint Louis University Hospital. He serves as an associate editor for Circulation: Heart Failure and blogs while staring out his office window at the Arch.

Just as spring training has begun, the National Institutes of Health has withdrawn funding for an important clinical trial, "Phosphodiesterase Type 5 Inhibition With Tadalafil Changes Outcomes in Heart Failure," or PITCH.

The role of PDE-5 inhibition in heart failure should be fully explored; the fact that the trial will not move forward now is a blow to the heart failure community and most importantly, patients. Although the details are not fully known, it appears that enrollment was slower than anticipated, a common phenomenon when clinical trials are initiated. (Full disclosure: I was in the process of submission of the regulatory paperwork and contracting to participate as a local principal investigator in PITCH when the trial was terminated.)

© Brocreative/Fotolia.com

PITCH is an example of translational medicine on steroids. A wealth of basic and preclinical data suggested that nitric oxide–induced vasodilation may impact outcomes in human heart failure. A lot of effort, much of it supported by the National Heart, Lung, and Blood Institute, was expended over the last two decades in this area. Indeed, just ask the Nobel Prize winners of 1998.

Is there any way for the investigators to get back "on the mound" to test the hypothesis? With patents expiring, don’t expect industry support to materialize. This leaves us with an important unanswered question. Quite unfortunate, when you think about how much we have examined inhibition of the renin-angiotensin system from every conceivable angle. PITCH needs a reliever. Who will it be?

Dr. Paul Hauptman is professor of internal medicine and assistant dean of clinical-translational research at Saint Louis University, and director of heart failure at Saint Louis University Hospital. He serves as an associate editor for Circulation: Heart Failure and blogs while staring out his office window at the Arch.

The release of top-line data from the sponsor of SYMPLICITY HTN-3, a large study of renal denervation in hypertension, provided a shock wave to the cardiovascular community.

To some degree, the findings of the study are not surprising. As always, patients who are in clinical trials do well, in this case the sham-operated patients who perhaps at long last were subjected to a focused effort at blood pressure lowering. We will have to wait a while to evaluate the data including subgroup analyses and substudies, but the much ballyhooed effects seen in earlier studies (Lancet 2009;373:1275-81; Lancet 2010;376:1903-9), which did not include a sham-operated arm, now seem to be a series of false leads.

In reading the obituaries, it sounds as if both the company and researchers have quickly opted to move on. But they shouldn’t. There is ample reason to believe that renal denervation may mitigate cardiorenal syndrome, a clinically challenging state that is associated with higher mortality in patients with heart failure. There are a number of small studies underway, the most prominent of which, PRESERVE (Promotion of Renal Sodium Excretion by Renal Sympathetic Denervation in Congestive Heart Failure), is supported by the National Heart, Lung, and Blood Institute. These studies should move forward. It would be a disservice to patients and medical science if one negative study in hypertension, albeit a big one, fails.

Will renal denervation work in heart failure? The studies must go on.

Dr. Hauptman is professor of internal medicine and assistant dean of clinical-translational research at Saint Louis University and director of heart failure at Saint Louis University Hospital. He is an associate editor for Circulation: Heart Failure and blogs while staring out his office window at the Arch.

The release of top-line data from the sponsor of SYMPLICITY HTN-3, a large study of renal denervation in hypertension, provided a shock wave to the cardiovascular community.

To some degree, the findings of the study are not surprising. As always, patients who are in clinical trials do well, in this case the sham-operated patients who perhaps at long last were subjected to a focused effort at blood pressure lowering. We will have to wait a while to evaluate the data including subgroup analyses and substudies, but the much ballyhooed effects seen in earlier studies (Lancet 2009;373:1275-81; Lancet 2010;376:1903-9), which did not include a sham-operated arm, now seem to be a series of false leads.

In reading the obituaries, it sounds as if both the company and researchers have quickly opted to move on. But they shouldn’t. There is ample reason to believe that renal denervation may mitigate cardiorenal syndrome, a clinically challenging state that is associated with higher mortality in patients with heart failure. There are a number of small studies underway, the most prominent of which, PRESERVE (Promotion of Renal Sodium Excretion by Renal Sympathetic Denervation in Congestive Heart Failure), is supported by the National Heart, Lung, and Blood Institute. These studies should move forward. It would be a disservice to patients and medical science if one negative study in hypertension, albeit a big one, fails.

