Norfolk County Cardiologist Association

How to survive a heart attack: After the first day

When you had your heart attack yesterday, both you and your doctor did everything right. With the sudden onset of chest pain, you didn't take antacids and wait it out; instead you called 911 and arrived in the emergency room within an hour. And your doctor, moving faster than you'd ever seen her move, gave you a "clot-busting" thrombolytic drug within 40 minutes of your arrival. Today they're telling you that the amount of heart muscle damage you suffered is minimal, and that you'll be home by this weekend, watching the playoffs as you'd planned.

Sure, you've had a heart attack, but they "caught it early," and soon everything will be pretty much the way it was before. So everything is good, right?

In an earlier article, we reviewed what should happen during the first 24 hours of a myocardial infarction (heart attack), emphasizing the steps you and your doctors need to take immediately to improve your chances of survival. Fortunately, in recent years most doctors and hospitals in the U.S. have become relatively good at recognizing and treating the acute phase of myocardial infarctions.

Once that first day is over, however, much work remains to be done to optimize your chances of long-term survival - and this is where doctors all too often drop the ball. In the rush to discharge the "uncomplicated" heart attack survivor 3 or 4 days after admission, vital steps are being neglected, and as a result thousands of patients are dying unnecessarily every year. In this article, we will review the important steps that must be taken in assuring that survivors of acute myocardial infarctions become long-term survivors. If you or a loved one has had a heart attack, you need to make sure that your doctors have paid attention to all these steps.

What is supposed to happen after the acute phase of a heart attack?

As we have seen, an acute myocardial infarction is caused by a sudden occlusion of a diseased coronary artery. That occlusion causes some or all of the heart muscle supplied by that artery to die. (The amount of muscle that dies is largely determined by the size of the occluded artery, and by whether the artery is successfully re-opened - by thrombolytic drugs or by angioplasty - within the first few hours.)

So after you've successfully negotiated the first 24 hours of a heart attack, we know at least three things about you that we probably didn't know before: 1) We know you've got coronary artery disease (a chronic, progressive problem) affecting at least one - and possibly multiple - coronary arteries. 2) We know that some portion of your heart muscle is being converted to scar tissue, and that the remaining normal heart muscle is working overtime to pick up the slack. 3) We know that, by virtue of the fact that you've now got scar tissue on your heart muscle, you may be at higher-than-normal risk for sudden death from heart arrhythmias.

Knowing these things, it's obviously too early to pat ourselves on the back with a "Job well done!" We've still got a lot of work to do.

We need to: a) assess the risk that your existing coronary artery disease will cause another heart attack in the near future, and take steps to prevent that from happening; b) accurately assess the amount of heart damage that has already occurred, and take steps to prevent heart failure; c) institute drugs and lifestyle changes to slow or halt the progression of your underlying coronary artery disease; and d) assess your risk of sudden death, and institute preventive therapy if necessary.

In the following sections we will address each one of these steps.

How can we prevent another heart attack in the near future?

Patients who survive a heart attack often have a high risk of experiencing another heart attack within weeks or months. Therefore, before you go home from the hospital after a heart attack, it is important to determine your risk of an early coronary event.

This risk assessment can be of one of two types - invasive, or noninvasive.

The invasive approach - cardiac catheterization and coronary angiography - is clearly the most direct and straightforward. All the coronary arteries are visualized, and any critical blockages can be noted and treated (with angioplasty and/or stents, or with bypass surgery). The advantage of the invasive approach is that any guesswork about the overall status of a patient's coronary arteries is removed. The disadvantages are that this approach is very expensive if widely used, and that with any invasive procedure there are risks and complications.

The noninvasive approach involves exercise stress testing. With the stress test, the patient walks on a treadmill or rides a stationary bicycle to a pre-determined level of exercise, while the ECG, heart rate and blood pressure are monitored for signs of cardiac ischemia (that is, for signs that a portion of the heart muscle is not getting sufficient blood flow). If signs of ischemia are seen, then the patient is referred for cardiac catheterization to define the precise anatomy of the coronary arteries. If signs of ischemia are not seen during exercise, the odds of having critical coronary artery disease (or an early recurrent heart attack) are statistically low.

