Practical management of dyslipidemia with elevated lipoprotein(a)

Abstract

To report a case and describe a practical approach to treating dyslipidemia in a very-high-risk patient with elevated lipoprotein(a) [Lp(a)]. Pharmacist-managed lipid clinic, from November 2006 to July 2007. A 50-year-old white woman with a recent history of multiple myocardial infarctions presented for management of dyslipidemia. At baseline, the patient had elevated low-density lipoprotein cholesterol (LDL-C), triglyceride (TG), total cholesterol (TC), and Lp(a) (306 nmol/L) levels and low high-density lipoprotein cholesterol (HDL-C) levels. Early initiation of combination therapy with a statin and niacin extended release (ER) titration was started. After 3 months, despite progressive weight gain caused by dietary indiscretion, LDL-C decreased by 24% and TG and TC levels reached goal. Lp(a) levels did not change. Niacin ER titration continued, pravastatin was maximized, and ezetimibe 10 mg daily was started. Despite dramatic 9-month weight gain (68 lb total), LDL-C and HDL-C reached goal and Lp(a) levels decreased by 33% (204 nmol/L) after niacin ER maximization. Lp(a) is an emerging risk factor in cardiovascular disease (CVD). Elevated Lp(a) (>30 mg/dL) has been implicated as both an independent and an additive risk factor for CVD and stroke, particularly in women. In this case, the patient did not reach the optimal goal (<30 mg/dL) but did experience more than 30% reduction in Lp(a) levels. Although multiple factors, including subclinical hypothyroidism, hormonal changes, and renal disease, increase Lp(a) levels, few beneficial treatment options exist (i.e., estrogen and niacin). Although the exact mechanism of action is unknown, niacin ER has been documented to reduce Lp(a) by 36% to 38%. Some effect of ezetimibe on Lp(a) in this patient cannot be ruled out. This case illustrates a practical use of currently available therapy options to address Lp(a) as a secondary cardiovascular risk factor. Niacin is a preferred option for Lp(a) lowering in very-high-risk patients with coronary heart disease and dyslipidemia. The importance of moderate reductions in Lp(a) is not known.