By definition, if you've suffered an MI, you have sustained a certain amount of damage to your heart muscle. If enough damage has been done, you may be at risk of developing heart failure.
Patients who suffer very large heart attacks have a very high risk of developing heart failure, and its onset can be quite acute, often within the first few hours or days of the MI. But even people with only a moderate amount of muscle damage can eventually experience heart failure. For these individuals, appropriate drug therapy and lifestyle changes can be critical in delaying or preventing the onset of heart failure.
It turns out that in patients who have had moderate-sized MIs, whether or not heart failure ensues depends to a large extent on how their remaining, normal heart muscle responds. The response the remaining normal heart muscle to the damage done by the MI is referred to as "remodeling."
What Is Remodeling, and Why Is It Bad?Remodeling works like this. After an MI, the normal heart muscle "stretches" in an attempt to take over the workload of the damaged muscle. This stretching of heart muscle leads to the enlargement of the heart. The heart enlargement that occurs after a heart attack is often called cardiac "remodeling."
Stretching helps the normal heart muscle contract more forcefully, 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" it has. 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 may ensue. Therefore, the remodeling that occurs after a heart attack may help the heart work better in the short term, but in the long term remodeling is a bad thing. If remodeling can be prevented or limited, the risk of developing heart failure diminishes.
How Is Remodeling Measured?An important part of assessing your health after an MI, therefore, is to estimate how much cardiac remodeling is taking place. This information can be obtained by doing a MUGA scan or an echocardiogram, two methods of noninvasively visualizing the left ventricle.
A good way to estimate the amount of heart muscle damage that has occurred after an MI, and the amount of remodeling you are having, is to measure the left ventricular ejection fraction (LVEF), which is the percentage of blood ejected by the left ventricle with each heart beat. With heart enlargement (that is, with remodeling), the ejection fraction falls. If the LVEF is less than 40% (normal being 50% or higher), then significant damage has occurred. The lower the LVEF, the greater the damage, the more remodeling - and the greater the risk of developing heart failure.
What can be done to prevent cardiac remodeling and heart failure?
Several randomized clinical trials have now shown that two classes of drugs can significantly reduce remodeling after an MI, and improve the survival of patients who have signs of impending heart failure. These drugs are the beta blockers and the ACE inhibitors.
Beta blockers work by blocking the effect of adrenaline on the heart, and they have significant beneficial effects in several types of heart disease. Beta blockers reduce the risk of angina in patients with coronary artery disease, improve the survival of patients with heart failure, reduce the risk of sudden death in patients after heart attacks, and delay or prevent cardiac remodeling after MIs. In patients with moderate to severe heart muscle damage due to MI, beta blockers can significantly improve survival. So, 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. The most commonly prescribed beta blockers after an MI are Tenormin (atenolol) and Lopressor (metoprolol).
ACE inhibitors block angiotensin converting enzyme, and by doing so they produce numerous beneficial effects on the cardiovascular system. The use of ACE inhibitors significantly improves long-term survival after an acute MI, and in addition, reduces the risk of developing heart failure (apparently by preventing or delaying remodeling). They also reduce the risk of recurrent MIs, stroke, and sudden death. ACE inhibitors, like the beta blockers, are considered a must if you have had a heart attack. Vasotec (enalapril) and Capoten (captopril) are the drugs most commonly used after an MI.
It is also important for you and your doctor to discuss more general measures that will improve your cardiovascular status and prevent heart failure. These include measures to improve your diet, cholesterol levels, exercise capacity, and to optimize your weight and your blood pressure. These measures, of course, are the same ones that will help you to slow the progression of the coronary artery disease that caused your heart attack in the first place.
In summary, after a heart attack it is very important that your doctor assess the condition of your heart muscle, and help you take the steps necessary to limit remodeling of your heart muscle and to prevent heart failure. Indeed, this is one of the main things you should be discussing with your doctor after a heart attack.