Evaluating cardiovascular pathophysiology and anatomy in atherosclerosis

Abstract

The process of atherosclerosis begins with endothelial dysfunction from impaired bioavailability of NO and progresses through multiple stages of plaque development. Impaired endothelial function decreases NO and increases oxidized macromolecules such as low-density lipoprotein cholesterol. Oxidized low-density lipoprotein cholesterol accumulates in subendothelial space, forming plaques that may eventually compromise the lumen. Acute coronary events result from plaque rupture and consequent thrombus formation and abrupt occlusion of the vessel lumen. New diagnostic methods such as flow-mediated dilation of the brachial artery can detect endothelial dysfunction, and intravascular ultrasound can detect early plaque formation in the arterial wall. These techniques may provide a means to identify patients at risk for adverse cardiovascular outcomes, thereby enabling physicians to potentially prevent adverse events by early initiation of lipid-lowering therapy.