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Coronary artery disease (CAD) is one of the leading causes of death worldwide. These rates are only likely to be buoyed in the future by the rising prevalence of obesity, diabetes, and metabolic syndrome. The pathogenesis of atherosclerosis, the main cause of CAD, has been a topic of great interest.1 As a brief review, dyslipidemia plays a key role. Beginning with the incorporation of serum low-density lipoprotein into the endothelium tunica intima, chemokines and endothelial adhesion molecules attract macrophages into the arterial wall. Eventually, cholesterol droplets are incorporated into the macrophage cytosol, become oxidized, and form the so-called ‘foam cell’. In a reciprocal exchange, inflammatory mediators released by foam cells trigger ongoing endothelial damage, fibrosis, and intimal hyperplasia. Eventually, coronary artery stenosis occurs; a condition at the basis of CAD and for which inflammation is a key component. |