Will renal denervation work in heart failure? The studies must go on.

Dr. Hauptman is professor of internal medicine and assistant dean of clinical-translational research at Saint Louis University and director of heart failure at Saint Louis University Hospital. He is an associate editor for Circulation: Heart Failure and blogs while staring out his office window at the Arch.

The release of top-line data from the sponsor of SYMPLICITY HTN-3, a large study of renal denervation in hypertension, provided a shock wave to the cardiovascular community.

To some degree, the findings of the study are not surprising. As always, patients who are in clinical trials do well, in this case the sham-operated patients who perhaps at long last were subjected to a focused effort at blood pressure lowering. We will have to wait a while to evaluate the data including subgroup analyses and substudies, but the much ballyhooed effects seen in earlier studies (Lancet 2009;373:1275-81; Lancet 2010;376:1903-9), which did not include a sham-operated arm, now seem to be a series of false leads.

In reading the obituaries, it sounds as if both the company and researchers have quickly opted to move on. But they shouldn’t. There is ample reason to believe that renal denervation may mitigate cardiorenal syndrome, a clinically challenging state that is associated with higher mortality in patients with heart failure. There are a number of small studies underway, the most prominent of which, PRESERVE (Promotion of Renal Sodium Excretion by Renal Sympathetic Denervation in Congestive Heart Failure), is supported by the National Heart, Lung, and Blood Institute. These studies should move forward. It would be a disservice to patients and medical science if one negative study in hypertension, albeit a big one, fails.

Will renal denervation work in heart failure? The studies must go on.

Dr. Hauptman is professor of internal medicine and assistant dean of clinical-translational research at Saint Louis University and director of heart failure at Saint Louis University Hospital. He is an associate editor for Circulation: Heart Failure and blogs while staring out his office window at the Arch.

Enough time has now passed to process the implications of studies presented at the 2013 annual scientific sessions of the American College of Cardiology. If you were in attendance at the "late breakers" session – or if you have been diligently reading articles from those sessions – you may find yourself saying this was the year of the negative study.

With the exception of the findings from some subgroup analyses, there were (as usual) many negative studies in heart failure: RED-HF (Reduction of Events With Darbepoetin Alfa in Heart Failure Trial), RELAX (Evaluating the Effectiveness of Sildenafil at Improving Health Outcomes and Exercise Ability in People With Diastolic Heart Failure), ASTRONAUT (Six Months Efficacy and Safety of Aliskiren Therapy on Top of Standard Therapy, on Morbidity and Mortality in Patients With Acute Decompensated Heart Failure), as well as in other disciplines; HPS2-THRIVE (Treatment of HDL to Reduce the Incidence of Vascular Events) and TERISA (Type 2 Diabetes Evaluation of Ranolazine in Subjects With Chronic Stable Angina).

So much for so-called bias against negative study findings!

Maybe as a result of a bumper crop of negative trials in recent years, the obsession with the late-breaker session has become muted of late. There are also fewer real potential blockbuster trials underway that have the potential to demonstrably change practice.

Yet downturns and disappointments affect many fields of endeavor. The stock market might trade sideways for extended periods of time. Sport teams may hover around the .500 mark for multiple seasons. Broadway might feature mostly revivals for a few years. But rest assured, change is underway and the appearance of stasis is just that – appearance. In fact, I think we tend to learn almost as much if not more when a study’s results disappoint.

Why didn’t sildenafil perform better in RELAX? Was it an issue of how the study was statistically powered?

Why is anemia a poor prognostic sign in heart failure, yet correction of anemia yields a big fat zero in affecting outcomes?

Yes, we can argue about the design of some these studies and maybe even the lack of perspective that might have led the sponsors astray. Rest assured, however, that we have moved forward in a slow if albeit inexorable way.

Cardiovascular medicine took a step forward at this year’s annual ACC meeting. Just don’t expect anything radical like a big leap in treatment advances right now. Don’t forget, for a time we were spoiled: Whether it was GUSTO (Global Use of Strategies to Open Occluded Coronary Arteries) or SAVE (Survival and Ventricular Enlargement) or 4S (Scandinavian Simvastatin Survival Study), everything seemed to hit for a while. But, on the other hand, we also had CAST (Cardiac Arrhythmia Suppression Trial) and BEST (Beta-blocker Evaluation of Survival Trial) and VEST (the Vesnarinone Trial).

