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Sudden cardiac death during exercise is of concern to a large number of sports-minded people because cardiovascular disease is so prevalent in this country. Common causes of sudden cardiac death among athletes include atherosclerosis (plaque build-up in the arteries) in persons over 35 years old, and hypertrophic cardiomyopathy (enlarged heart with disease to the myocardium, middle layer of the walls of the heart), which is more common among younger individuals. A retrospective study of cases of exercise and non-exercise-related sudden cardiac deaths reported in the state of Maryland between 1981 and 1988 was performed. Subjects were between the ages of 14 and 40 years. The medical conditions most often associated with sudden death during exercise were examined. There were 656 non-exercise and 34 exercise-related deaths. In the exercise-related group, over 90 percent were men (31 of 34) and the average age was 26 years. Causes of death in this group were attributed to atherosclerosis (nine cases), hypertrophic cardiomyopathy (eight cases), malformed coronary arteries (four cases), ventricular hypertrophy (three cases), myocarditis (two cases), one case each of arrhythmogenic right ventricle and Kawasaki disease, and six unexplained cases. In the non-exercise-related group, over 75 percent were men (501 of 656) and the average age was 32 years. Severe atherosclerosis was more frequent in total non-exercise-related deaths (307 of 656), and hypertrophic cardiomyopathy was the cause of more exercise-related deaths (8 of 34). These results suggest that patients with hypertrophic cardiomyopathy have an increased risk of suffering sudden cardiac death during exercise. (Consumer Summary produced by Reliance Medical Information, Inc.)

People who recover from cardiac arrest are at risk of suffering a recurrent episode. A subset of this group (60 to 80 percent) exhibits abnormalities in heart function during electrocardiogram (ECG) testing; these patients respond well to medication that alleviates the abnormalities. This improvement appears to prevent recurrence of cardiac arrest. The remaining 20 to 40 percent of patients show no abnormalities during ECG testing; this group is thought to be at a particularly high risk for sudden cardiac death. Seventy-one survivors of a single episode of cardiac arrest were evaluated. During testing, 26 of these patients had no inducible ECG abnormalities, such as ventricular tachycardia (abnormally rapid patterns of contraction of the ventricle). After a 16-month follow-up, 11 of the 26 patients suffered recurrent cardiac arrest, and 10 of these patients died. Analysis of the clinical data pertaining to these patients revealed that several variables were more likely to be associated with recurrent cardiac arrest. Among the 11 patients who suffered a recurrence, 55 percent had dilated cardiomyopathy (a defect in the functioning of the heart muscle), and 64 percent experienced premature ventricular contractions. Twenty-four-hour ambulatory ECG-guided therapy (wearing a portable ECG machine) did not improve the survival rate for these patients. Further studies are needed to determine the optimal treatment strategy for this high-risk group of patients. (Consumer Summary produced by Reliance Medical Information, Inc.)

Heart attacks are caused by loss of circulation to the heart muscle. Abnormal contractions of the heart (''stunned myocardium'') often accompanies restored circulation following a heart attack, and this has been thought to be caused by generation of oxygen free radicals, which are very reactive charged oxygen molecules. The relationship between oxygen free radicals and damaged heart function during the diastolic (filling) and systolic (contracting) phases of heart action have been investigated. Infusion of chemically generated free radicals into the hearts of experimental animals did not cause ischemia (loss of blood flow) nor death of heart muscle cells. However, systolic function decreased by 40 percent, and this was reversed by free radical scavengers (proteins which destroy free radicals). Free radicals had no effect on diastolic function, and it appears likely that other mechanisms are responsible for the changes in diastole which follow heart attacks. (Consumer Summary produced by Reliance Medical Information, Inc.)