title: The re-emergence of lipoprotein(a) in a broader clinical arena.
abstract: 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.
authors: Division of Cardiovascular Medicine, Sulpizio Cardiovascular Center, University of California San Diego, La Jolla, CA. Electronic address: stsimikas@ucsd.edu.
authors: Sotirios
authors: S
authors: Tsimikas
mesh_terms: D001021:Aortic Valve / Q000378:metabolism / Q000473:pathology*; D001024:Aortic Valve Stenosis / Q000235:genetics / Q000378:metabolism / Q000628:therapy; D002114:Calcinosis / Q000235:genetics / Q000378:metabolism / Q000628:therapy; D002318:Cardiovascular Diseases / Q000453:epidemiology / Q000517:prevention & control; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000009:adverse effects* / Q000494:pharmacology; D017270:Lipoprotein(a) / Q000378:metabolism*; D054539:Medication Therapy Management / Q000639:trends; D012307:Risk Factors
chemical_list: D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D017270:Lipoprotein(a)
keywords: Aortic stenosis; Cardiovascular disease; Genome-wide association studies; Lipoprotein(a); Therapy