EDITORIAL A Role for Pharmacogenetics? See Article by Parish, Hopewell, and Hill et al Michael B. Boffa, PhD Marlys L. Koschinsky, PhD e are on the cusp of having elevated plasma concentrations of lipoprotein(a) as a therapeutic target for cardiovascular disease (CVD). WRecent large population studies and meta-analyses, genome-wide asso- ciation studies, and Mendelian randomization studies have identified elevated lipoprotein(a) as an independent, causal risk factor for coronary heart disease and other atherothrombotic disorders. Elevated lipoprotein(a) is also emerging as a key risk factor for calcific aortic valve disease. Several therapeutic modalities capable of lowering lipoprotein(a) are in the marketplace or are in clinical trials. Yet, sev- eral obstacles remain. Most importantly, it has not been directly demonstrated that lowering lipoprotein(a) produces a clinical benefit, and to what extent lipoprotein(a) must be lowered to derive such a benefit. Beyond this, there remain fundamental unanswered questions on how lipoprotein(a) concentrations are established and the mechanisms underlying the lipoprotein(a)-lowering effects of current therapies. The article by Parish et al in this issue, describing a substudy of the Heart Protec- tion Study 2–Treatment of HDL to Reduce the Incidence of Vascular Events (HPS2- THRIVE) randomized controlled trial of niacin/laropiprant, sheds interesting new
Circulation: Cardiovascular Genetics – Wolters Kluwer Health
Published: Feb 1, 2018
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