What do we find in Human Atherosclerosis that Provides Insight into the Hemodynamic Factors in Atherogenesis?

Abstract

A prominent feature of human atherosclerosis is that despite a number of systemic influences, plaque deposition tends to be a focal process with predominant localization at arterial branch points and bifurcations. Furthermore, certain arteries such as the carotid and coronary arteries and those of the lower extremity are particularly prone to plaque formation while others such as those of the upper extremity are rarely affected. Both the focal and selective distribution of plaques have been attributed to local differences in hemodynamic conditions. For many years it was thought that high shear stress damaged the endothelium and was an initiating factor in plaque formation (1, 2). The proposed relationship among high shear stress, endothelial injury and plaque deposition was based on in vitro experimental observations and in vivo observations in experimental animals. Not until the distribution of human atherosclerotic plaques was studied by making precise quantitative correlations of plaque localization with hemodynamic conditions did it become apparent that quite the opposite was true (3).