Chronic heart failure following hemorrhagic myocardial infarction: mechanism, treatment and outlook

Authors:

Shing Fai Chan1, Keyur Vora1 and Rohan Dharmakumar1,*
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Affiliations:

1 Krannert Cardiovascular Research Center, Indiana University School of Medicine/IU Health Cardiovascular Institute.

Keywords: 

myocardial infarction, intramyocardial hemorrhage, heart failure, deferiprone, fatty infiltration, iron

Corresponding Author(s):

Rohan Dharmakumar, Krannert Cardiovascular Research Center. Indiana University School of Medicine/IU Health Cardiovascular Institute. Indianapolis, USA 46202; Phone: (317) 274-5652; rdkumar@iu.edu

Conflict of interest statement:

Dr. Dharmakumar has ownership interest in Cardio-Theranostics, LLC. The remaining authors declare no competing interests.

Please cite this article as:

Shing Fai Chan, Keyur Vora and Rohan Dharmakumar (2023). Chronic heart failure following hemorrhagic myocardial infarction: mechanism, treatment and outlook. Cell Stress 7(2): 7-11. doi: 10.15698/cst2023.02.276

© 2023 Chan et al. This is an open-access article released under the terms of the Creative Commons Attribution (CC BY) license, which allows the unrestricted use, distribution, and reproduction in any medium, provided the original author and source are acknowledged.

Abstract:

Myocardial infarction (MI), the blockage of arterial blood supply of the heart, is among the most common causes of death worldwide. Even when patients receive immediate treatment by re-opening blocked arteries, they often develop chronic heart failure (CHF) in the aftermath of MI events. Yet, the factors that contribute to the development of MI-associated CHF are poorly understood. In our recent study (Nat Commun 13:6394), we link intramyocardial hemorrhage, an injury which can occur during reperfusion of areas affected by MI, to an increased risk of CHF. Mechanistically, our data suggest that an iron-induced adverse cascade of events after hemorrhagic MI drives fatty degeneration of infarcted tissue, which ultimately contributes to negative cardiac remodeling. In this Microreview, we discuss the implications of our findings regarding the molecular mechanism, more targeted treatment options as well as perspectives in the clinical care of CHF after hemorrhagic MI.