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Making the heart resistant to infarction: how can we further decrease infarct size?
Renaud Tissier1, Alain Berdeaux, Bijan Ghaleh
1INSERM, Unite 841, Creteil, F-94000 France.
Insights
New cardioprotective strategies target the Reperfusion Injury Salvage Kinase (RISK) pathway to reduce heart damage after acute myocardial infarction (AMI). These approaches, including pharmacological agents and myocardial cooling, aim to improve outcomes beyond standard reperfusion therapy.
Area of Science:
- Cardiology
- Biochemistry
- Pharmacology
Background:
- Acute myocardial infarction (AMI) is a leading cause of death globally.
- Current treatment relies on reperfusion therapy, with limited options for further myocardial salvage.
- The Reperfusion Injury Salvage Kinase (RISK) pathway has emerged as a novel target for cardioprotection.
Purpose of the Study:
- To review the efficacy of emerging cardioprotective strategies for acute myocardial infarction.
- To explore interventions targeting the RISK pathway and adverse reperfusion events.
- To evaluate the potential of myocardial cooling as an anti-infarct intervention.
Main Methods:
- Review of existing literature on cardioprotective agents and strategies.
- Analysis of mechanisms involving the RISK pathway, preconditioning, and postconditioning.
- Examination of interventions aimed at mitigating reperfusion injury, such as calcium overload and free radical damage.
Main Results:
- The RISK pathway plays a crucial role in mediating cardioprotection.
- Pharmacological interventions activating the RISK pathway show promise.
- Strategies addressing reperfusion injury and myocardial cooling are under investigation for improved efficacy.
Conclusions:
- Activating the RISK pathway offers a promising therapeutic avenue for reducing infarct size in AMI.
- Novel pharmacological agents and myocardial cooling represent potential advancements in anti-infarct therapy.
- Further clinical trials are needed to confirm the efficacy of these strategies in improving patient outcomes.
Abstract:
Acute myocardial infarction (AMI) following coronary artery occlusion is a common cause of mortality and morbidity world-wide. Patients currently receive reperfusion therapy as the only anti-infarct intervention. A number of agents have been evaluated to further improve myocardial salvage, but until recently, none has demonstrated clear efficacy in clinical trials. A new target of cardioprotection, the Reperfusion Injury Salvage Kinase (RISK) pathway, has been proposed. These kinases are involved in mediating the cardioprotection of myocardial preconditioning and postconditioning induced by short non-lethal cycles of ischemia/reperfusion performed before (preconditioning) or just after (postconditioning) a lethal ischemic insult. Many pharmacological interventions are now available that protect the heart by activating the RISK pathway at the time of reperfusion. The present review will examine the efficacy of several strategies that have been proposed to protect the acutely ischemic myocardium including (1) those intended to directly alter adverse reperfusion events (e.g., calcium overload and free radical attack), (2) those based on activation of the RISK pathway including postconditioning, and (3) myocardial cooling.
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