TY - JOUR
T1 - NHLBI Working Group Recommendations to Reduce Lipoprotein(a)-Mediated Risk of Cardiovascular Disease and Aortic Stenosis
AU - Tsimikas, Sotirios
AU - Fazio, Sergio
AU - Ferdinand, Keith C.
AU - Ginsberg, Henry N.
AU - Koschinsky, Marlys L.
AU - Marcovina, Santica M.
AU - Moriarty, Patrick M.
AU - Rader, Daniel J.
AU - Remaley, Alan T.
AU - Reyes-Soffer, Gissette
AU - Santos, Raul D.
AU - Thanassoulis, George
AU - Witztum, Joseph L.
AU - Danthi, Simhan
AU - Olive, Michelle
AU - Liu, Lijuan
N1 - Publisher Copyright:
© 2018 American College of Cardiology Foundation
PY - 2018/1/16
Y1 - 2018/1/16
N2 - 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.
AB - 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.
KW - aortic stenosis
KW - cardiovascular disease
KW - lipoprotein(a)
KW - metabolism
KW - pathophysiology
KW - therapy
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U2 - 10.1016/j.jacc.2017.11.014
DO - 10.1016/j.jacc.2017.11.014
M3 - Review article
C2 - 29325642
AN - SCOPUS:85040634118
SN - 0735-1097
VL - 71
SP - 177
EP - 192
JO - Journal of the American College of Cardiology
JF - Journal of the American College of Cardiology
IS - 2
ER -