It wasn’t as easy as we would like to think, but we learned a lot.

So the bottom line is: See you in Dallas at the scientific sessions of the American Health Association in the fall!

Enough time has now passed to process the implications of studies presented at the 2013 annual scientific sessions of the American College of Cardiology. If you were in attendance at the "late breakers" session – or if you have been diligently reading articles from those sessions – you may find yourself saying this was the year of the negative study.

With the exception of the findings from some subgroup analyses, there were (as usual) many negative studies in heart failure: RED-HF (Reduction of Events With Darbepoetin Alfa in Heart Failure Trial), RELAX (Evaluating the Effectiveness of Sildenafil at Improving Health Outcomes and Exercise Ability in People With Diastolic Heart Failure), ASTRONAUT (Six Months Efficacy and Safety of Aliskiren Therapy on Top of Standard Therapy, on Morbidity and Mortality in Patients With Acute Decompensated Heart Failure), as well as in other disciplines; HPS2-THRIVE (Treatment of HDL to Reduce the Incidence of Vascular Events) and TERISA (Type 2 Diabetes Evaluation of Ranolazine in Subjects With Chronic Stable Angina).

So much for so-called bias against negative study findings!

Maybe as a result of a bumper crop of negative trials in recent years, the obsession with the late-breaker session has become muted of late. There are also fewer real potential blockbuster trials underway that have the potential to demonstrably change practice.

Yet downturns and disappointments affect many fields of endeavor. The stock market might trade sideways for extended periods of time. Sport teams may hover around the .500 mark for multiple seasons. Broadway might feature mostly revivals for a few years. But rest assured, change is underway and the appearance of stasis is just that – appearance. In fact, I think we tend to learn almost as much if not more when a study’s results disappoint.

Why didn’t sildenafil perform better in RELAX? Was it an issue of how the study was statistically powered?

Why is anemia a poor prognostic sign in heart failure, yet correction of anemia yields a big fat zero in affecting outcomes?

Yes, we can argue about the design of some these studies and maybe even the lack of perspective that might have led the sponsors astray. Rest assured, however, that we have moved forward in a slow if albeit inexorable way.

Cardiovascular medicine took a step forward at this year’s annual ACC meeting. Just don’t expect anything radical like a big leap in treatment advances right now. Don’t forget, for a time we were spoiled: Whether it was GUSTO (Global Use of Strategies to Open Occluded Coronary Arteries) or SAVE (Survival and Ventricular Enlargement) or 4S (Scandinavian Simvastatin Survival Study), everything seemed to hit for a while. But, on the other hand, we also had CAST (Cardiac Arrhythmia Suppression Trial) and BEST (Beta-blocker Evaluation of Survival Trial) and VEST (the Vesnarinone Trial).

It wasn’t as easy as we would like to think, but we learned a lot.

So the bottom line is: See you in Dallas at the scientific sessions of the American Health Association in the fall!

Enough time has now passed to process the implications of studies presented at the 2013 annual scientific sessions of the American College of Cardiology. If you were in attendance at the "late breakers" session – or if you have been diligently reading articles from those sessions – you may find yourself saying this was the year of the negative study.

With the exception of the findings from some subgroup analyses, there were (as usual) many negative studies in heart failure: RED-HF (Reduction of Events With Darbepoetin Alfa in Heart Failure Trial), RELAX (Evaluating the Effectiveness of Sildenafil at Improving Health Outcomes and Exercise Ability in People With Diastolic Heart Failure), ASTRONAUT (Six Months Efficacy and Safety of Aliskiren Therapy on Top of Standard Therapy, on Morbidity and Mortality in Patients With Acute Decompensated Heart Failure), as well as in other disciplines; HPS2-THRIVE (Treatment of HDL to Reduce the Incidence of Vascular Events) and TERISA (Type 2 Diabetes Evaluation of Ranolazine in Subjects With Chronic Stable Angina).

So much for so-called bias against negative study findings!

Maybe as a result of a bumper crop of negative trials in recent years, the obsession with the late-breaker session has become muted of late. There are also fewer real potential blockbuster trials underway that have the potential to demonstrably change practice.

