Calcium channel blockers and atherogenesis

Abstract

The events involved in atherogenesis include platelet deposition on damaged endothelial surfaces; migration and proliferation of smooth muscle cells; the formation of elastin, collagen, and glycosaminoglycans, followed by the penetration and complexing of lipoproteins; and, calcification. Since calcium is involved in these and other events, considerable data exist on the effects of altering calcium influx in experimental atherosclerosis. Interventions that increase calcium deposition tend to increase the severity of experimental atherosclerosis, whereas interventions that reduce calcium entry into cells tend to reduce its progression. Using rabbits, researchers have recently focused on the ability of calcium channel blockers, such as nifedipine, verapamil, and diltiazem, to attenuate the development of experimental atherosclerosis. Studies also suggest that although calcium channel blockers may protect against the development of experimental atherosclerosis, they are less effective in inducing its regression. Further, studies with calcium channel blockers in rabbits deficient in low-density lipoprotein receptors did not show protection against the development of atherosclerosis. However, no clinical studies are yet available to judge the potential protective effects of calcium channel blockers in humans. Since many patients are now receiving long-term calcium blocker therapy for hypertension, these findings may be relevant in the selection of antihypertensive therapy, provided that protective effects can be demonstrated.