Is functional improvement after myocardial infarction predicted with myocardial enhancement patterns at multidetector CT?

Purpose: To prospectively evaluate the sensitivity of myocardial early perfusion defects (EDs) and late enhancement (LE) at multidetector computed tomography (CT) following acute myocardial infarction (AMI) to predict segment myocardial dysfunction and myocardial functional recovery (MFR), by using echocardiography as the reference standard. Materials and Methods: Institutional review board approval and informed consent were obtained. Twenty-six patients (25 men, one woman; mean age, 53 years ± 9 [standard deviation]), underwent baseline multidetector CT, coronary angiography, and echocardiography within a week of AMI and a follow-up echocardiography at 3 months. ED, LE, and late hypoattenuation were compared with regional left ventricular function and MFR. A logistic regression model and generalized estimating equation analysis were applied to estimate the predictive effect of ED and LE. Differences between groups were evaluated by using nonpaired Student t tests. Results: All EDs and LE corresponded with AMI location determined by using angiography and echocardiography. For occluded arteries (n = 5), no relationship was found between the presence of ED or LE and MFR. For patent arteries (n = 21), presence of LE had a respective sensitivity and specificity of 73% and 85% for predicting follow-up segment dysfunction, compared with 57% and 90% for ED. In abnormal baseline segments, nonrecovery was clearly related to the presence and size of segment defect area for both ED (odds ratio: 1.95 [95% confidence interval: 0.9, 4.1] per square centimeter) and LE (odds ratio: 1.85 [95% confidence interval: 1.2, 2.9] per square centimeter). Segments that recovered had significantly lower prevalence of ED and LE, and if present, were significantly smaller than in segments remaining abnormal (P <.05). Conclusion: The presence and size of ED and LE at multidetector CT is closely related to follow-up segment myocardial dysfunction and MFR.