Dyslipidemia and Its Role in the Pathogenesis of Atherosclerotic Cardiovascular Disease: Implications for Evaluation and Targets for Treatment of Dyslipidemia Based on Recent Guidelines

Abstract

The clinical presentations of atherosclerotic disease are the result of a constellation of diverse metabolic and immunologic mechanisms ultimately set into motion by the formation of fatty acid streaks and the accompanying inflammatory cell activation, endothelial damage, smooth muscle proliferation, vascular fibrosis, and end-organ infarction and necrosis. At the heart of atherosclerosis are the byprod-ucts of lipid metabolism, lipoproteins containing triglycerides, phospholipids, and cholesterol, and the changes they undergo that eventually lead to macrophage activation, foam cell formation, and other downstream atherosclerotic changes. Understanding the functionality of cholesterol, triglycerides, and lipoproteins in the cascade of atherosclerotic pathways has tremendous implications on current guidelines for the evaluation and targets in the management of dyslipidemia, and serves as the foundation for future investigations into targets of atherosclerotic therapies.