The Clinical Profile of Atherosclerosis

Abstract

Current thinking supports the belief that underlying the onset of the atherosclerotic lesion is chronic injury to the arterial endothelium. The action of shear stress as a consequence of patterns of blood flow, whether turbulent or laminar, and as engendered by branch points and flow dividers, may be the origin of the injury. A number of factors such as hypercholesterolemia, cigarette smoking, hypertension and immune complexes may act synergistically with chronic endothelial injury to increase the degree and rate of plaque formation. That the response to these risk factors, such as flow disturbances, may be influenced by variations of susceptibility of endothelial cells is suggested by the great variability of the age at onset, rate of progression among individuals, and extent of plaque size in different anatomical beds. The predisposition to the development of symptomatic atherosclerotic lesions of the extracranial carotid artery, the coronary circulation, particularly at branch points, the infrarenal aorta, the iliofemoral tract of the lower extremities, and the renal arteries, particularly their ostia, is well known. By contrast, the vessels of the upper extremity, the mid descending thoracic aorta, most of the visceral vessels, with the occasional exception of the orifices of the celiac axis and the superior mesenteric artery are rarely the site of atherosclerotic disease and even more rarely productive of symptoms. This variation in vulnerability from arterial bed to arterial bed supports the concept of heterogeneity of endothelial response.