Lp(a) is an independent risk factor for recurrent atherosclerotic heart disease in men and women after menopause. Excess levels of Lp(a) are seen in both males and females, more common in Africans, African Americans, and Asian populations than in whites. Since the standard lipid profile does not report Lp(a), it has to be ordered separately. Screening for Lp(a) should be considered under the following circumstances: (a) patient or family history of premature atherosclerotic heart disease, (b) familial history of hyperlipidemia, (c) established atherosclerotic heart disease with a normal routine lipid profile, (d) hyperlipidemia refractory to therapy, and (e) history of recurrent arterial stenosis. Treatment options are (a) a new extended-release form of niacin 3 to 4 g daily (although most effective in lowering Lp(a) and in reducing atherosclerotic heart disease mortality rates, its use may be limited because of side effects); (b) estrogen replacement after menopause, (however, concomitant progesterone therapy dilutes the effectiveness of estrogens); (c) lowering LDL with statins (generally effective in atherosclerotic heart disease but has no effect on Lp(a) levels), (d) aspirin and antibiotics (may be effective when C-reactive protein levels are high); and (e) folic acid (reduces homocysteine levels). The general measures that halt the progression of CAD should always be adhered to, namely, maintaining normal weight, a daily exercise program, blood pressure control, a low-cholesterol-forming diet, and daily aspirin.

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