Beta Blockers in Heart Failure

From Richard N. Fogoros, M.D.,
They're GOOD for patients with heart failure.
For years, evidence has been accumulating that beta blockers are useful drugs in patients with heart disease due to dilated cardiomyopathy. This information has been taken up only slowly by much of the medical profession, because doctors had been taught for generations that if one thing is true, it's that you don’t use beta blockers in patients with heart failure. Consequently, tens of thousands of patients with coronary artery disease are being treated inappropriately.

If there was final nail in the coffin of the mistaken belief that beta blockers are bad for patients with heart failure, that nail came with the COPERNICUS trial. Approximately 2200 patients with severe cardiac problem were enrolled in this trial. They all received optimal medical therapy with ACE inhibitors, diuretics, and digitalis. They were then randomly assigned to receive either carvedilol or placebo. The resulting analysis showed a 35% improvement in survival among patients receiving carvedilol. The improvement in survival was even greater in patients with particularly severe heart failure.
Furthermore, patients receiving the beta blocker had no more side effects than those receiving the inactive placebo. The results of the COPERNICUS trial are in line with other recent studies examining the use of beta blockers in patients with heart failure. Trials using bisoprolol and metoprolol showed similar results.
The "proof" in favor of using beta blockers in heart failure is about as strong as "proof" in medicine ever gets. And the compelling benefit is not “merely” some difficult-to-measure quality of life parameter – the compelling benefit is a significant improvement in survival.
The survival benefits are so striking that one would think doctors would be rushing to place all their heart failure patients on beta blockers as soon as possible. Unfortunately, this is not happening.
Indeed, doctors seem to be ignoring the evidence in droves. The fact is, despite the striking evidence to the contrary, the notion that beta blockers are beneficial in heart failure is just too radical for many doctors to accept without mulling it over for a few years. It appears that a minority of heart disease patients likely to be helped by beta blockers are actually receiving those drugs today.

What to do if you have heart failure
If you have heart failure, what you should not do is wait expectantly for your doctor’s delicate sensibilities to come around. Beta blockers are not the only new and strikingly effective therapy for heart failure that your doctor might be ignoring.

Atrial Fibrillation

From Richard N. Fogoros, M.D,
The Basics
Atrial fibrillation is one of the most common of the heart rhythm disturbances. While it is a benign arrhythmia, the lack of highly effective and safe therapies makes it one of the most frustrating of arrhythmias to deal with for both patients and doctors.
In these articles, we will review the causes, symptoms and diagnosis of this arrhythmia, but our main goal is to simplify the confusing array of options for treating atrial fibrillation.

What is atrial fibrillation?
Atrial fibrillation is a rapid and highly irregular heart arrhythmia, caused by chaotic electrical impulses in the atria of the heart. The AV node are therefore bombarded with frequent, irregular electrical impulses.

What causes atrial fibrillation?
Atrial fibrillation is associated with underlying valvular heart disease, longstanding hypertension, coronary artery disease, alcohol use, hyperthyroidism, pericarditis, cardiac surgery, heart attack, and virtually all other varieties of heart disease. When an underlying cause can be identified, then often, treating that underlying cause also improves the atrial fibrillation. In many patients, no particular underlying cause for atrial fibrillation can be identified, in which case the atrial fibrillation is said to be “idiopathic.”
When idiopathic atrial fibrillation is seen in younger patients, the term “lone atrial fibrillation” is frequently used. This term reflects the fact that no identifiable cause for the arrhythmia is present, so it is the “lone” abnormality present. What are the symptoms of atrial fibrillation, and how dangerous is it? The symptoms of atrial fibrillation are related to the rapid heart rate, and to the loss of coordination between the atria and ventricles. People who have atrial fibrillation often complain of palpitations, easy fatigability, shortness of breath, and (occasionally) lightheadedness. In addition, people with underlying coronary artery disease can develop angina from the rapid heart rate; and people with underlying cardiomyopathy can have an acute episode of heart attack.
Possibly the biggest problem with atrial fibrillation is that, if the arrhythmia is sustained for a day or two, the ineffective pumping action of the atria (caused by the chaotic electrical activity) allow blood clots to form. If these blood clots break off and get into the bloodstream, a stroke can result. Thus, patients who are in prolonged or chronic atrial fibrillation have a significantly increased risk of stroke.