Deciding whether the invasive or noninvasive approach ought to be used is controversial. Most cardiologists prefer the invasive approach since it removes the guesswork. Most managed care companies prefer the noninvasive approach since it is much cheaper, and because there is little direct evidence that sending everybody for catheterization yields an improved overall result. (Of course, one advantage of performing immediate angioplasty instead of using thrombolytic therapy during the acute heart attack is that all coronary artery lesions are identified during the catheterization, and the "invasive vs. noninvasive" debate becomes moot.)

A reasonable compromise is to use the noninvasive approach in patients who are judged on clinical grounds to fall into a low-risk category for recurrent coronary events, and to send the remaining patients for catheterization. (Low risk patients are under 60, have had no angina or signs of heart failure, have few if any risk factors, have had a heart attack involving the right coronary artery, do not have diabetes, and have normal blood pressure.)

But the point is, when you've had a heart attack, whichever method is used, SOME method of assessing the risk of early coronary events MUST be performed prior to discharge. Unfortunately, this rule is being violated more and more often by the imperative toward early hospital discharge.

How can we prevent heart failure?

By definition, if you've suffered a heart attack you've sustained a certain amount of heart muscle death. Whether or not you develop heart failure as a result is largely dependent on the amount of heart muscle that has been damaged - the more damage, the higher the risk of heart failure.

Obviously, patients who suffer large heart attacks have a high risk of developing heart failure, and its onset can be quite acute - often within the first few hours or days.

But even patients with only a moderate amount of muscle damage can eventually experience heart failure. For these patients, appropriate drug therapy can often delay or prevent the onset of heart failure. Our understanding of the mechanism of heart failure in these patients has advanced in the past few years, and consequently so has the drug therapy we now know to be effective.

It turns out that for patient with only moderate muscle damage, whether heart failure ensues depends to a large extent on how the remaining normal heart muscle behaves. The behavior of the normal heart muscle in response to damage to another portion of heart muscle is referred to as remodeling.

Remodeling works like this. After a heart attack, the normal heart muscle stretches in an attempt to pick up the slack for the muscle that has been damaged. The stretching increases the force of contraction in normal muscle, and allows it to do more work. In this way, the heart muscle behaves something like a rubber band - the more you stretch it, the more "snap." However, if you overstretch a rubber band, or keep stretching it over and over for a long period of time, it eventually loses its "snap" and becomes flaccid. Unfortunately, the heart muscle does the same thing. Chronically stretching normal heart muscle causes it to weaken, and heart failure ensues. Therefore, the ventricular remodeling that occurs after a heart attack is bad, and ought to be prevented if possible.

An important part of assessing any patient after a heart attack, therefore, is to quantify the amount of heart damage that has been done, and the amount of "stretching" that has occurred. This information can be obtained by doing a MUGA scan or an echocardiogram, two methods of noninvasively visualizing the left ventricle.

A good index of the amount of heart muscle damage that has occurred after a heart attack is to measure the left ventricular ejection fraction (LVEF), which is the percentage of blood ejected by the left ventricle with each heart beat. If the LVEF is less than 40%, then significant damage has occurred. The lower the LVEF, the more the damage, and the worse the patient's prognosis.

The amount of stretching that has occurred can be assessed by measuring the dimensions of the left ventricle - stretching of the heart muscle produces dilation of the ventricle, so greater-than-normal left ventricular dimensions indicates that significant ventricular remodeling is occurring. The greater the dilation of the ventricle, the poorer the patient's prognosis.

Over the past several years, numerous randomized clinical trials have been completed that show that two classes of drugs can significantly improve the overall survival of patients who have signs of impending heart failure (either low LVEF or increased ventricular dilation). These drugs are the beta blockers and the ACE inhibitors.

