Lp(a) may accelerate atherosclerotic damage (atheroma) by increasing the size of plaque/atheroma in artery walls. It is retained in the artery wall more than LDL cholesterol as it binds to the artery lining through apolipoprotein (a). Lp(a) is also thought to increase risk of heart attacks by interfering with clotting mechanisms and therefore promoting clot development on the inner surface of blood vessels.

This dual action may explain the role of Lp(a) in the promotion of cardiovascular disease (CVD).

Lp(a) concentrations within the blood are genetically determined and will remain fairly constant in an individual over a lifetime. Concentration is not affected by diet, exercise, and other lifestyle modifications used to lower lipids within the blood. Lp(a) concentrations are slightly lower in men than in women and increase slightly in women after the menopause. The concentration of Lp(a) also varies with ethnicity: patients of African American descent can have concentrations up to 4 times higher than Caucasians, but they may not have a higher risk for CAD.