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The challenge for therapies targeting perfusion abnormalities is to identify and evaluate the region of interest. The aim of this study was to compare rest and stress myocardial perfusion measured by cardiac multi-detector computed tomography (MDCT) and cardiac magnetic resonance (CMR) imaging in patients with invasive coronary angiography demonstrated occluded vessels. Twenty-four patients with refractory angina due to occluded coronary arteries underwent perfusion imaging obtained by 320-MDCT scanner and 1.5 T MR scanner. Rest and adenosine stress images were obtained and interpreted using the modified 17-segment American Heart Association model. For the qualitative analysis, each segment was graded according to the following scoring system: 0 = no defect, 1 = hypoperfusion transmural extent <1/3, 2 = 1/3-1/2, 3 = >1/2, and 4 = infarct stigmata. In the semiquantitative analysis the perfusion was either scored 0 (normal) or 1 (abnormal). The summed rest and stress scores were calculated. MDCT and CMR had a high probability to identify perfusion defects. An excellent correlation between MDCT and CMR summed rest (r = 0.916) and stress scores (r = 0.915) was found. The interobserver reproducibility was high for MDCT and CMR images. The qualitative and semiquantitative MDCT against CMR analysis of rest and stress images showed high concordance to detect perfusion defects per vascular territory and on a per myocardial segment basis. 320-MDCT and CMR perfusion imaging can be used clinically to identify myocardial perfusion defects and potentially evaluate the effect of therapy targeting perfusion abnormalities.

To evaluate the myocardial area at risk (AAR) measured by the endocardial surface area (ESA) method on late gadolinium enhancement (LGE) cardiovascular magnetic resonance (CMR) when applied after scar remodeling (3 months after index infarction) compared to T2-weighted CMR imaging. One hundred and sixty nine patients with ST-elevation myocardial infarction, treated with primary percutaneous coronary intervention, underwent one CMR within 1 week after index treatment to determine the AAR with T2-weighted imaging and a second scan 3 months after to measure AAR with the ESA method. There was a moderate correlation between the two methods (r = 0.86; P < 0.001). The AAR was significantly higher measured with T2-weighted imaging than with the ESA methods (32 ± 11% of left ventricle (LV) vs. 26 ± 10%LV; P < 0.001). The mean difference was 6 ± 6%LV. Furthermore, the mean difference between the two methods was statistical higher in the patients with myocardial salvage index ≥0.90 than in the remaining patients (9 ± 8%LV vs. 6 ± 5%LV; P = 0.02). The ESA method performed after scar remodeling (3 months following STEMI) yields significantly lower AAR's and myocardial salvage indices compared to the T2-weighted method. Therefore, T2-weighted CMR plus LGE is the method of choice to assess AAR and myocardial salvage index using CMR. However, the ESA method is an easy and valid method for determining AAR, which can be used in settings where T2-weighted imaging has not been obtained in the acute phase.