Hemorrhagic myocardial infarctions demonstrated persistent T2* losses at 6 months compared to nonhemorrhagic territories (P<0.001), indicating chronic iron deposition.
Observational (n=15)
Does hemorrhagic myocardial infarction lead to chronic iron deposition and prolonged inflammatory burden?
Hemorrhagic myocardial infarction leads to chronic iron deposition within the infarct zone, which is associated with persistent macrophage recruitment and prolonged inflammatory burden.
p-value: p=<0.001
BACKGROUND: Intramyocardial hemorrhage frequently accompanies large reperfused myocardial infarctions. However, its influence on the makeup 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 percutaneous coronary intervention for first segment-elevation myocardial infarction, underwent cardiovascular magnetic resonance imaging on day 3 and month 6 after percutaneous coronary intervention. Patients with hemorrhagic (Hemo+) infarctions, as determined by T2* cardiovascular magnetic resonance on day 3 (n=11), showed persistent T2* losses colocalized with scar tissue on the follow-up scans, suggesting chronic iron deposition. T2* values of Hemo+ territories were significantly higher than nonhemorrhagic (Hemo-) and remote territories (P<0.001); however, T2* values of nonhemorrhagic (Hemo-) and remote territories were not different (P=0.51). Canines (n=20) subjected to ischemia-reperfusion injury (n=14) underwent cardiovascular magnetic resonance on days 3 and 56 after ischemia-reperfusion injury. Similarly, sham-operated animals (Shams; n=3) were imaged using cardiovascular magnetic resonance at similar time points. Subsequently, hearts were explanted and 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 with the other (control) groups (P<0.001), and Perls stain confirmed localized iron deposition. Mean Fe of Hemo+ was nearly an order of magnitude greater than that of the control groups (P<0.001), but no significant differences were observed among the control groups. A strong linear relationship was observed between log(T2*) and -log(Fe); R(2)=0.7 and P<0.001. The monoclonal antibody Mac387 stains, along with Perls 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 the chronic phase of myocardial infarction.
Kali et al. (Wed,) conducted a observational in segment-elevation myocardial infarction (n=15). Hemorrhagic myocardial infarction vs. Nonhemorrhagic myocardial infarction was evaluated on T2* values on cardiovascular magnetic resonance (p=<0.001). Hemorrhagic myocardial infarctions demonstrated persistent T2* losses at 6 months compared to nonhemorrhagic territories (P<0.001), indicating chronic iron deposition.
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