Lp(a): A Toolkit for Health Care Professionals

8 The Challenge • Lifestyle therapy, including diet and physical exercise, has no significant effect on Lp(a) levels. 6 • Statin therapy doesn’t decrease Lp(a) levels. Patients with a history of ASCVD who are taking statins and have an Lp(a) ≥50 mg/dL are at increased risk for ASCVD 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 studies that PCSK9 inhibitors lower Lp(a) to a modest degree, but the contribution of Lp(a) reduction in lowering their ASCVD risk remains undetermined and requires further studies. • Lipoprotein apheresis is the only FDA-approved treatment for lowering Lp(a) and can be used for those with elevated Lp(a) and recurrent ASCVD events. 6 How Does Lp(a) Work? Lp(a) is pro-inflammatory. Despite the link between Lp(a) level and both ASCVD and calcific aortic valve disease, the exact pathophysiologic mechanism isn’t clear. Recent evidence suggests that oxidized phospholipids present on Lp(a) promote endothelial dysfunction, inflammation and calcification in vasculature. 19 Lp(a) has also been detected in the blood vessel wall, where it appears to be retained more avidly than LDL. 20 Similarly, growing evidence links elevated Lp(a) to calcific aortic stenosis. 21