Lp(a)-lowering therapies remain limited despite proven links to residual cardiovascular risk, aortic stenosis and peripheral arterial disease, a review (Curr Treat Options Cardiovasc Med 2017)

Cardiovascular disease is a leading cause of morbidity and mortality in the USA and around the world. While we are now able to achieve significant low-density lipoprotein cholesterol (LDL-C) lowering with current therapies, many patients remain at risk for cardiovascular disease (CVD). Elevated lipoprotein(a) [Lp(a)] has been shown to be an independent risk factor for CVD and accounts for some of the residual CVD risk after LDL-C lowering in several large clinical trials. Moreover, there is now strong evidence supporting the causal relationship between Lp(a) and aortic stenosis as well as peripheral arterial disease. Despite the growing interest in this lipoprotein, the current therapeutic options for Lp(a) reduction are limited. Our general approach in patients with elevated Lp(a) levels is to aggressively manage other modifiable cardiovascular risk factors including lifestyle modification, consideration of aspirin therapy, and LDL-C lowering. Unfortunately, there are conflicting reports on how effective this strategy is at reducing the risk for cardiovascular events attributed to elevated Lp(a). As a result, targeted Lp(a)-lowering strategies are needed. Lp(a) therapeutics is an active area of research with several promising classes of pharmacotherapies under investigation to address this causal biomarker.