THE ANTIATHEROGENIC EFFECTS OF CALCIUM-ANTAGONISTS

Evidence that calcium antagonists can suppress diet-induced atherosclerosis in the thoracic aorta of animals has existed for a decade. Recently, the results of quantitative angiographic trials of calcium antagonists in humans have become available, confirming their beneficial effect on coronary artery disease. Nifedipine treatment reduces the rate of new lesion development in patients with mild-to-moderate coronary artery disease, reduces disease progression, and, in some cases, induces lesion regression. There is evidence that the use of verapamil may be associated with lesion regression and stenosis prevention, and that nicardipine may influence the progression of minimal coronary lesions. Theoretically, a wide range of explanations for an effect of calcium antagonists on atherogenesis is possible. Potential mechanisms include preventing calcium overload, upregulating LDL receptors with enhanced LDL clearance, inhibiting cell migration into the arterial wall, and antiplatelet effects. The exact mechanism remains unclear, but alteration of serum lipid levels and blood pressure does not appear to be the common pathway. Work with humans is still preliminary, and longer follow-up and further trials are required to determine the appropriate clinical application of calcium timing for their introduction.