How is atrial fibrillation diagnosed?
Atrial fibrillation is easy to diagnose in patients who are having the arrhythmia at the time they visit the doctor. A simple electrocardiogram (ECG) will reveal the diagnosis in virtually all such patients. However, many patients with atrial fibrillation have transient episodes lasting from minutes to hours. These patients will generally complain of the sudden episodes of palpitations and perhaps shortness of breath. If the episode has ended by the time they receive medical attention, no sign of atrial fibrillation will be found. In these patients, some form of outpatient monitoring is necessary to make a diagnosis.

Palpitations

From Richard N. Fogoros, M.D,
What causes them, and how should they be evaluated?
Palpitations, an unusual awareness of the heart beat, is an extremely common symptom. Most people who complain of palpitations describe them either as “skips” in the heartbeat (that is, a pause, often followed by a particularly strong beat,) or as periods of rapid and/or irregular heartbeats.
While many people with palpitations can ignore them, others find them extremely disturbing and frightening, and often worry that they are about to die at any moment. Fortunately, the vast majority of palpitations are not associated with life threatening heart rhythm disturbances.
When a patient complains to a doctor about palpitations, it becomes the doctor’s obligation to do two things:
a) identify the cause of the palpitations, and
b) provide optimal therapy for that cause.

What kinds of arrhythmias produce palpitations?
Most people with palpitations have some type of cardiac arrhythmia.
Virtually any arrhythmia can cause palpitations, but the most common causes of palpitations are premature atrial complexes (PACs), premature ventricular complexes (PVCs), episodes of atrial fibrillation, and episodes of supraventricular tachycardia (SVT).
However, in some cases palpitations can be caused by more dangerous arrhythmias, such as ventricular tachycardia. Life-threatening arrhythmias are usually seen in patients with underlying heart disease, however, so it is especially important to identify what is causing palpitations in individuals who have underlying heart disease. The same thing holds for patients with palpitations who also have significant risk factors for heart disease.

How palpitations should be evaluated
The first order of business when a patient complains of palpitations is to find out whether the palpitations are caused by a heart rhythm disturbance, and if so, to identify the particular arrhythmia that is causing the palpitations.
This should be relatively straightforward to do, so it always amazes to see how much trouble doctors seem to have in accomplishing this feat. The trick is simply to record an electrocardiogram (ECG)at the time the patient is having symptoms. That’s it.
But doctors commonly make two major mistakes in their attempt to determine whether an arrhythmia is causing the palpitations: they often miss the arrhythmia that is causing the palpitations, and they often attribute the palpitations to an arrhythmia that is not causing them.

Mistake 1: The doctor will order an ECG or a Holter monitor study, and during that time the patient will not experience palpitations. Then, not seeing an arrhythmia, the doctor will declare that there is no arrhythmia causing the palpitations. Worse, the doctor may tell the patient that the symptoms are “all in your head.” But often, the arrhythmia that is causing the palpitations just happened not to occur during the arbitrary monitoring period. The doctor’s workup was inadequate.
To make a correct diagnosis, the palpitations and ECG must occur at the same time. If the palpitations occur only intermittently, and especially if they do not occur every single day, instead of doing an ECG or a 24-hour Holter study, the doctor should order an event recorder study. The event recorder study can continuously record the heart rhythm for weeks at a time – however long it takes to “capture” an episode of palpitations. It’s really quite simple – record the ECG for as long as it takes for the patient to have an episode of palpitations, then look to see what the heart rhythm is during the palpitations.

Mistake 2: The doctor will see an arrhythmia during monitoring that is not associated with palpitations, and blame the palpitations on that arrhythmia. This is wrong. To say an arrhythmia is causing palpitations, the arrhythmia and the palpitations must occur at the same time. Once again, monitoring must continue until palpitations occur, so that the heart rhythm can be examined at the time of the palpitations. Since doctors frequently make these two mistakes, it is important for patients to keep in mind the simple rule: To make a correct diagnosis, the ECG must be recorded at the very time the palpitations are taking place. If this has not been accomplished, the patient must redirect the physician's efforts through gentle reminders, guile, appeals to reason, righteous indignation, or whatever it takes.