Yet downturns and disappointments affect many fields of endeavor. The stock market might trade sideways for extended periods of time. Sport teams may hover around the .500 mark for multiple seasons. Broadway might feature mostly revivals for a few years. But rest assured, change is underway and the appearance of stasis is just that – appearance. In fact, I think we tend to learn almost as much if not more when a study’s results disappoint.

Why didn’t sildenafil perform better in RELAX? Was it an issue of how the study was statistically powered?

Why is anemia a poor prognostic sign in heart failure, yet correction of anemia yields a big fat zero in affecting outcomes?

Yes, we can argue about the design of some these studies and maybe even the lack of perspective that might have led the sponsors astray. Rest assured, however, that we have moved forward in a slow if albeit inexorable way.

Cardiovascular medicine took a step forward at this year’s annual ACC meeting. Just don’t expect anything radical like a big leap in treatment advances right now. Don’t forget, for a time we were spoiled: Whether it was GUSTO (Global Use of Strategies to Open Occluded Coronary Arteries) or SAVE (Survival and Ventricular Enlargement) or 4S (Scandinavian Simvastatin Survival Study), everything seemed to hit for a while. But, on the other hand, we also had CAST (Cardiac Arrhythmia Suppression Trial) and BEST (Beta-blocker Evaluation of Survival Trial) and VEST (the Vesnarinone Trial).

It wasn’t as easy as we would like to think, but we learned a lot.

So the bottom line is: See you in Dallas at the scientific sessions of the American Health Association in the fall!

Another academic year is upon us and so, too, is an attempt to reconfigure how we train our interns and residents.

The decline in medical education began with the Bell Commission and the first law passed by New York State in 1989 designed to limit residents’ hours. Since then the rules have become more draconian, and internship as we knew it is no more. A lot can be said about the consequences, but I’ll just mention one that impacts cardiology: It’s the lack of exposure to clinical medicine, a galling end-product of regulations that were created to correct a perceived wrong without the benefit of a foundation of critical data.

CCat82/iStockphoto

That 3:00 a.m. STEMI call is more likely than ever to be witnessed by a "night float" than a resident on a cardiology rotation. When morning comes, the course of events has become at most a 15-second summation given to the incoming resident; it is no longer a meaningful "at the bedside" exchange. Without such experiences, the complications of a myocardial infarction are now merely items to be memorized from a textbook, ECG interpretation is becoming a lost art, and any complaint of "chest pain" on the internal medicine service leads to a call for a cardiology consultation.

At least cardiology fellowship remains in demand, and the fellows seem to be engaged. Indeed, their enthusiasm and interest provide much needed reassurance; after all, we are training the physicians who will be our physicians or our children’s physicians in the future.

Another academic year is upon us and so, too, is an attempt to reconfigure how we train our interns and residents.

The decline in medical education began with the Bell Commission and the first law passed by New York State in 1989 designed to limit residents’ hours. Since then the rules have become more draconian, and internship as we knew it is no more. A lot can be said about the consequences, but I’ll just mention one that impacts cardiology: It’s the lack of exposure to clinical medicine, a galling end-product of regulations that were created to correct a perceived wrong without the benefit of a foundation of critical data.

CCat82/iStockphoto

That 3:00 a.m. STEMI call is more likely than ever to be witnessed by a "night float" than a resident on a cardiology rotation. When morning comes, the course of events has become at most a 15-second summation given to the incoming resident; it is no longer a meaningful "at the bedside" exchange. Without such experiences, the complications of a myocardial infarction are now merely items to be memorized from a textbook, ECG interpretation is becoming a lost art, and any complaint of "chest pain" on the internal medicine service leads to a call for a cardiology consultation.

At least cardiology fellowship remains in demand, and the fellows seem to be engaged. Indeed, their enthusiasm and interest provide much needed reassurance; after all, we are training the physicians who will be our physicians or our children’s physicians in the future.

Another academic year is upon us and so, too, is an attempt to reconfigure how we train our interns and residents.

The decline in medical education began with the Bell Commission and the first law passed by New York State in 1989 designed to limit residents’ hours. Since then the rules have become more draconian, and internship as we knew it is no more. A lot can be said about the consequences, but I’ll just mention one that impacts cardiology: It’s the lack of exposure to clinical medicine, a galling end-product of regulations that were created to correct a perceived wrong without the benefit of a foundation of critical data.

