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Updated: Feb 25, 2026

Postconditioning with Lactate-enriched Blood for Cardioprotection in ST-segment Elevation Myocardial Infarction
Published on: May 28, 2019
New and revisited approaches to preserving the reperfused myocardium
Robert A Kloner1,2, David A Brown3,4,5, Marie Csete1,6
1Cardiovascular Research Institute, Huntington Medical Research Institutes, 99 North El Molino Avenue, Pasadena, California 91101, USA.
Insights
Protecting the heart after ST-elevation myocardial infarction (STEMI) is crucial. This review explores novel therapies targeting mitochondrial function, cell death pathways, and anaesthetics to preserve reperfused myocardium and prevent adverse remodelling.
Area of Science:
- Cardiovascular Medicine
- Regenerative Medicine
- Pharmacology
Background:
- Early reperfusion in ST-elevation myocardial infarction (STEMI) improves outcomes but high morbidity and mortality persist.
- Key issues include impaired cardiac pump function due to rapid muscle infarction and adverse left ventricular remodelling post-STEMI.
- Current strategies to reduce infarct size beyond reperfusion have yielded disappointing results, necessitating new therapeutic approaches.
Purpose of the Study:
- To review emerging therapies for preserving reperfused myocardium in STEMI patients.
- To discuss strategies targeting cellular mechanisms and pharmacological agents for cardioprotection.
- To explore treatments for the no-reflow phenomenon and its impact on cardiac healing and remodelling.
Main Methods:
- Literature review of current research on myocardial protection post-reperfusion.
- Analysis of therapeutic targets including mitochondrial bioenergetics, pyroptosis, and autophagy.
- Evaluation of inhaled anaesthetics and treatments for the no-reflow phenomenon.
Main Results:
- Several promising therapeutic avenues are being explored to protect the heart during and after myocardial infarction.
- Targeting cellular pathways like mitochondrial function and programmed cell death shows potential for reducing myocardial damage.
- Inhaled anaesthetics and interventions for no-reflow may mitigate adverse cardiac remodelling.
Conclusions:
- Despite advances in reperfusion therapy, significant unmet needs remain in managing STEMI.
- Novel therapeutic strategies targeting cellular protection and addressing the no-reflow phenomenon are essential for improving long-term outcomes.
- Further research into these approaches holds promise for reducing mortality and morbidity in STEMI patients.
Abstract:
Early coronary artery reperfusion improves outcomes for patients with ST-segment elevation myocardial infarction (STEMI), but morbidity and mortality after STEMI remain unacceptably high. The primary deficits seen in these patients include inadequate pump function, owing to rapid infarction of muscle in the first few hours of treatment, and adverse remodelling of the heart in the months that follow. Given that attempts to further reduce myocardial infarct size beyond early reperfusion in clinical trials have so far been disappointing, effective therapies are still needed to protect the reperfused myocardium. In this Review, we discuss several approaches to preserving the reperfused heart, such as therapies that target the mechanisms involved in mitochondrial bioenergetics, pyroptosis, and autophagy, as well as treatments that harness the cardioprotective properties of inhaled anaesthetic agents. We also discuss potential therapies focused on correcting the no-reflow phenomenon and its effect on healing and adverse left ventricular remodelling.

