Heart Associates     Commonly Asked Questions

"Can exercise produce heart attacks?"

    Can exercise induce heart attacks?
    Is exercise dangerous in survivors of heart attacks?
    How much exercise could a heart attack patient do?
    These are some of the concerns and questions I hear with
        respect to exercise and heart attacks.
About 50% of all acute MI’s are “triggered” by activities or adverse situations, which are commonly called “acute risk factors”.

Vigorous physical activity in a deconditioned patient accounts for about 10-20% of acute myocardial infarctions as a trigger factor. In addition, severe emotional stress, earthquakes, and acute exposure to cold weather are well-recognized trigger factors. It is noted that the early morning hours of the first working day of the week (Monday) also has a trigger effect with increased incidence of acute myocardial infarctions.

While it is well known from epidemiological studies that habitual physical activity that conditions the cardiovascular system can reduce the incidence of myocardial infarction and sudden cardiac death in the general population, it might appear paradoxical when I say that vigorous physical activity, particularly in adverse conditions, can actually increase the incidence of myocardial infarction and sudden cardiac death. Whereas acute myocardial infarctions happen during or immediately after vigorous physical activity, strenuous physical activity becomes one of the most important triggers of an acute myocardial infarction.

An asymptomatic diabetic smoker with sedentary habits, who has hyperlipidemia and evidence of heart failure, constitutes the parameters of a person who has a high potential to develop exercise-induced myocardial infarctions. It is felt that rupture of a lipid-rich coronary plaque is responsible for the sudden deterioration into myocardial infarction and sudden cardiac death in this subset of patients. Angiography and postmortem studies have shown that these patients were more likely to have single-vessel coronary artery disease rather than three-vessel disease, and that they had more chance of having a blood clot in the infarct-related vessel.

An asymptomatic diabetic smoker with sedentary habits, who has hyperlipidemia and evidence of heart failure, constitutes the parameters of a person who has a high potential to develop exercise-induced MI’s.

Normally exercise increases the diameter of the coronary arteries, and the blood flow increases multifold. In addition, the bodies’ own built-in clot-lysing factors are also activated. However, in a sedentary smoker, exercise can lead to real constriction of the vessels (exercise-induced coronary spasm), and can even trigger clot formation by stimulating the platelets (exercise-induced platelet aggregation). Moreover, the rapid rise in heart rate and blood pressure associated with strenuous exercise can exponentially increase the shearing forces in the coronary system creating a cleft in the cholesterol plaque leading to erosion, rupture, thrombosis, and occlusion of the artery resulting in an acute myocardial infarction.

In general, we can give some recommendations to individuals who are predisposed to exercise-induced acute myocardial infarction:

  1. Individuals with high risk for myocardial infarction and sudden death must be aware of such situations and avoid unaccustomed vigorous exercise.

  2. Modify cardiac risk factors as described above

  3. Must have a formal treadmill exercise test (TET) by a cardiologist before undertaking graded levels of exercise. The patient must follow some guidelines pertaining to the duration of exercise and the maximum pulse rate during exercise. These guidelines can be generated from a formal TET.

Case History

I have witnessed the tragic story of a 39 year-old gentleman weighing 340 pounds, a diabetic, heavy smoker with hyperlipidemia, who came to a cardiologist’s office for the first treadmill exercise test. He ran for 3 minutes with a heart rate of 158 and blood pressure of 220/100. During the late recovery phase he had minor EKG changes of about 1.0 mm of ST depression with moderate shortness of breath. The young cardiologist prescribed aspirin, calcium channel blockers, and nitrates, and sent him home. On the way to the parking lot, the patient collapsed with a cardiac arrest. CPR was initiated within a few seconds. He was taken to the ED, which was very close by. With the full support of the ACLS team, resuscitation was attempted, but finally unsuccessful. Postmortem examination revealed severe three-vessel coronary artery disease, with almost a fully occluded circumflex artery with a fresh clot in it. It is concluded that this patient had a plaque rupture at the time of exercise leading to AMI and death. He did not have chest pain most likely due to diabetes.

Caveat

After having noted minor EKG changes late in the recovery phase of the exercise, it would have been ideal to delay the final EKG for another thirty minutes before the patient left the office.

It is very difficult to make predictions, particularly when it refers to the future.

Dan Quayle

Phone: (585) 338-2322

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