The re-emergence of lipoprotein(a) in a broader clinical arena

Lipoprotein(a) [Lp(a)] is a genetic, independent and likely causal risk factor for cardiovascular disease (CVD) and calcific aortic valve stenosis (CAVS). Lp(a) levels are primarily genetically determined and tend to fluctuate only mildly around a pre-determined level. In primary care settings, one Lp(a) measurement can reclassify up to 40% of patients in intermediate risk score categories. In secondary care settings, recent data from the JUPITER and AIM-HIGH trials demonstrate that elevated Lp(a) remains part of the “residual risk” despite achievement of low-density lipoprotein cholesterol levels <70 mg/dL. Recent reports suggest that statins can increase Lp(a) levels, potentially further contributing to this residual risk. Current therapies to lower Lp(a) are limited to niacin, mipomersen and proprotein convertase subtilisin kexin-type 9 inhibitors, but these drugs are limited by weak efficacy and not specifically approved for Lp(a) lowering. Emerging therapies to lower Lp(a) may shed new light into the potential clinical benefit of lowering Lp(a) in CVD and CAVS.