Characterizing the Inflammatory Tissue Response to Acute Myocardial Infarction by Clinical Multimodality Noninvasive Imaging

OBJECTIVES: Myocardial infarction (MI) triggers a systemic inflammatory response which determines subsequent healing. Experimentally, cardiac positron (PET) and magnetic resonance(CMR) imaging has been used successfully to obtain mechanistic insights. We explored the translational potential in patients early after MI.

METHODS: PET/CT and CMR were performed in 15 patients <7 days after first MI. CMR showed regional transmural late gadolinium enhancement (LE) and edema exceeding the area of LE.

RESULTS: Using F-18 deoxyglucose with heparin pretreatment, metabolic rate of glucose (MRGlc) was significantly increased in infarct vs remote myocardium (median 2.0 vs 0.4mg/min/100ml;P=0.0001). Infarct correlated with MRGlc in remote myocardium (ρ=0.64;P=0.01), spleen(ρ=0.82;P=0.0002) and bone marrow(ρ=0.57;P=0.03), but not with muscle or liver. Regionally, FDG-score was highest in segments with LE vs edema only and remote (median 2.0 vs 1.8 vs 0.4;P<0.0001). Patients requiring repeat intervention during preliminary follow-up of 11±5 months tended to have higher early post-MI MRGlc. Five patients with chronic, stable MI served as controls. Opposite to acute MI, MRGlc was lower in infarct (median infarct/remote ratio 0.6 vs 3.2 for acute MI; P=0.001), and there was no correlation with bone marrow or spleen MRGlc.

CONCLUSIONS: Increased glucose utilization following heparin-induced suppression of myocyte uptake appears to mostly reflect inflammatory activity in damaged myocardium early after MI. Consistent with prior preclinical observations, and in contrast to chronic MI, this is associated with activity in spleen and bone marrow as sources of inflammatory cells. PET and CMR multimodality characterization of the acutely infarcted, inflamed myocardium may provide multi-parametric endpoints for clinical studies aiming at support of infarct healing. Ahkello Witherspoon Jersey

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