Coronary artery disease (CAD) results from progressive atherosclerosis of the coronary arteries, a chronic inflammatory process that begins with endothelial dysfunction and culminates in luminal narrowing, plaque rupture, and acute coronary syndromes. Understanding the cellular pathogenesis is essential for nurses because it explains why risk factor modification is effective, why certain medications are used, and how stable angina differs from unstable angina at the tissue level. Atherosclerosis pathogenesis follows a predictable sequence: (1) Endothelial dysfunction: Risk factors (hypertension, smoking, diabetes, hyperlipidemia) damage the endothelial cell layer lining coronary arteries, reducing nitric oxide production and increasing permeability to lipoproteins. (2) Lipid accumulation: Low-density lipoprotein (LDL) particles infiltrate the subendothelial space and become oxidized. Oxidized LDL is highly inflammatory and activates endothelial cells to express adhesion molecules (VCAM-1, ICAM-1) that recruit circulating monocytes. (3) Foam cell formation: Monocytes migrate into the intima, differentiate into macrophages, and engulf oxidized LDL via scavenger receptors (CD36, SR-A). These lipid-laden macrophages become foam cells, forming the fatty streak — the earliest visible lesion of atherosclerosis (present in some teenagers). (4) Fibrous plaque development: Smooth muscle cells...