NHLBI Working Group Recommendations to Reduce Lipoprotein(a)-Mediated Risk of Cardiovascular Disease and Aortic Stenosis

JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY

卷:71

Review

Tsimikas, Sotirios¹  Fazio, Sergio²  Ferdinand, Keith C.³  Ginsberg, Henry N.⁴  Koschinsky, Marlys L.^5,6  Marcovina, Santica M.⁷  Moriarty, Patrick M.⁸  Rader, Daniel J.⁹  Remaley, Alan T.¹⁰  Reyes-Soffer, Gissette⁴  Santos, Raul D.^11,12  Thanassoulis, George¹³  Witztum, Joseph L.¹⁴  Danthi, Simhan¹⁰  Olive, Michelle¹⁰  Liu, Lijuan¹⁰ 

[1] Univ Calif San Diego, Dept Med, Div Cardiol, Vasc Med Program,Sulpizio Cardiovasc Ctr, La Jolla, CA 92093 USA

[2] Oregon Hlth & Sci Univ, Portland, OR 97201 USA

[3] Tulane Univ Med Ctr Hosp & Clin, New Orleans, LA USA

[4] Columbia Univ, Coll Phys & Surg, New York, NY USA

[5] Univ Western Ontario, Schulich Sch Med & Dent, Robarts Res Inst, London, ON, Canada

[6] Univ Western Ontario, Schulich Sch Med & Dent, Dept Physiol & Pharmacol, London, ON, Canada

[7] Univ Washington, Dept Med, Seattle, WA USA

[8] Univ Kansas, Med Ctr, Kansas City, MO USA

[9] Univ Penn, Perelman Sch Med, Philadelphia, PA 19104 USA

[10] NHLBI, NIH, Bldg 10, Bethesda, MD 20892 USA

[11] Univ Sao Paulo, Med Sch Hosp, Heart Inst InCor, Sao Paulo, Brazil

[12] Hosp Israelita Albert Einstein, Sao Paulo, Brazil

[13] McGill Univ, Ctr Hlth, Montreal, PQ, Canada

[14] Univ Calif San Diego, Dept Med, Div Endocrinol, La Jolla, CA 92093 USA

关键词: aortic stenosis;    cardiovascular disease;    lipoprotein(a);    metabolism;    pathophysiology;    therapy;   

DOI  :  10.1016/j.jacc.2017.11.014

来源: Elsevier

【 摘 要 】

Pathophysiological, epidemiological, and genetic studies provide strong evidence that lipoprotein(a) [Lp(a)] is a causal mediator of cardiovascular disease (CVD) and calcific aortic valve disease (CAVD). Specific therapies to address Lp(a)-mediated CVD and CAVD are in clinical development. Due to knowledge gaps, the National Heart, Lung, and Blood Institute organized a working group that identified challenges in fully understanding the role of Lp(a) in CVD/CAVD. These included the lack of research funding, inadequate experimental models, lack of globally standardized Lp(a) assays, and inadequate understanding of the mechanisms underlying current drug therapies on Lp(a) levels. Specific recommendations were provided to facilitate basic, mechanistic, preclinical, and clinical research on Lp(a); foster collaborative research and resource sharing; leverage expertise of different groups and centers with complementary skills; and use existing National Heart, Lung, and Blood Institute resources. Concerted efforts to understand Lp(a) pathophysiology, together with diagnostic and therapeutic advances, are required to reduce Lp(a)-mediated risk of CVD and CAVD. (c) 2018 by the American College of Cardiology Foundation.

【 授权许可】

Free