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J Am Coll Cardiol. 2018 Jan 16;71(2):177-192. doi: 10.1016/j.jacc.2017.11.014.

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

Author information

1
Vascular Medicine Program, Sulpizio Cardiovascular Center, Division of Cardiology, Department of Medicine, University of California San Diego, La Jolla, California. Electronic address: stsimikas@ucsd.edu.
2
Oregon Health & Science University, Portland, Oregon.
3
Tulane Medical Center, New Orleans, Louisiana.
4
College of Physicians and Surgeons, Columbia University, New York, New York.
5
Robarts Research Institute and Department of Physiology & Pharmacology Schulich School of Medicine & Dentistry, University of Western Ontario, London, Ontario, Canada.
6
Department of Medicine, University of Washington, Seattle, Washington.
7
University of Kansas Medical Center, Kansas City, Missouri.
8
Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania.
9
National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland.
10
Heart Institute (InCor) University of Sao Paulo Medical School Hospital and Hospital Israelita Albert Einstein, Sao Paulo, Brazil.
11
McGill University Health Center, Montreal, Quebec, Canada.
12
Division of Endocrinology, Department of Medicine, University of California San Diego, La Jolla, California.

Abstract

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.

KEYWORDS:

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

PMID:
29325642
PMCID:
PMC5868960
[Available on 2019-01-16]
DOI:
10.1016/j.jacc.2017.11.014

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