CCat82/iStockphoto

That 3:00 a.m. STEMI call is more likely than ever to be witnessed by a "night float" than a resident on a cardiology rotation. When morning comes, the course of events has become at most a 15-second summation given to the incoming resident; it is no longer a meaningful "at the bedside" exchange. Without such experiences, the complications of a myocardial infarction are now merely items to be memorized from a textbook, ECG interpretation is becoming a lost art, and any complaint of "chest pain" on the internal medicine service leads to a call for a cardiology consultation.

At least cardiology fellowship remains in demand, and the fellows seem to be engaged. Indeed, their enthusiasm and interest provide much needed reassurance; after all, we are training the physicians who will be our physicians or our children’s physicians in the future.

Our knowledge base in cardiovascular diseases has progressed in the last 20 years largely on the strength of randomized clinical trials. We pay special attention to "megatrials" because of their statistical heft, and often apply the lessons learned to the patients we treat.

But critics abound, and with good reason. A personal favorite: "Randomised controlled trials are primarily about medical interventions and not patients," that is, randomization permits comparisons of interventions not confounded by the individuality of patients." The paradox of the clinical trial is that it is the best way to assess whether an intervention works, but is arguably the worst way to assess who will benefit from it (Lancet 1999;353:743-6).

Photo:CarolinaSmith/iStockphoto.com

So therein lies the core of the debate about RCTs: How representative are they? If simvastatin worked in the 4S Study (Lancet 1994;344:1383-9), would the drug work in American, non-Scandinavian patients? If implantable cardioverter defibrillators reduced mortality in a primary prevention cohort with a mean age in the lower 60s, would they work in octogenarians (Arch. Intern. Med. 2012: 2012;172:67-8)? A combination of hydralazine and nitrates worked in black patients with heart failure treated in A-HeFT (N. Engl. J. Med. 2004;351:2049-57), but do the findings apply to Caucasians?

Krumholz and colleagues pointed out 10 years ago that women and the elderly were underrepresented in clinical trials of heart failure interventions (Arch. Intern. Med. 2002; 1682-8), andthese findings have remained germane (Arch. Intern. Med. 2011;171:550-6). Recently, Dhruva and Redberg proposed with ample justification (JAMA 2012;307:1145-6) that device trials increase representation of women and that the Food and Drug Administration should be focused on enforcing this directive.

The problem is that there are limits to how completely we can "cover the waterfront," since patient factors that likely influence response (ethnicity, race, sex and other related inherent genetic, biological and social parameters) can be so varied. Shall we set a minimum enrollment for elderly Asian females without diabetes? What about young Hispanic males who smoke more than one pack of cigarettes a day? And how do we handle in-group differences? To some degree, this line of questioning is pure nonsense. We have learned something from the science of clinical trials; namely, subgroups should be prespecified, and stratification at time of randomization is necessary. However, these requirements represent an impossible statistical barrier if multiple potential subgroups are determined to be of interest.

There is no easy answer to the proposal of Dhruva and Redberg. To simply state "Registry" or "Pharmacogenomics" is not sufficient. On the other hand, the potential "Balkanization" of clinical trials in which each defined subgroup is given its own trial is not tenable. Selection of one favored subgroup for greater representation will not solve the problem either. The thorny representation issues of randomized trials must be addressed. The future of RCTs lies in the balance.

Our knowledge base in cardiovascular diseases has progressed in the last 20 years largely on the strength of randomized clinical trials. We pay special attention to "megatrials" because of their statistical heft, and often apply the lessons learned to the patients we treat.

But critics abound, and with good reason. A personal favorite: "Randomised controlled trials are primarily about medical interventions and not patients," that is, randomization permits comparisons of interventions not confounded by the individuality of patients." The paradox of the clinical trial is that it is the best way to assess whether an intervention works, but is arguably the worst way to assess who will benefit from it (Lancet 1999;353:743-6).

Photo:CarolinaSmith/iStockphoto.com

So therein lies the core of the debate about RCTs: How representative are they? If simvastatin worked in the 4S Study (Lancet 1994;344:1383-9), would the drug work in American, non-Scandinavian patients? If implantable cardioverter defibrillators reduced mortality in a primary prevention cohort with a mean age in the lower 60s, would they work in octogenarians (Arch. Intern. Med. 2012: 2012;172:67-8)? A combination of hydralazine and nitrates worked in black patients with heart failure treated in A-HeFT (N. Engl. J. Med. 2004;351:2049-57), but do the findings apply to Caucasians?

