Beta-blocker therapy post AMI

 

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.

It took almost 2 decades before beta-blocker therapy became part of the standard therapy for AMI, but in the interval beta-blockers had been used widely for the treatment of hypertension and angina. One important finding in BHAT was that patients with heart failure associated with the AMI event received the largest mortality benefit. This observation led to the subsequent clinical trials emphasizing the role of beta-blockade in the treatment of heart failure with or without ischemic etiology.

The role of beta-blockers in the treatment of the contemporary AMI has been challenged recently. Reasonable questions have been raised as to the wisdom of throwing the full bag of therapy at this population rather than a more selective choice of drugs. In order to gain further insight into the benefits of beta-blocker therapy in the total spectrum of post MI therapy, large populations studies using a variety of statistical gymnastics have tried to identify the unique benefit that can be attributed to beta-blocker therapy relative to the other drugs and surgical interventions used in the post-AMI populations. The result has been a mixed message without any clear guidance. One can make a good case for carrying out clinical trials in specific subsets of the currently defined post-AMI population. Such an endeavor is unlikely. Pharma is clearly not interested in old drug research and the National Heart, Lung, and Blood Institute doesn’t have the funds. So it comes down to clinician’s decisions.

As an avowed beta-blocker enthusiast, I use it in most of my post-AMI patients, particularly if they have left ventricular dysfunction, and in patients with concomitant hypertension. I do not use it in patents with transitory troponin elevations without convincing evidence of clinical symptoms. I will continue beta-blockade as long as I am able to write the prescription or until someone has answered the question.
 

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.

It took almost 2 decades before beta-blocker therapy became part of the standard therapy for AMI, but in the interval beta-blockers had been used widely for the treatment of hypertension and angina. One important finding in BHAT was that patients with heart failure associated with the AMI event received the largest mortality benefit. This observation led to the subsequent clinical trials emphasizing the role of beta-blockade in the treatment of heart failure with or without ischemic etiology.

The role of beta-blockers in the treatment of the contemporary AMI has been challenged recently. Reasonable questions have been raised as to the wisdom of throwing the full bag of therapy at this population rather than a more selective choice of drugs. In order to gain further insight into the benefits of beta-blocker therapy in the total spectrum of post MI therapy, large populations studies using a variety of statistical gymnastics have tried to identify the unique benefit that can be attributed to beta-blocker therapy relative to the other drugs and surgical interventions used in the post-AMI populations. The result has been a mixed message without any clear guidance. One can make a good case for carrying out clinical trials in specific subsets of the currently defined post-AMI population. Such an endeavor is unlikely. Pharma is clearly not interested in old drug research and the National Heart, Lung, and Blood Institute doesn’t have the funds. So it comes down to clinician’s decisions.

As an avowed beta-blocker enthusiast, I use it in most of my post-AMI patients, particularly if they have left ventricular dysfunction, and in patients with concomitant hypertension. I do not use it in patents with transitory troponin elevations without convincing evidence of clinical symptoms. I will continue beta-blockade as long as I am able to write the prescription or until someone has answered the question.
 

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.

It took almost 2 decades before beta-blocker therapy became part of the standard therapy for AMI, but in the interval beta-blockers had been used widely for the treatment of hypertension and angina. One important finding in BHAT was that patients with heart failure associated with the AMI event received the largest mortality benefit. This observation led to the subsequent clinical trials emphasizing the role of beta-blockade in the treatment of heart failure with or without ischemic etiology.

The role of beta-blockers in the treatment of the contemporary AMI has been challenged recently. Reasonable questions have been raised as to the wisdom of throwing the full bag of therapy at this population rather than a more selective choice of drugs. In order to gain further insight into the benefits of beta-blocker therapy in the total spectrum of post MI therapy, large populations studies using a variety of statistical gymnastics have tried to identify the unique benefit that can be attributed to beta-blocker therapy relative to the other drugs and surgical interventions used in the post-AMI populations. The result has been a mixed message without any clear guidance. One can make a good case for carrying out clinical trials in specific subsets of the currently defined post-AMI population. Such an endeavor is unlikely. Pharma is clearly not interested in old drug research and the National Heart, Lung, and Blood Institute doesn’t have the funds. So it comes down to clinician’s decisions.

As an avowed beta-blocker enthusiast, I use it in most of my post-AMI patients, particularly if they have left ventricular dysfunction, and in patients with concomitant hypertension. I do not use it in patents with transitory troponin elevations without convincing evidence of clinical symptoms. I will continue beta-blockade as long as I am able to write the prescription or until someone has answered the question.
 

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.