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Updated: Aug 8, 2026
Postconditioning with Lactate-enriched Blood for Cardioprotection in ST-segment Elevation Myocardial Infarction
Published on: May 28, 2019
[Postconditioning: lethal reperfusion injury as a therapeutic target]
1Hôpital cardiologique et pneumologique, Louis-Pradel, 59, boulevard Pinel, 69394 Lyon 03, Lyon, France. ovize@sante.univ-lyon1.fr
Insights
Ischemic postconditioning significantly reduces heart attack damage by using brief reperfusion periods. This cardioprotective method may involve specific cell signaling pathways, offering hope for new treatments.
Area of Science:
- Cardiology
- Cellular Biology
- Pharmacology
Context:
- Acute myocardial infarction (AMI) is a primary cause of death globally.
- Ischemic postconditioning is a cardioprotective strategy involving brief reperfusion episodes after prolonged ischemia.
- Current treatments aim to limit infarct size and preserve cardiac function.
Purpose:
- To summarize the protective mechanisms of ischemic postconditioning.
- To highlight its potential in reducing infarct size in acute myocardial infarction.
- To explore the development of pharmacological agents mimicking postconditioning.
Summary:
- Ischemic postconditioning, a technique of repeated brief ischemia-reperfusion, significantly reduces infarct size following acute myocardial infarction.
- This cardioprotective effect is associated with the activation of the PI3-kinase-Akt-eNOS signaling pathway and inhibition of the mitochondrial permeability transition pore.
- A recent clinical study confirmed the protective benefits of postconditioning in the human heart.
Impact:
- Provides a foundation for developing novel pharmacological therapies for acute myocardial infarction.
- Suggests that mimicking postconditioning could offer a new treatment strategy for patients with ongoing heart attacks.
- Emphasizes the need for further research into pharmacologic agents that replicate postconditioning's benefits.
Abstract:
Acute myocardial infarction is the leading cause of morbidity and mortality in western countries. Ischemic postconditioning, that consists of repeated brief episodes of ischemia-reperfusion performed just after reflow following a prolonged ischemic insult, dramatically reduces infarct size. Recent data indicate that it might involve the activation of the PI3-kinase-Akt-eNOS signalling pathway and inhibition of the opening of the permeability transition pore. A recent clinical study demonstrated that postconditioning protects the human heart. Further research is needed to find new pharmacological agents that would mimick postconditioning in order to treat all patients with ongoing acute myocardial infarction.
