Prediction of myocardial viability by MRI.

In this regard, the temporal pattern of myocardial contrast enhancement on MRI is reported in this issue of Circulation to be a predictive index of potential myocardial viability for reperfused myocardial infarctions.1 With fast MRI, the firstpass distribution of MRI contrast media indicated that despite patency of the target coronary artery with TIMI 3 flow in all patients, reperfusion at the tissue level was impeded in more than half of the injured regions. This sign of impeded perfusion (“no-reflow” phenomenon) was predictive of poorer contractile recovery 7 weeks after the acute event. These results are similar to earlier reports, such as that of Ito et al,2 that used myocardial contrast echocardiography to assess myocardial reperfusion after patency of acutely occluded epicardial coronary arteries was established. Recovery of regional and global LV function was worse in the group of patients with residual contrast defects. MRI and echocardiographic estimates of tissue perfusion after coronary recanalization seem to reflect the severity of microvascular disruption, occlusion, or extravascular compression by edema or hemorrhage. Thus, the depicted perfusion pattern serves as a surrogate of the severity of myocardial injury rather than a direct indicator of myocardial cellular viability. A number of other promising MRI techniques for predicting myocardial viability of potentially salvageable myocardium in a region of acute ischemic injury have been proposed. These MRI approaches can be conveniently divided into 3 categories: assessment of tissue perfusion after recanalization, evaluation of myocardial contractile reserve, and characterization of myocardial cellular membrane function. The report by Rogers et al1 exemplifies the first approach. It examined the myocardial contract enhancement pattern on both first-pass and pseudoequilibrium-phase (delayed) MRI images and identified that hypoenhancement on first-pass imaging was an indictor of poorer recovery of function 7 weeks after the acute event. A prior report by Wu et al3 suggested that contrast-enhanced MRI could estimate the extent of microvascular obstruction after acute coronary occlusion in 44 patients using pseudoequilibrium-phase (1 to 2 minutes after injection) images. MRI performed 1066 days after infarction demonstrated hypoenhanced areas within the infarct zone in 11 patients who were therefore considered to have microvascular obstruction in the core of the infarction. Hyperenhancement was observed in the periphery of the infarction in these 11 patients, whereas hyperenhancement of the entire infarction was present in the remaining patients. The group with hypoenhanced regions, which was presumed to represent microvascular obstruction, had significantly more future cardiovascular event and more severe LV remodeling. Saeed et al4 also demonstrated in an animal model of reperfused myocardial infarction that reperfusion at the tissue level is characterized on inversion recovery echo-planar imaging as enhancement to a level approaching that of normal myocardium 20 seconds after injection, followed by progressive further enhancement, whereas the signal intensity of normal myocardium declines. This study, using methodology with high temporal resolution, actually demonstrated that the first-pass enhancement kinetics of even adequately reperfused myocardium is not identical to normal myocardium, but rather there is decreased upslope and delay in the early peak of enhancement of the infarcted compared with normal myocardium. It seems clear from a number of studies that lack of enhancement of the core of acute infarctions after recanalization either on first-pass or pseudoequilibrium MRI acquisitions is predictive of more severe injury, less recovery of regional function, and poorer outcome. The second MRI approach for predicting myocardial viability simulates techniques used with echocardiography by demonstrating residual contractile response to inotropic drugs in an ischemically injured or chronically ischemic region. This MRI approach to predicting viability not only assesses contractile response but also incorporates the precise measurement of wall thickness afforded by MRI as an additional parameter. MRI-defined diastolic wall thickness $5.5 mm and dobutamine-induced systolic wall thickening $2 mm were shown to be predictive of contractile recovery after myocardial revascularization.5,6 Quantitative assessment of dobutamine-induced systolic wall thickening on cine MRI was shown to be a reliable indicator of improvement of regional LV function and ejection function after revascularization.5 With the use of F-fluorodeoxyglucose PET as the determinant of residual viability, dobutamine transesophageal echocardiography (TEE) and dobutamine cine MRI were compared in 43 patients with prior myocardial infarction.6 Sensitivity and specificity of dobutamine TEE and cine MRI for PET-defined viability were 77% versus 81% and 94% versus 100%, respectively. A potential advantage of the MRI The opinions expressed in this editorial are not necessarily those of the editors or of the American Heart Association. Correspondence to Charles B. Higgins, MD, Professor and Vice Chairman of Radiology, Department of Radiology, Box 0628, 505 Parnassus Ave, Suite L308, San Francisco, CA 94143-0618. E-mail [email protected] (Circulation. 1999;99:727-729.) © 1999 American Heart Association, Inc.