ANGPTL3 Deficiency and Protection Against Coronary Artery Disease


Nathan O. Stitziel, MD, PHD, Amit V. Khera, MD, Xiao Wang, PHD, Andrew J. Bierhals, MD, MPH, A. Christina Vourakis, BA, Alexandra E. Sperry, BA, Pradeep Natarajan, MD, Derek Klarin, MD, Connor A. Emdin, DPHIL, Seyedeh M. Zekavat, BSc, Akihiro Nomura, MD, Jeanette Erdmann, PHD, Heribert Schunkert, MD, Nilesh J. Samani, MD,m,n William E. Kraus, MD, Svati H. Shah, MD, MPH, Bing Yu, PHD, Eric Boerwinkle, PHD, Daniel J. Rader, MD, Namrata Gupta, PHD, Philippe M. Frossard, PHD, Asif Rasheed, MBBS, John Danesh, DPHIL, Eric S. Lander, PHD, Stacey Gabriel, PHD, Danish Saleheen, MBBS, PHD, Kiran Musunuru, MD, PHD, MPH, Sekar Kathiresan, MD, for the PROMIS and Myocardial Infarction Genetics Consortium Investigators.

BACKGROUND: Familial combined hypolipidemia, a Mendelian condition characterized by substantial reductions in all 3 major lipid fractions, is caused by mutations that inactivate the gene angiopoietin-like 3 (ANGPTL3). Whether ANGPTL3 deficiency reduces risk of coronary artery disease (CAD) is unknown.

CONCLUSIONS: ANGPTL3 deficiency is associated with protection from CAD.

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