Protection of myocardium by the compensatory mechanism of coronary collaterals after total occlusion of major coronary arteries shown in patients with familial hypercholesterolemia.

We report 11 in a group of 21 asymptomatic patients with heterozygous familial hypercholesterolemia (FH) and progressive coronary artery disease to evaluate the role of compensatory mechanism(s), especially coronary collaterals, in providing adequate blood supply to the myocardium, following complete occlusion of one or more major coronary arteries. Diet-colestipol-nicotinic acid treatment decreased their plasma total cholesterol and low density lipoprotein cholesterol (mg/dl, mean +/- SEM) from 442.9 +/- 25.8 and 363.0 +/-24.1, respectively, to 231.2 +/- 11.8 and 185.3 +/- 14.2, respectively, for 6 to 9 years. The initially stenotic lesions of these 11 patients slowly progressed to complete occlusion, while the patients remained free of myocardial ischemia or infarction and exhibited no abnormality on 24-hour ambulatory ECG monitoring, exercise stress, and thallium 201 stress tests. We conclude that coronary occlusion can be retarded in FH patients by strenuous hypocholesterolemic therapy to allow the development of compensatory mechanism including coronary collaterals. Apparently, the angiographically visualizable collaterals combined with subendocardial anastomosis can give adequate myocardial blood supply to this series of FH patients following occlusion of one or more of their major coronary arteries.