Chronic MIs in STEMI and NSTEMI patients can be reliably characterized using threshold-based detection on native T1 maps at 3-T. Visual detection of chronic MIs on native T1 maps in both patient populations has high specificity, but modest sensitivity.

Background LGE CMR is a powerful method for characterizing MI, but the requisite gadolinium infusion is estimated to be contraindicated in nearly 20% of MI patients due to end-stage chronic kidney disease. The purpose of this study is to investigate whether T1 Cardiovascular-Magnetic-Resonance Imaging (CMR) obtained without contrast agents at 3T could be an alternative to Late-Gadolinium-Enhanced (LGE) CMR for characterizing chronic myocardial infarctions (MIs) using a canine model of MI. Methods and Results Canines (n=29) underwent CMR at 7 days (acute, AMI) and 4 months (chronic, CMI) post-MI. Infarct location, size and transmurality measured using native T1 maps and LGE images at 1.5T and 3T were compared. Resolution of edema between AMI and CMI was examined with T2 maps. T1 maps overestimated infarct size and transmurality relative to LGE images in AMI (p=0.016 and p=0.007, respectively), which was not observed in CMI (p=0.49 and p=0.81, respectively), at 3T. T1 maps underestimated infarct size and transmurality relative to LGE images in AMI and CMI (p<0.001), at 1.5T. Relative to the remote territories, T1 of the infarcted myocardium was increased in CMI and AMI (p<0.05); and T2 of the infarcted myocardium was increased in AMI (p<0.001), but not in CMI (p >0.20) at both field strengths. Histology showed extensive replacement fibrosis within the CMI territories. CMI detection sensitivity and specificity of T1 CMR at 3T were 95% and 97%, respectively. Conclusions Native T1 maps at 3T can determine the location, size and transmurality of CMI with high diagnostic accuracy. Patient studies are necessary for clinical translation.

Free-breathing T2-prepared myocardial BOLD MR imaging showed that hypercapnia of 10 mm Hg may provide a cardiac hyperemic stimulus similar to adenosine.

Background Emerging evidence indicates that persistent microvascular obstruction (PMO) is more predictive of major adverse cardiovascular events than myocardial infarct (MI) size. But, it remains unclear how PMO, a phenomenon limited to the acute/sub-acute period of MI, drives adverse remodeling in chronic MI setting. We hypothesized that PMO resolves into chronic iron crystals within MI territories, which in turn are proinflammatory and favor adverse remodeling post-MI. Methods and Results Canines (n=40) were studied with cardiac MRI to characterize the spatiotemporal relationships among PMO, iron deposition, infarct resorption, and LV remodeling between day 7 (acute) and week 8 (chronic) post-MI. Histology was used to assess iron deposition, and to examine relationships between iron content with macrophage infiltration, pro-inflammatory cytokine synthesis, and matrix metalloproteinase activation. Atomic-resolution TEM was used to determine iron crystallinity and energy-dispersive X-ray spectroscopy was used to identify the chemical composition of the iron composite. PMO with or without reperfusion hemorrhage led to chronic iron deposition and the extent of this deposition was strongly related to PMO volume (r>0.8). Iron deposits were found within macrophages as aggregates of nanocrystals (~2.5 nm diameter) in the ferric state. Extent of iron deposits was strongly correlated with proinflammatory burden, collagen degrading enzyme activity, infarct resorption, and adverse structural remodeling (r>0.5). Conclusions Crystalized iron deposition from PMO is directly related to proinflammatory burden, infarct resorption, and adverse LV remodeling in the chronic phase of MI in canines. Therapeutic strategies to combat adverse remodeling could potentially benefit from taking into account the chronic iron-driven inflammatory process.