CLINICIAN GUIDE · CHOLESTEROL & CARDIOVASCULAR PREVENTION · SECTION 1 OF 3
Understand lipid measures, plaque formation, and inherited risk.
The body needs cholesterol for cells and hormones. The clinical concern is prolonged exposure to atherogenic lipoproteins, which can enter artery walls and promote plaque. High cholesterol usually produces no symptoms; waiting for chest pain misses the prevention opportunity.[1]
Cholesterol within LDL particles; the main treatment target.
Total cholesterol minus HDL-C; includes cholesterol carried in multiple atherogenic particles.
A risk marker. High HDL does not cancel elevated LDL or other risk factors.
Reflect triglyceride-rich lipoproteins; marked elevations add pancreatitis risk.
A marker of atherogenic particle number; useful selectively when standard cholesterol measures underestimate risk.
A largely inherited lipoprotein associated with additional ASCVD risk.
Primary prevention: reduce the chance of a first ASCVD event. Secondary prevention: reduce recurrent events in established ASCVD, such as coronary disease, atherosclerotic stroke, or peripheral arterial disease.
Risk reflects age, BP, smoking, diabetes, kidney disease, family history, and cumulative lipid exposure. The same LDL value can warrant different treatment in different patients. A young adult’s low 10-year risk can conceal substantial lifetime exposure.[3][4]
Untreated LDL-C ≥190 mg/dL, premature ASCVD, or a striking family history should raise concern for familial hypercholesterolemia (FH). The LDL threshold alone does not prove FH.
Measure Lp(a) at least once in adulthood. Elevated Lp(a) supports more intensive overall risk reduction. Report the laboratory’s units; mg/dL and nmol/L are not interchangeable through a universal conversion.[3][5]
Adult clinician education · References reviewed October 11, 2026.