Abstract

Acute myocardial infarction (AMI) and the heart failure that often follows, are major causes of death and disability worldwide. As such, new therapies are required to limit myocardial infarct (MI) size, prevent adverse left ventricular (LV) remodeling, and reduce the onset of heart failure following AMI. The inflammatory response to AMI, plays a critical role in determining MI size, and a persistent pro-inflammatory reaction can contribute to adverse post-MI LV remodeling, making inflammation an important therapeutic target for improving outcomes following AMI. In this article, we provide an overview of the multiple players (and their dynamic roles) involved in the complex inflammatory response to AMI and subsequent LV remodeling, and highlight future opportunities for targeting inflammation as a therapeutic strategy for limiting MI size, preventing adverse LV remodeling, and reducing heart failure in AMI patients.

Highlights

  • The initial pro-inflammatory response to AMIAcute myocardial infarction (AMI) and the heart failure that often follows, are among the leading causes of death and disability worldwide

  • In this article we provide an overview of the multiple players in the complex inflammatory response to Acute myocardial infarction (AMI) and subsequent left ventricular (LV) remodeling, and highlight future opportunities for targeting inflammation as a therapeutic strategy for limiting myocardial infarct (MI) size and preventing heart failure following AMI

  • In the first 24–72 h following AMI, the cardiac fibroblasts act as pro-inflammatory mediators, activating the inflammasome and producing cytokines, chemokines and exhibiting matrix-degrading properties, thereby helping to clear the wound of dead cells and remove matrix debris — this process is facilitated by specific pro-inflammatory cytokines, which delay the transformation of fibroblasts into myofibroblasts

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Summary

The initial pro-inflammatory response to AMI

Acute myocardial infarction (AMI) and the heart failure that often follows, are among the leading causes of death and disability worldwide. The inflammatory response to acute IRI plays a critical role in determining acute MI size and subsequent post-MI adverse LV remodeling, making it a potential therapeutic target for improving clinical outcomes in AMI patients. There is an increasing amount of experimental evidence, that a number of different players are involved in the inflammatory response, and they have been shown to contribute to the detrimental effects of acute myocardial IRI, making them important therapeutic targets for cardioprotection. In this article we provide an overview of the multiple players (and their dynamic roles involved) in the complex inflammatory response to AMI and subsequent LV remodeling, and highlight future opportunities for targeting inflammation as a therapeutic strategy for limiting MI size and preventing heart failure following AMI

The inflammatory response to acute myocardial IRI
The anti-inflammatory reparative phase following AMI
Therapeutic targeting of inflammation following MI
Complement cascade inhibition
Neutrophils
P-selectin Ab
25 STEMI PPCI pooled analysis
Therapeutic targeting of inflammatory cytokines
Why have so many anti-inflammatory therapies failed to protect in AMI?
Future therapeutic approaches to target inflammation
Findings
Conclusion

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