Review ArticleSpatiotemporal Dynamics of Immune Cells in Early Left Ventricular Remodeling After Acute Myocardial Infarction in MiceBejjani, Anthony T. BSc*; Saab, Sally A. MSc*; Muhieddine, Dina H. MSc†; Habeichi, Nada J. MSc†; Booz, George W. PhD‡; Zouein, Fouad A. PhD†Author Information Departments of *Biology; and †Pharmacology and Toxicology, Faculty of Medicine, American University of Beirut Medical Center, Beirut, Lebanon; and ‡Department of Pharmacology and Toxicology, School of Medicine, University of Mississippi Medical Center, Jackson, MS. Reprints: Fouad A. Zouein, PhD, FAHA or Dina H. Muhieddine, Msc, Department of Pharmacology and Toxicology, American University of Beirut & Medical Center, Riad El-Solh, Beirut 1107 2020, Lebanon (e-mail: email@example.com or Dina.firstname.lastname@example.org). This work has been funded with supports of the Medical Practice Plan (MPP), the Faculty of Medicine of the American University of Beirut, MPP-320145 (to F.A.Z.). The authors report no conflicts of interest. A. T. Bejjani and S. A. Saab have contributed equally. Received August 07, 2019 Accepted October 23, 2019 Journal of Cardiovascular Pharmacology: February 2020 - Volume 75 - Issue 2 - p 112-122 doi: 10.1097/FJC.0000000000000777 Buy Metrics Abstract Myocardial infarction remains a leading cause of morbidity and death. Insufficient delivery of oxygen to the myocardium sets into play a complicated process of repair that involves the temporal recruitment of different immune cells so as to remove debris and necrotic cells expeditiously and to form effective scar tissue. Clearly defined and overlapping phases have been identified in the process, which transitions from an overall proinflammatory to anti-inflammatory phenotype with time. Variations in the strength of the phases as well as in the co-ordination among them have profound consequences. Too strong of an inflammatory phase can result in left ventricular wall thinning and eventual rupture, whereas too strong of an anti-inflammatory phase can lead to cardiac stiffening, arrhythmias, or ventricular aneurisms. In both cases, heart failure is an intermediate consequence with death being the likely outcome. Here, we summarize the role of key immune cells in the repair process of the heart after left ventricular myocardial infarction, along with the associated cytokines and chemokines. A better understanding of the immune response ought to lead hopefully to improved therapies that exploit the natural repair process for mending the infarcted heart. Copyright © 2020 Wolters Kluwer Health, Inc. All rights reserved.