If a plaque ruptures within a vital artery, a blood clot forms and may obstruct the flow of oxygenated blood to the heart or brain, resulting in an acute coronary syndrome (ACS), myocardial infarction (MI), or stroke, with potentially irreversible damage to the tissue of the heart or brain. Control and reduction of CVD risk factors, including high cholesterol levels, elevated blood pressure, insulin resistance, elevated blood glucose levels, smoking, poor dietary habits, and a sedentary lifestyle, can contribute to a reduction in CVD morbidity and mortality. a The abbreviation CVD will be used throughout this CPG. For the purposes of this guideline, CVD includes atherosclerotic cardiovascular disease. Although serum cholesterol and its components have been well established as independent risk factors for CVD, they contribute only marginally to risk calculators in estimating CVD risk, the principal driver for the management of lipids in the primary prevention of CVD. Aside from familial hypercholesterolemia (FH) and other genetically mediated forms of extreme lipid levels, dyslipidemia has traditionally been defined as one or more of the following: low-density lipoprotein cholesterol (LDL-C) 130 milligrams per deciliter (mg/dL), high-density lipoprotein cholesterol (HDL-C) <40 mg/dL, or triglycerides (TGs) 200 mg/dL. However, in patients with known CVD or elevated risk for CVD, even normal lipids levels warrant intervention for CVD risk reduction. Treatment of dyslipidemia involves lifestyle changes and lipid-lowering drugs. However, the management of dyslipidemia has shifted away from treating dyslipidemia itself as a discrete entity and moved toward managing dyslipidemia in the context of overall risk for CVD. For this reason, much of our evidence is based on CV risk reduction and does not require lipid levels for inclusion criteria. 