Beta blockers work by blocking the effect of adrenaline on the heart, and have been noted to have numerous beneficial effects in several types of heart disease. Beta blockers reduce the risk of angina in patients with coronary artery disease, significantly improve the survival of patients with heart failure, significantly reduce the risk of sudden death in patients after heart attacks, and appear to delay or prevent the remodeling seen in the left ventricle after heart attacks. Unless there are strong reasons not to use them (some patients with severe asthma or other lung disease simply cannot take these drugs), virtually every heart attack survivor should be placed on beta blockers.

ACE inhibitors block angiotensin converting enzyme, and thereby produce numerous salutary effects on the cardiovascular system. This class of drugs significantly improves long-term survival among survivors of acute myocardial infarction, and in addition reduces the incidence of heart failure (apparently by preventing or delaying remodeling), recurrent heart attacks, stroke, and sudden death. These drugs also are a "must" for survivors of heart attacks.

Thus, assessing the condition of the heart muscle, and taking steps to limit ventricular remodeling and prevent heart failure, are vital steps after a myocardial infarction.

How can we delay the progression of coronary artery disease, and reduce the long-term risk of repeated heart attacks?

As we have noted, atherosclerosis, the disease process causing blockages in coronary arteries, is a chronic, progressive process. An acute myocardial infarction often merely represents one of a series of untoward events that occur during this progressive disease.

Once a patient has been identified as having coronary artery disease (perhaps by suffering a myocardial infarction), then every effort must be made to slow or halt the progression of the underlying disease process. Doing so involves using each of two major strategies: the pharmacological strategy, and the non-pharmacological strategy.

The pharmacological strategy uses drugs to either slow the progression of the coronary artery disease, or to prevent the sudden occlusion of a diseased coronary artery (by preventing the acute clotting phenomenon that causes the occlusion). The following drugs are important in this regard:

Aspirin: Aspirin reduces the "stickiness" of platelets, and thus reduces the chances of developing a blood clot at the site of an atherosclerotic plaque. (Click here to review the blood clotting mechanism, and how it causes heart attacks). Aspirin has been shown to significantly reduce vascular mortality in patients with known coronary artery disease, and without question should be used in every heart attack survivor, unless there are strong reasons not to.

Statins: Several randomized clinical trials now show that prescribing statin drugs after a heart attack in patients with elevated LDL cholesterol levels will significantly reduce the risk of recurrent myocardial infarction, and will significantly reduce mortality. Every patient who has had a heart attack should have lipids measured, and a statin should be begun immediately if the LDL level is high. (Click here for a review of cholesterol and triglycerides, and their treatment).

The non-pharmacological strategy for slowing the progression of coronary artery disease involves reducing any risk factors the patient may have. These include weight loss, beginning a low fat - low cholesterol - low saturated fat diet, smoking cessation, excellent control of diabetes and hypertension if present, and regular aerobic exercise. All patients should receive extensive training on how to modify these risk factors after a heart attack. Unfortunately, the push to get people out of the hospital quickly after a heart attack nearly precludes adequate instruction on risk-factor modification.

How can we reduce the risk of sudden death?

Of all the measures that can be taken to improve the prognosis of patients after a heart attack, this is the one most frequently neglected. Nearly 300,000 people die suddenly from ventricular arrhythmias in the U.S. alone each year, and a large majority of the victims of sudden death are survivors of myocardial infarctions. (This is a huge number, and may be difficult to believe at first. But most individuals in the U.S. over the age of 25 will be able to think of at least one close family member or friend who has died suddenly. Sudden arrhythmic death is a problem that touches the lives of almost everyone sooner or later.)

The scar that forms on the ventricular muscle after a heart attack tends to create significant electrical instability. This electrical instability often leads to the sudden, unexpected development of ventricular tachycardia or ventricular fibrillation - arrhythmias that often produce instantaneous loss of consciousness, and death within a few minutes. These arrhythmias most often occur without any warning, in people who seem to be in their usual state of health.

