Invited Review ArticleInhibiting NLRP3 Inflammasome Activity in Acute Myocardial Infarction: A Review of Pharmacologic Agents and Clinical OutcomesBuckley, Leo F. PharmD*; Libby, Peter MD†Author Information *Department of Pharmacy Services, Brigham and Women's Hospital, Boston, MA; and †Division of Cardiovascular Medicine, Harvard Medical School, Boston, MA. Reprints: Leo F. Buckley, PharmD, Department of Pharmacy Services, Brigham and Women's Hospital, 75 Francis St, PB-AB-314, Boston, MA 02120 (e-mail: [email protected]). P. Libby is supported by the National Heart, Lung, and Blood Institute: (R01HL080472); American Heart Association (18CSA34080399); RRM Charitable Fund. P. Libby is an unpaid consultant to, or involved in clinical trials for Amgen, AstraZeneca, Esperion Therapeutics, Ionis Pharmaceuticals, Kowa Pharmaceuticals, Novartis, Pfizer, Sanofi-Regeneron, and XBiotech, Inc. P. Libby is a member of scientific advisory board for Amgen, Corvidia Therapeutics, DalCor Pharmaceuticals, IFM Therapeutics, Kowa Pharmaceuticals, Olatec Therapeutics, Medimmune, Novartis, and XBiotech, Inc. P. Libby's laboratory has received research funding in the last 2 years from Novartis. The remaining author reports no conflicts of interest. Journal of Cardiovascular Pharmacology: October 2019 - Volume 74 - Issue 4 - p 297-305 doi: 10.1097/FJC.0000000000000701 Buy Metrics Abstract The NLRP3 inflammasome is an intracellular, multimeric protein complex that initiates a potent inflammatory response to danger signals. After acute myocardial infarction, NLRP3 inflammasome-dependent inflammation promotes adverse left ventricular remodeling and recurrent atherosclerotic events. Selective and nonselective inhibitors of the NLRP3 inflammasome or its downstream effectors (interleukin-1β and interleukin-18) may prevent adverse left ventricular remodeling and recurrent atherosclerotic events. In this review, we highlight strategies to inhibit NLRP3 inflammasome activity and their potential roles in the management of acute myocardial infarction. Copyright © 2019 Wolters Kluwer Health, Inc. All rights reserved.