Effect of Intravenous TRO40303 as an Adjunct to Primary Percutaneous Coronary Intervention for Acute ST-Elevation Myocardial Infarction: MITOCARE Study Results

Study Questions:

What is the efficacy and safety of TRO40303 for the reduction of reperfusion injury in patients undergoing revascularization for ST-segment elevation myocardial infarction (STEMI)?


Patients in the MITOCARE study presenting with STEMI within 6 hours of the onset of pain randomly received TRO40303 (n = 83) or placebo (n = 80) via intravenous bolus injection prior to balloon inflation during primary percutaneous coronary intervention in a double-blind manner. The primary endpoint was infarct size expressed as area under the curve (AUC) for creatine kinase (CK) and for troponin I (TnI) over 3 days. Secondary endpoints included measures of infarct size using cardiac magnetic resonance (CMR) and safety outcomes.


The median pain-to-balloon time was 180 minutes for both groups, and the median (mean) door-to-balloon time was 60 (38) minutes for all sites. Infarct size, as measured by CK and TnI AUCs at 3 days, was not significantly different between treatment groups. There were no significant differences in the CMR-assessed myocardial salvage index (1-infarct size/myocardium at risk) (mean 52 vs. 58% with placebo, p = 0.1000), mean CMR-assessed infarct size (21.9 g vs. 20.0 g, or 17 vs. 15% of left ventricular [LV] mass) or LV ejection fraction (LVEF) (46 vs. 48%), or in the mean 30-day echocardiographic LVEF (51.5 vs. 52.2%) between TRO40303 and placebo. A greater number of adjudicated safety events occurred in the TRO40303 group for unexplained reasons.


The authors concluded that in STEMI patients treated with contemporary mechanical revascularization principles, there was no effect of TRO40303 in limiting reperfusion injury of the ischemic myocardium.


The MITOCARE study of TRO40303 failed to show reductions in infarct size, as measured by the co-primary endpoints of reduction in AUC(0–72) for the cardiac biomarkers CK and TnI. Analysis of secondary endpoints, as measured by CMR and echocardiography, confirmed that there were no significant differences between TRO40303 and placebo in reducing reperfusion injury. This implies that treatment of STEMI patients with immediate mechanical revascularization and contemporary supportive pharmacotherapy does not support the role for TRO40303 to limit reperfusion injury of the infarcted myocardium. Additional research is indicated to provide further insight into the nature of reperfusion injury and potential mechanisms to mitigate it.

Clinical Topics: Invasive Cardiovascular Angiography and Intervention, Noninvasive Imaging, Vascular Medicine, Interventions and Imaging, Interventions and Vascular Medicine, Echocardiography/Ultrasound

Keywords: Myocardial Infarction, Reperfusion Injury, Oximes, Creatine Kinase, Troponin I, Myocardium, Magnetic Resonance Spectroscopy, Myocardial Reperfusion, Echocardiography, Percutaneous Coronary Intervention, ESC Congress

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