Accelerated atherosclerosis

The process of accelerated atherosclerosis appears to share common pathophysiologic mechanisms, namely, endothelial injury with early platelet involvement and subsequent progressive smooth muscle cell proliferation and thrombosis leading to vascular occlusion. Understanding the mechanisms of this process has made it possible to include strategies to limit vascular injury and reduce subsequent thrombotic and proliferating cellular responses. In contrast to spontaneous atherosclerosis, a more significant denuding endothelial injury appears to be the critical initiating event, followed by intense platelet involvement and thrombus formation, leading to an initial predominant process of smooth muscle cell proliferation in accelerated atherosclerosis. Risk factors like cigarette smoking and hypertension play an important role in this process. This accelerated proliferative process appears to be the cause of premature coronary occlusion in patients undergoing heart and kidney transplantation, coronary vein graft bypass and percutaneous transluminal coronary angioplasty and diabetes. This accounts for significant morbidity and mortality in these patients. Prophylactic anticalcinotic vasoprotection by suitable calcium antagonists may offer a more appropriate way of anti-arteriosclerotic arterial protection than the other procedures hitherto used. Calcium channel blockers have positive effects on a number of processes that may be associated with restenosis, including reduction of platelet aggregation, minimisation of vasospasm and inhibition of mitogens. In this article the role of nifedipine in accelerated atherosclerosis has been reviewed.