The sudden deaths that result from these arrhythmias are most often mislabeled "a massive heart attack" by the attending physician. In fact, less than 20% of these 300,000 yearly sudden deaths are related to acute myocardial infarctions. The remainder are due to ventricular arrhythmias (though the arrhythmias themselves are ultimately related to a heart attack that occurred in the past.)

While sudden death is an all-too-common (and an always devastating) occurrence in patients who have survived heart attacks, assessing the risk of sudden death is seldom brought up by the attending physician, and doing something about that risk is done even less often. This is because assessing the risk is not particularly easy, straightforward, or cheap, and doing something about a high risk of sudden death is very expensive. There almost seems to be a tacit agreement among many doctors to simply ignore the issue altogether as being so impractical as not to warrant consideration.

However, the data from randomized trials are compelling - heart attack survivors with a high risk of sudden death can be identified, and once identified, their risk of dying from ventricular arrhythmias can be virtually eliminated. And in most large university centers these measures are being followed routinely. There is no reason to expect less to be done in your own case.

How high risk is identified: Patients are at high risk for sudden death if they have and LVEF less than 40%, and have episodes of non-sustained ventricular tachycardia on Holter monitoring, and subsequently are found to have ventricular tachycardia on electrophysiologic testing. Thus, identifying high-risk patients involves measuring the LVEF (which ought to be done routinely anyway), and if less than 40%, doing a Holter study. If the Holter study is positive, the patient should be referred for electrophysiologic testing.

How high risk patients should be treated: The data is now definitive. Patients who are identified as having a high risk for sudden death will have that risk virtually eliminated - and their overall chances for long-term survival significantly increased - by insertion of an implantable defibrillator. (These are pacemaker-like devices that monitor the heart rhythm continuously, and if a potentially fatal arrhythmia occurs, automatically administer a defibrillating shock to the heart to restore the rhythm to normal.)

Resistance on the part of doctors to identifying and treating high risk patients is multifactorial. Both electrophysiologic testing and the implantable defibrillator are expensive. Electrophysiologic testing is not performed in all hospitals, so getting the testing done often means sending the patient away to another institution - itself an expensive proposition, and one that often results in the patient being "stolen" forever. And finally, subtle pressure by managed care organizations makes it very difficult for doctors to embark on potentially expensive undertakings unless they are compelled (by law, by peer pressure, or by their patients' expectations) to do so. Here, none of these compelling forces are in play.

As it now stands, most of the patients who receive the necessary assessment and treatment are either being cared for in major university centers, or themselves push for it. So the major message here is: Push for it. Insist on it. Sudden death after heart attacks is very common, and it can be prevented.

Summary - What you need to do to save your own skin

After you've survived the first day of a heart attack, you've got a lot to learn about and a lot to think about. While in the good old days you might have had a week or two of hospitalization to go through all the testing, risk assessment, education, and initiation of therapy necessary to optimize your long-term prognosis, today whatever is going to get done must happen in the first three (or four, if you've got a liberal health plan) days.

Doctors and hospitals have mobilized nicely to provide adequate acute care for the patient presenting with a heart attack. But for the most part they have completely neglected approaching the necessary subacute care (the care after the first 24 hours) in an organized fashion. As a consequence, it is the rare patient who receives all the assessment, training, and treatment that has been shown to be vital to an optimal outcome. For instance, recent studies show that less than half the patients who need statin drugs receive them. Other studies show that only a minority of heart attack survivors receive beta blockers. And the proportion of patients who get an adequate assessment for the risk of sudden death - let alone who receive the implantable defibrillator - is laughable.

Until doctors and hospitals get their act together, the key to successfully navigating a heart attack is you. You need to insist that the appropriate tests are done, the appropriate referrals are made, and the appropriate medications are begun. To this end we provide a convenient check list of the things that should be done prior to discharge after a heart attack.

Doctors really do want to do the right thing. It's just that, given all the pressure and constraints they're operating under, sometimes they need for their patients to remind them of who they're really beholden to, and what the expectations in that regard truly are.