8 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.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 The Challenge • Lifestyle therapy, including heart-healthy eating and regular physical activity, has no significant effect on Lp(a) levels.7 • Statin therapy doesn’t decrease Lp(a) levels. Patients with a history of CVD who are taking statins and have an Lp(a) ≥50 mg/dL are at increased risk for vascular events, independent of other risk factors.6 • 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. In other randomized trials, use of niacin has been associated with enhanced side effects and even adverse events.6 • 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 FDAapproved treatment for lowering Lp(a). FDA approved for Lp(a) lowering when: • Patient has heterozygous familial hypercholesterolemia and • LDL-C > 100mg/dL and • Patient has established coronary artery disease or peripheral artery disease and • Lp(a) > 60 mg/dL26
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