Contrast-enhanced cardiac MRI is superior to non-contrast mapping to predict left ventricular remodeling at 6 months after acute myocardial infarction

Figures

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  Fig. 1. Cardiac T2-weighted CMR image (a), LGE image (b), ECV, native T2 and T1 maps (c). For quantitative analysis of lesion size, a large region of interest (ROI) was placed in remote myocardium to quantify mean signal intensity or mean relaxation times, including standard deviations as shown in a and b. The threshold was set at >2 SDs to define lesion size in the infarct area. Care was taken not to include the blood volume or the epicardial fat in the measurements by precise placement of the endo- and epicardial myocardial borders, as shown in the colored T2-weighted and LGE images. ECV, extracellular volume; LGE, late gadolinium enhancement; SD, standard deviation

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  Fig. 2. Comparisons of mapping and standard CMR parameters at baseline between patients with and without adverse LV remodeling. Mapping CMR at baseline (left column) shows patients who developed adverse LV remodeling at 6 months had significantly higher ECVinfarct and native T2infarct but similar native T1infarct. Standard CMR at baseline (right column) shows patients who developed adverse LV remodeling had larger edema size and infarct size than those without remodeling. ECV, extracellular volume; LV, left ventricular

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  Fig. 3. Changes of LV mass index (a), edema size (b), and infarct size (c) in patients with and without adverse LV remodeling at 6 months following AMI. AMI, acute myocardial infarct; LV, left ventricular

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  Fig. 4. Receiver-operating characteristic curve analysis for the prediction of adverse LV remodeling at 6 months following AMI with mapping (a) and standard CMR (b). ECVinfarct and infarct size by LGE were the best predictors of adverse LV remodeling with AUCs of 0.843 (p < 0.01) and 0.789 (p < 0.01), respectively. Native T1infarct had the lowest AUC of 0.549 (p = 0.668) and was inferior to edema size by T2-weighted (AUC = 0.720; p < 0.05) and native T2infarct (AUC = 0.766; p < 0.01) in predicting adverse LV remodeling. AMI, acute myocardial infarct; AUC, area under the curve; ECV, extracellular volume; LV, left ventricular

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  Fig. 5. Correlation of ECVinfarct and infarct size at baseline with change in LVEDVi at 6 months following AMI. △LVEDVi is calculated by dividing the change in LVEDVi by initial LVEDVi. A positive correlation was found between ECVinfarct (a) and infarct size (b) at baseline and △LVEDVi. Variables above the horizontal dashed line indicate the increase in LVEDVi; conversely, below the horizontal dashed line indicates the decrease in LVEDVi at 6 months after AMI. Triangles represent these patients developed adverse LV remodeling, who had an obvious tendency in higher ECVinfarct and larger infarct size as well as significant increase in LVEDVi. AMI, acute myocardial infarct; ECV, extracellular volume; LVEDVi, left ventricular end-diastolic volume index