8 The Challenge • Lifestyle therapy, including heart-healthy eating and regular physical activity, has no significant effect on Lp(a) levels.8 • Statin therapy doesn’t decrease Lp(a) levels. Patients with a history of CVD who are taking statins and have an Lp(a) ≥125 nmol/L (≥50 mg/dL) are still at increased risk for vascular events, independent of other risk factors.7, 22 • Niacin lowers Lp(a); yet, to date, there are no randomized trials in people with high Lp(a) to determine if this is beneficial or not. Randomized Clinical Trials do not support use of niacin as an add-on drug to statin therapy as it has been associated with enhanced side effects and even adverse events.4,7 How Does Lp(a) Work? Despite the link between Lp(a) level and a variety of CVD events, the exact pathophysiological roles of Lp(a) are not clear. Lp(a) accumulates in the blood vessel wall, where it appears to be retained more avidly than LDL-C.24 Recent evidence suggests that proinflammatory oxidized phospholipids present on Lp(a) promote the processes of endothelial dysfunction, inflammation and calcification in vasculature.24 The role of Lp(a) as a prothrombotic factor is controversial, with evidence both for and against this possibility.25 • It is suggested by post hoc analyses that PCSK9 inhibitors lower Lp(a) to a modest degree, but the specific contribution of Lp(a) reduction in lowering CVD risk in treated patients remains unclear. • Lipoprotein apheresis (LA) is currently the only FDA approved treatment for lowering Lp(a). FDA approved for Lp(a) lowering when: • Clinically diagnosed familial hypercholesterolemic heterozygotes and • Either documented coronary artery disease or documented peripheral artery disease and • Lp(a) ≥130 nmol/L (≥60mg/dL) 4
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