Dyslipidemia, atherosclerosis, and vulnerable plaques: the effect of atorvastatin on atherosclerosis and plaque structure

Atherosclerotic vascular disease is characterized by inflammation and lipid accumulation resulting from detrimental effects of several risk factors on vascular structure, including dyslipidemia. The disease progresses slowly and insidiously resulting in acute coronary syndromes when the plaque ruptures. The plaques having a high propensity to rupture are defined as vulnerable. The vulnerability of the plaque is determined by several factors such as its lipid content, degree of inflammation, strength of the fibrous cap, degree of apoptosis, necrosis, and neovascularization. The patient's risk profile and characteristics are also related to the vulnerability of plaques. The main aim in preventive cardiology is to prevent the formation of atherosclerotic plaques or to stabilize the existing plaques to decrease cardiovascular events. Lifestyle modifications, reduction in risk factors, and some pharmacologic measures can improve plaque stabilization. Statins contribute to plaque stabilization by their lipid lowering and pleiotropic effects. Several studies have shown that, with statin treatment, the plaque becomes more stable, resulting in a decrease in cardiovascular events. This review summarizes the studies about plaque-stabilizing effects of atorvastatin.