Unstable Angina (Part I)

From Richard N. Fogoros, M.D.,
In this article we will review unstable angina – what causes it, how it differs from a classic heart attack, how it is diagnosed, and how it ought to be treated.
As recently as the mid-1990s, it is likely that a heart patient would have been sent home from most emergency rooms with the diagnosis of a “simple angina,” or even “chest pain of non-cardiac origin.” And until a few months ago, even with the correct diagnosis, it is likely he would have been managed much more conservatively, with outpatient drug therapy only.
What has changed? Two things: our understanding of the cause of unstable angina, and our understanding of the best way of diagnosing and treating it.

What is unstable angina?
Stable angina, unstable angina and myocardial infarctions ultimately are all caused by the same process – coronary artery disease. A myocardial infarction, or heart attack, occurs when a plaque ruptures in a coronary artery, leading to the sudden formation of a blood clot superimposed on the plaque. The blood clot often totally occludes the artery, leading to death of the heart muscle being supplied by that artery. And a myocardial infarction is the death of heart muscle.
Unstable angina occurs when a blood clot forms on a plaque, suddenly increasing the degree of blockage in a coronary artery. By definition, in unstable angina the clot does not completely occlude the artery, but merely increases the degree of blockage. Because blood flow across the blockage suddenly becomes more sluggish, angina occurs even at rest.
Indeed, the blood flow can become so sluggish, and the angina can persist for so long, that some of the heart muscle cells being supplied by the partially occluded artery can actually die in patients with unstable angina. Since the death of heart cells is the definition of a myocardial infarction, once some of the cells die, the patient has “officially” had a heart attack.
Our ability to detect cell death in patients with unstable angina has greatly improved over the past few years, mainly by the development of more sensitive assays for the enzyme, troponin. Troponin is a heart muscle protein that is released into the bloodstream when heart muscle cell death occurs. As our ability to measure troponin increases, more and more patients with unstable angina are being diagnosed with heart attacks.

Unstable Angina (Part II)

From Richard N. Fogoros, M.D.
How is unstable angina diagnosed?
Anybody with a history of coronary artery disease should suspect unstable angina if their angina occurs at a markedly lower-than-normal level of exercise, if it occurs at rest, if it persists longer than usual or is more difficult to relieve with nitroglycerin, or especially if it wakes them up at night. Any of these symptoms can indicate a suddenly “narrower” coronary artery, implying that a blood clot has superimposed itself on an atherosclerotic plaque.
People without any history of coronary artery disease can also develop unstable angina, but these individuals seem to be at higher risk because they often don’t recognize the symptoms.
The classic symptoms of angina include chest pressure or pain, sometimes squeezing or “heavy” in character, often radiating to the jaw or left arm. Unfortunately, many patients with angina do not have classic symptoms. Their discomfort may be very mild, and may be localized to the back, abdomen, shoulders, or either or both arms. Nausea or merely a feeling of heartburn may be the only symptom. What this means, essentially, is that anyone middle aged or older, especially anyone with one or more risk factors for coronary artery disease, should be alert to symptoms that might represent angina.
Not surprisingly, most people presenting with unstable angina have a history of known coronary artery disease. This is likely because they know what these symptoms mean, and they get themselves to the hospital before cardiac damage becomes irreversible. People without known coronary artery disease, on the other hand, tend to stay at home, explaining away their disturbing symptoms as something they ate or something they lifted – and they most often either die there, or finally come to the hospital once they’ve had a completed heart attack. Unstable angina is largely a condition of experience.

How is unstable angina diagnosed?
Unstable angina is usually diagnosed by the medical history and by the ECG. Patients complaining of symptoms consistent with angina, occurring at rest or with minimal exertion, especially when they have a history of coronary artery disease, should be presumed to have unstable angina.
Especially if the patient’s pain has been relatively prolonged, the doctor checks cardiac enzymes to determine whether heart muscle damage (i.e., a heart attack) has occurred. Until a few years ago, the chief cardiac enzyme that was measured was CPK. Rises in heart –muscle-specific CPK levels were unusual with unstable angina, so most of these patients were felt not to have muscle damage. However, in the past few years, since the enzyme troponin has been commonly measured, it has become apparent that a substantial proportion of patients presenting with typical unstable angina actually do have death of cardiac cells.

