Lipid management is centered on reducing atherosclerotic cardiovascular disease (ASCVD) risk through modification of lipoprotein metabolism. Lipoproteins are macromolecular complexes that transport hydrophobic lipids (cholesterol, triglycerides) through the aqueous bloodstream. The primary atherogenic lipoprotein is low-density lipoprotein (LDL), which carries approximately 70% of circulating cholesterol. The atherosclerotic process begins when LDL particles penetrate the arterial intima and become oxidized. Oxidized LDL triggers endothelial activation, recruiting monocytes that differentiate into macrophages, which engulf oxidized LDL via scavenger receptors and become foam cells. Foam cell accumulation forms fatty streaks, which progress to fibrous plaques through smooth muscle cell migration, extracellular matrix deposition, and neovascularization. Vulnerable plaques with thin fibrous caps and large lipid cores are prone to rupture, exposing thrombogenic contents to blood and triggering acute coronary syndrome. Statins are the cornerstone of lipid management. They inhibit HMG-CoA reductase, the rate-limiting enzyme in the cholesterol biosynthesis pathway, reducing intrahepatic cholesterol production. This upregulates hepatic LDL receptor expression, increasing LDL clearance from the blood. Statins additionally have pleiotropic effects: improved endothelial function, anti-inflammatory effects (reduced CRP), plaque stabilization, and antithrombotic properties. The 2018...