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.
