Abstract
Coronary artery disease (CAD) is a significant health concern characterized by reduced blood flow to the heart muscle, primarily due to the buildup of atherosclerotic plaques in the coronary arteries. This process begins with endothelial injury, leading to a cascade of biological responses contributing to plaque formation. Endothelial injury attracts the migration of monocytes which differentiate into macrophages upon uptake of oxidized low-density lipoproteins, changing into lipid-laden macrophage or "foam cells." The process of plaque formation is influenced by many factors which have been studied extensively in literature such as smoking, hypertension, and diabetes mellitus. Chronic inflammatory illnesses are often associated with a high prevalence of coronary artery syndromes, prompting the evaluation of markers of inflammation such as white blood cell count and inflammatory markers as independent risk factors for CAD. White blood cells play a remarkable role in the pathophysiology of disease formation and progression. The article below aims to discuss the pathophysiology and epidemiology of leukocytosis as a risk factor for CAD.
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