In order to bring you the best possible user experience, this site uses Javascript. If you are seeing this message, it is likely that the Javascript option in your browser is disabled. For optimal viewing of this site, please ensure that Javascript is enabled for your browser.
Did you know that your browser is out of date? To get the best experience using our website we recommend that you upgrade to a newer version. Learn more.

We use cookies to optimise the design of this website and make continuous improvement. By continuing your visit, you consent to the use of cookies. Learn more

Effect of intravenous TRO40303 as an adjunct to primary percutaneous coronary intervention for acute ST-elevation myocardial infarction: Results of the MITOCARE study

ESC Congress 2014 - Hot Line report

Acute Coronary Syndromes (ACS)



By Dan Atar, FESC (Oslo, Norway)
View Discussant report

Read the press release
Open the Presentation
Watch the Webcast
Resources are published as they become available during the congress

List of Authors:
D. Atar(1), H. Arheden (2), P. Clemmensen (3), N. Danchin (4), D. Erlinge (5), H. Firat (6), S. Halvorsen (1), W. Hauke (7), E. Vicaut (8), S. Eggert Jensen (9)

(1) Oslo University Hospital, Dept of Cardiology B, Oslo, Norway;
(2) Skane University Hospital, Dept. of Clinical Physiology, Lund, Sweden;
(3) Rigshospitalet, Copenhagen University Hospital, Dept. of Cardiology, Copenhagen, Denmark
(4) European Hospital Georges Pompidou, Dept. of Cardiology, Paris, France
(5) Skane University Hospital, Dept. of Cardiology, Lund, Sweden
(6) FIRALIS SAS, Huningue, France
(7) Trophos SA, Luminy Biotech Enterprises, Marseille, France
(8) Hospital Lariboisiere, Clinical Research Unit, Paris, France
(9) Aalborg University Hospital, Dept. of Cardiology, Aalborg, Denmark


The MITOCARE study evaluated the efficacy and safety of TRO40303 for the reduction of reperfusion injury in patients undergoing revascularization for ST-elevation myocardial infarction (STEMI).
Patients presenting with STEMI within 6 hours of onset of pain randomly received TRO40303 (n=83) or placebo (n=80) via intravenous bolus injection prior to balloon inflation during primary PCI 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 three days. Secondary endpoints included measures of infarct size using cardiac magnetic resonance (CMR) and safety outcomes.
Median pain-to-balloon time was 180 minutes for both groups, and 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 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 LV-mass) or left ventricular 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.
This study in STEMI patients treated with contemporary mechanical revascularization principles did not show any effect of TRO40303 in limiting reperfusion injury of the ischemic myocardium


By Hans Erik Botker, FESC (Aarhus N, Denmark)
See Presenter abstract
Open the presentation
Watch the Webcast





Hot Line: Myocardial Infarction

The content of this article reflects the personal opinion of the author/s and is not necessarily the official position of the European Society of Cardiology.