Spatiotemporal Dynamics of Immune Cells in Early Left Ventricular Remodeling After Acute Myocardial Infarction in Mice

• Published in: Journal of cardiovascular pharmacology Vol. 75; no. 2; pp. 112 - 122
• Main Authors: Bejjani, Anthony T., Saab, Sally A., Muhieddine, Dina H., Habeichi, Nada J., Booz, George W., Zouein, Fouad A.
• Format: Journal Article
• Language: English
• Published: United States Journal of Cardiovascular Pharmacology 01-02-2020; Copyright Wolters Kluwer Health, Inc. All rights reserved
• Subjects: Animals; Cytokines - metabolism; Disease Models, Animal; Immune System - immunology; Immune System - metabolism; Immune System - pathology; Inflammation Mediators - metabolism; Mice; Myocardial Infarction - immunology; Myocardial Infarction - metabolism; Myocardial Infarction - pathology; Myocardial Infarction - physiopathology; Myocardium - immunology; Myocardium - metabolism; Myocardium - pathology; Time Factors; Ventricular Function, Left; Ventricular Remodeling
• ISSN: 0160-2446; 1533-4023
• DOI: 10.1097/FJC.0000000000000777

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.