Chronic Iron Deposition following Acute Hemorrhagic Myocardial Infarction: A Cardiovascular Magnetic Resonance Study

Introduction - Intramyocardial hemorrhage frequently occurs in large reperfused myocardial infarctions (MI). However, its long-term fate remains unexplored. Hypothesis - We hypothesize that intramyocardial hemorrhage, secondary to reperfused MI, results in chronic iron deposition within infarcted territories. Methods - We studied 15 patients by Cardiovascular Magnetic Resonance (CMR) T2* mapping (1.5T) on day 3 and 6 months after successful percutaneous coronary intervention for first STEMI. Using the same CMR protocol, we also studied 20 canines, on days 3 and 56 post ischemia-reperfusion injury, of which 3 animals received sham procedures. Subsequently, canine hearts were explanted, imaged ex-vivo, and samples of hemorrhagic infarcts (Hemo+), non-hemorrhagic infarcts (Hemo-), remote and sham myocardium were isolated, sectioned and mass spectrometry was performed. Results - Eleven patients had Hemo+ (verified by T2* CMR on day 3) and their scar tissue T2* values remained significantly lower after 6 months, when compared to Hemo- and remote myocardium (Fig 1; p<0.001). In canines, Hemo+ territories showed a significant T2* reduction compared to the other groups (Fig 2; p<0.001). Mean iron content ([Fe]) of Hemo+ on day 56 was 10-fold greater than that observed in control groups (p<0.001), while no differences were observed among the control groups (p=0.14). A strong linear relationship was observed between log(T2*) and -log([Fe]) (R2 = 0.74; p