Krumholz and colleagues pointed out 10 years ago that women and the elderly were underrepresented in clinical trials of heart failure interventions (Arch. Intern. Med. 2002; 1682-8), andthese findings have remained germane (Arch. Intern. Med. 2011;171:550-6). Recently, Dhruva and Redberg proposed with ample justification (JAMA 2012;307:1145-6) that device trials increase representation of women and that the Food and Drug Administration should be focused on enforcing this directive.

The problem is that there are limits to how completely we can "cover the waterfront," since patient factors that likely influence response (ethnicity, race, sex and other related inherent genetic, biological and social parameters) can be so varied. Shall we set a minimum enrollment for elderly Asian females without diabetes? What about young Hispanic males who smoke more than one pack of cigarettes a day? And how do we handle in-group differences? To some degree, this line of questioning is pure nonsense. We have learned something from the science of clinical trials; namely, subgroups should be prespecified, and stratification at time of randomization is necessary. However, these requirements represent an impossible statistical barrier if multiple potential subgroups are determined to be of interest.

There is no easy answer to the proposal of Dhruva and Redberg. To simply state "Registry" or "Pharmacogenomics" is not sufficient. On the other hand, the potential "Balkanization" of clinical trials in which each defined subgroup is given its own trial is not tenable. Selection of one favored subgroup for greater representation will not solve the problem either. The thorny representation issues of randomized trials must be addressed. The future of RCTs lies in the balance.

Our knowledge base in cardiovascular diseases has progressed in the last 20 years largely on the strength of randomized clinical trials. We pay special attention to "megatrials" because of their statistical heft, and often apply the lessons learned to the patients we treat.

But critics abound, and with good reason. A personal favorite: "Randomised controlled trials are primarily about medical interventions and not patients," that is, randomization permits comparisons of interventions not confounded by the individuality of patients." The paradox of the clinical trial is that it is the best way to assess whether an intervention works, but is arguably the worst way to assess who will benefit from it (Lancet 1999;353:743-6).

Photo:CarolinaSmith/iStockphoto.com

So therein lies the core of the debate about RCTs: How representative are they? If simvastatin worked in the 4S Study (Lancet 1994;344:1383-9), would the drug work in American, non-Scandinavian patients? If implantable cardioverter defibrillators reduced mortality in a primary prevention cohort with a mean age in the lower 60s, would they work in octogenarians (Arch. Intern. Med. 2012: 2012;172:67-8)? A combination of hydralazine and nitrates worked in black patients with heart failure treated in A-HeFT (N. Engl. J. Med. 2004;351:2049-57), but do the findings apply to Caucasians?

Krumholz and colleagues pointed out 10 years ago that women and the elderly were underrepresented in clinical trials of heart failure interventions (Arch. Intern. Med. 2002; 1682-8), andthese findings have remained germane (Arch. Intern. Med. 2011;171:550-6). Recently, Dhruva and Redberg proposed with ample justification (JAMA 2012;307:1145-6) that device trials increase representation of women and that the Food and Drug Administration should be focused on enforcing this directive.

The problem is that there are limits to how completely we can "cover the waterfront," since patient factors that likely influence response (ethnicity, race, sex and other related inherent genetic, biological and social parameters) can be so varied. Shall we set a minimum enrollment for elderly Asian females without diabetes? What about young Hispanic males who smoke more than one pack of cigarettes a day? And how do we handle in-group differences? To some degree, this line of questioning is pure nonsense. We have learned something from the science of clinical trials; namely, subgroups should be prespecified, and stratification at time of randomization is necessary. However, these requirements represent an impossible statistical barrier if multiple potential subgroups are determined to be of interest.

There is no easy answer to the proposal of Dhruva and Redberg. To simply state "Registry" or "Pharmacogenomics" is not sufficient. On the other hand, the potential "Balkanization" of clinical trials in which each defined subgroup is given its own trial is not tenable. Selection of one favored subgroup for greater representation will not solve the problem either. The thorny representation issues of randomized trials must be addressed. The future of RCTs lies in the balance.