How should unstable angina be treated?
Until a few years ago, unstable angina was generally considered as basically an exacerbation of typical angina – that is, the pattern of angina changed for the worse, but because no heart cell damage occurred, the goal of therapy was simply to “quiet down” the angina with drugs, and send the patient home. If this could be accomplished, it was assumed, the patient was no worse off than before the angina became unstable.
However, it has now become clear that many patients presenting with unstable angina have a greatly increased risk, over the next few weeks to months, of having a full-blown heart attack, and even death. This, along with a better understanding of what causes unstable angina (that is, a blood clot forming at the site of an atherosclerotic plaque that slows but does not totally occlude blood flow) has led to the notion that much more aggressive management is needed.
Two general approaches to therapy have evolved:
a) treat aggressively with drugs to stabilize the ischemia, then evaluate non-invasively (the Wait and See approach,) or
b) treat aggressively with drugs to stabilize the ischemia, while at the same time planning for early invasive intervention (the Aggressive approach.)

Unstable Angina (Part III)

From Richard N. Fogoros, M.D.
What drugs are used to “stabilize” unstable angina?
Both the Wait and See and the Aggressive approaches involve the intensive use of medication to stabilize or eliminate the cardiac ischemia. These medications are generally aimed at either protecting the jeopardized heart muscle, or preventing further progression of the blood clot.
In the former category are beta blockers and intravenous nitroglycerin, both of which are started immediately. Beta blockers reduce the effect of adrenalin on the heart muscle, and nitroglycerin reduces the cardiac workload by lowering cardiac muscle tension. Both of these effects reduce the amount of blood flow needed by the cardiac muscle. In “clot stabilizing” category are either heparin or enoxaparin (drugs that inhibit the thrombin clotting system) and aspirin and/or IIb/IIIa inhibitors (drugs that inhibit platelets).

What is the Wait and See approach?
Using this approach, patients are carefully observed in the coronary care unit for signs of continuing ischemia. Such signs include more chest discomfort, further changes in the ECG, or continuing rises in cardiac enzymes.
If there are no further signs of ischemia, then patients are converted to an all-oral drug regimen they can continue at home. Before discharge from the hospital, a stress and thallium study is done to assess the patient’s potential for developing further ischemia. If the stress test is favorable, they are discharged to home. If, on the other hand, signs of early ischemia are seen on the treadmill test, they are sent for catheterization and angiography, in order to be evaluated for possible revascularization (angioplasty and/or stent, or bypass surgery.)
Using the Wait and See approach, approximately half the patients are discharged from the hospital without receiving catheterization.

What is the aggressive approach?
The aggressive approach begins the same way as the Wait and See approach, that is, with intensive drug therapy to stabilize the ischemia. But while this is being done, arrangements are being made to perform catheterization and angiography, with the clear goal in mind of doing angioplasty and/or stent. This procedure is performed as soon as it can be done practically.

Which approach is better?
This has been a very controversial question. Many patients do very well with the more conservative Wait and See approach to unstable angina.
What can we say about the appropriateness of the conservative approach vs. the aggressive approach? Thanks to data accumulated over the past year or two, we can say the following regarding therapy given to patients with unstable angina:
1) In patients with ECG changes and elevated troponin levels, early interventional therapy yields a significantly reduced incidence of full-blown myocardial infarction, and of death. In these patients, the Aggressive approach should now be considered as standard.
2) In patients with no ECG changes and with normal troponin levels, there is no evidence to date that aggressive early catheterization yields better results. In these patients, the Wait and See approach is entirely appropriate.

Summary
We now know that in most patients, unstable angina represents an acute deterioration in a previously stable atherosclerotic plaque. Indeed, the essential difference between unstable angina and a classic myocardial infarction is simply that in unstable angina, the acute blood clot only partially occludes the coronary artery instead of completely occluding it. For this reason, and because patients who are “stabilized” using medical therapy are now known to have a high incidence of having a classic heart attack in the near future, unstable angina probably is best thought of as being an “incomplete myocardial infarction. This fact justifies an aggressive early approach in many patients with unstable angina.
At this point in time, many doctors in many emergency rooms have not yet gotten “up to speed” in the appropriate treatment of unstable angina. They still think of unstable angina in terms of being somewhat-worse-than-usual angina, instead of being a somewhat-milder-than-usual heart attack. This is a problem. Even the Wait and See approach to unstable angina is far more aggressive than the treatment used for routine angina. Patients whose doctors who do not treat unstable angina with sufficient respect are at extremely high risk for a poor outcome.

