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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.
The common (spontaneous atherosclerosis) 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.