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Updated: May 2, 2026
Postconditioning with Lactate-enriched Blood for Cardioprotection in ST-segment Elevation Myocardial Infarction
Published on: May 28, 2019
Ischemic postconditioning: mechanisms, comorbidities, and clinical application
Bruno Buchholz1, Martín Donato, Verónica D'Annunzio
1Department of Pathology, School of Medicine, Institute of Cardiovascular Physiopathology, University of Buenos Aires, JE Uriburu 950 - 2nd Floor, C1114AAD, Buenos Aires, Argentina.
Insights
Ischemic postconditioning, brief reperfusion episodes, reduces heart attack damage. Pharmacological agents mimicking this effect show promise for treating ischemic heart disease (IHD).
Area of Science:
- Cardiology
- Cardiovascular Research
- Translational Medicine
Background:
- Ischemic heart disease (IHD) is a leading cause of mortality and heart failure.
- Acute myocardial infarction (heart attack) necessitates novel therapeutic strategies.
- Ischemic postconditioning, brief ischemia/reperfusion at reperfusion onset, reduces infarct size.
Purpose of the Study:
- To review the mechanisms of ischemic postconditioning.
- To discuss the role of autacoids, cytokines, and signaling pathways.
- To evaluate the clinical applicability of ischemic postconditioning in IHD.
Main Methods:
- Review of existing research on ischemic postconditioning mechanisms.
- Analysis of autacoid and cytokine involvement (e.g., adenosine, bradykinin, opioids).
- Exploration of kinase signaling pathways and mitochondrial modulation.
Main Results:
- Ischemic postconditioning involves complex signaling pathways and mediators.
- Pharmacological agents can mimic cardioprotective effects of ischemic postconditioning.
- Comorbidities may influence the efficacy of postconditioning strategies.
Conclusions:
- Ischemic postconditioning and pharmacological mimics offer potential therapeutic avenues for IHD.
- Further large-scale, randomized clinical trials are essential.
- Determining the clinical benefit for IHD patients requires rigorous evaluation.
Abstract:
Since ischemic heart disease (IHD) is a major cause of mortality and heart failure, novel therapeutic strategies are expected to improve the clinical outcomes of patients with acute myocardial infarction. Brief episodes of ischemia/reperfusion performed at the onset of reperfusion can reduce infarct size; a phenomenon termed "ischemic postconditioning." Extensive research has determined that different autacoids (e.g., adenosine, bradykinin, opioid, etc.) and cytokines, their respective receptors, kinase signaling pathways, and mitochondrial modulation are involved in ischemic conditioning. Modification of these factors by pharmacological agents mimics the cardioprotection by ischemic postconditioning. Here, the potential mechanisms of ischemic postconditioning, the presence of comorbidities, and the possible extrapolation to the clinical setting are reviewed. In the near future, large, multicentered, randomized, placebo-controlled, clinical trials will be required to determine whether pharmacological and/or ischemic postconditioning can improve the clinical outcomes of patients with IHD.
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