A novel approach for treating myocardial infarction Every year, millions of cardiac reperfusion procedures are performed worldwide for treatment of heart tissue death or myocardial infarction (MI). The serious side-effects of this procedure have prompted scientists to look for alternative approaches that provide cardiac recovery while reducing the infarct size. Health © Julien Veys Current treatment for MI involves the restoration of blood flow in the heart muscle — a process known as reperfusion — through thrombolysis or percutaneous coronary intervention (PCI). However, myocardial reperfusion itself can paradoxically induce damage or death to cardiomyocytes, hampering the clinical benefits. As a result, the EU-funded MITOCARE project wishes to develop a complementary therapy that would prevent or limit myocardial reperfusion injury. Also, it aims to understand the pathophysiology of ischaemia-reperfusion injury (IRI) and which factors influence patient recovery or response to treatment. More details can be found on the project website. Evidence indicates that mitochondrial permeability transition pore (mPTP) opening is responsible for IRI, suggesting that it could be used as a therapeutic target. For this purpose, the MITOCARE consortium is performing a medium-scale clinical study to test TRO40303 as a new modulator of the mPTP. Alongside patient response to treatment with TRO40303, researchers are monitoring various other parameters such as confounding factors that may influence treatment outcome and biomarkers. On an experimental basis, MITOCARE partners are comparing the use of TRO40303 in rodent, rabbit and pig models of ischaemia/reperfusion with the positive effects of hypothermia to reduce mPTP opening. The strong protection of hypothermia initiated before ischemia and the specific protection afforded by TRO40303 on reperfusion injury were both confirmed. When completed, the MITOCARE study will provide solid evidence regarding the validity of a novel therapeutic approach against IRI. Also, the clinical benefit of a new mitochondrial-targeted compound will be demonstrated, thereby reducing the need for future regenerative therapies.
