Morphology of Atherosclerotic Lesions

Abstract

Atherosclerosis is a multifactorial and multipart progressive disease manifested by the focal development within the arterial wall of lesions – the atherosclerotic plaques – in response to various deleterious insults that affect the vessel wall’s cells. Among the risk factors, as identified by classical epidemiology, there are dyslipidemia, vasoconstrictor hormones incriminated in hypertension, products of glycoxidation associated with hyperglycemia, pro-inflammatory cytokines and smoking, out of which the first is a prerequisite for the initiation and progression of about half of arterial lesions. In other instances, an inflammatory reaction induced by putative antigens that stimulate T lymphocytes, certain heat shock proteins, components of plasma lipoproteins, and potentially, microbial structures induce atherosclerotic plaque in the absence of systemic hypercholesterolemia [1, 2]. Thus, the process is more complex than previously thought. The conventional view that stressed the role of dyslipidemia in the generation of atherosclerosis was rounded by extensive evidence that inflammation is a key contributor to all stages of this disease, from the initial lesion to the ruptured plaque [2]. In all cases, the atheroma formation entails a progressive process in which the gradual implication of various cells and their secretory products define a sequence of events that leads from the fatty streak to fibro-lipid plaque, and ultimately to plaque rupture and atherothrombosis.