@article{eprints1509,
            note = {Published online before print February 12, 2013},
          author = {Avinash Kali and Andreas Kumar and Ivan Cokic and Richard Tang and Sotirios A. Tsaftaris and Matthias G Friedrich and Rohan Dharmakumar},
           title = {Chronic Manifestation of Post-Reperfusion Intramyocardial Hemorrhage as Regional Iron Deposition: A Cardiovascular MR Study with Ex-vivo Validation},
       publisher = {American Heart Association},
         journal = {Circulation: Cardiovascular Imaging},
            year = {2013},
           month = {February},
             url = {http://eprints.imtlucca.it/1509/},
        abstract = {Background{--}Intramyocardial hemorrhage frequently accompanies large reperfused myocardial infarctions. However, its influence on the make-up and the ensuing effect on the infarcted tissue during the chronic phase remain unexplored.

Methods and Results{--}Patients (n = 15; 3 women), recruited after successful PCI for first ST-elevation myocardial infarction, underwent Cardiovascular Magnetic Resonance (CMR) imaging on day 3 and month 6 post-PCI. Patients with hemorrhagic (Hemo+) infarctions, as determined by T2* CMR on day 3 (n = 11), showed persistent T2* losses co-localized with scar tissue on the follow-up scans, suggesting chronic iron deposition. T2* values of Hemo+ territories were significantly higher than non-hemorrhagic (Hemo-) and remote territories (p{\ensuremath{<}}0.001); however, T2* values of non-hemorrhagic (Hemo-) and remote territories were not different (p=0.51. Canines (n = 20), subjected to ischemia-reperfusion (I/R) injury (n = 14), underwent CMR on days 3 and 56 post I/R injury. Similarly, sham-operated animals (Shams; n = 3) were imaged using CMR at similar time points. Subsequently, hearts were explanted, imaged ex-vivo, and samples of Hemo+, Hemo-, remote and Sham myocardium were isolated and stained. The extent of iron deposition ([Fe]) within each sample was measured using mass spectrometry. Hemo+ infarcts showed significant T2* losses compared to the other (control) groups (p{\ensuremath{<}}0.001), and Perl's stain confirmed localized iron deposition. Mean [Fe] of Hemo+ was nearly an order of magnitude greater than the control groups (p{\ensuremath{<}}0.001), but no significant differences were observed among the control groups. A strong linear relationship was observed between log(T2*) and -log([Fe]) (R2=0.7; p{\ensuremath{<}}0.001). The monoclonal antibody Mac387 stains, along with Perl's stains, showed preferential localization of newly recruited macrophages at the site of chronic iron deposition.

Conclusions{--}Hemorrhagic myocardial infarction can lead to iron depositions within the infarct zones, which can be a source of prolonged inflammatory burden in chronic phase of myocardial infarction. },
        keywords = {acute myocardial infarction; cardiac magnetic resonance imaging; hemorrhage; inflammation}
}