Sudden Death After Heart Attacks (Part I)

From Richard N. Fogoros, M.D.,
Very common, but very preventable
Most of the thousands of deaths are not due to repeat heart attack (that is, to repeat blockage of a coronary artery.) Instead, most are due to the sudden appearance of a lethal heart arrhythmia known as ventricular fibrillation. When ventricular fibrillation occurs, it usually occurs suddenly, without a shred of warning. And unless the heart is defibrillated within a few minutes, death ensues. (Defibrillation is usually accomplished by placing the electrode "paddles" of a heart defibrillator on the chest and administering a high-voltage shock.)
Thankfully, ventricular fibrillation is an extremely rare occurrence in people with normal hearts. But in people who have suffered almost any form of heart muscle damage - heart attacks being by far the most common cause of heart muscle damage - ventricular fibrillation is disturbingly likely. (The heart muscle damage itself makes the heart electrically unstable, and produces the environment necessary for ventricular fibrillation to occur.) Indeed, the more muscle damage one has sustained, the higher the risk of having sudden death from this arrhythmia.
There is a treatment that could prevent many of these sudden deaths - the implantable defibrillator. The implantable defibrillator is a pacemaker-like device that is implanted under the skin near the upper chest. It monitors the heart rhythm continuously, and if ventricular fibrillation occurs it automatically delivers a large shock to the heart, restoring the rhythm to normal. Often, the shock is delivered within a few seconds of the onset of the lethal arrhythmia. Implantable defibrillators have been used in patients for over 20 years, and have proven more than 99% effective in restoring the heart rhythm to normal, and in preventing sudden death.

Sudden Death After Heart Attacks (Part II)

From Richard N. Fogoros, M.D.
MADIT II and the appropriate use of the implantable defibrillator
Unfortunately, there has been no formal "indication" for using implantable defibrillators in heart attack survivors. These devices have been reserved for patients who have already had cardiac arrests from ventricular fibrillation, and who were fortunate enough to be resuscitated - a relatively very small population of individuals. The reticence to use implantable defibrillators in larger groups of patients was originally based on the "newness" of the therapy - did it really work as well as it was supposed to? - and on the fact that for the first decade or so of its use, the surgery necessary for implanting this device was a major undertaking. Today, when the necessary surgery is nearly as simple as implanting a standard pacemaker, and when the device has proven its effectiveness to an astounding degree, the reticence to apply it to larger groups is based on cost.
This week in the New England Journal of Medicine, such a study was reported. The MADIT II trial enrolled more than a thousand patients who had prior heart attacks and whose left ventricular ejection fractions (a measure of the pumping efficiency of the heart) was less than 30% were randomized to receive either standard medical therapy, or the same standard medical therapy plus the implantable defibrillator. The results were striking: patients who received the defibrillator experienced a 30% reduction in mortality compared to patients without the defibrillator. As a result of MADIT II, the FDA is being petitioned to allow use of the implantable defibrillator in heart attack survivors with reduced ejection fractions. The FDA is expected to grant this new indication relatively soon.
But based on the reaction of doctors and insurers to this new data, a sudden surge in defibrillator implantations may not occur.

Why preventing sudden death is low on everyone's priority list
Three reasons:
1) Insurance companies and the feds (i.e. Medicare) like sudden death. It is not only the cheapest way to die, but also its victims (most of whom have some form of underlying heart disease) immediately stop consuming precious health care dollars.
2) Doctors don't like to think about sudden death because doing something to prevent it is expensive.
3) Unlike AIDS, breast cancer, or the heartbreak of psoriasis, sudden death has no constituency among patient groups. By the time a person realizes it's a problem, he/she may have enough time to utter a gasp but certainly not enough time to found a political action committee. Patients simply aren't demanding that reluctant doctors implant these devices, or that insurance companies pay for them.
So for nearly everyone in the health care system, the course of least resistance - and the safest course of action - is simply to ignore the problem. Frankly, unless heart attack survivors specifically ask about the possibility of sudden death - which is a reasonably likely occurrence in many patients who have survived a heart attack - the topic is unlikely to come up.