Myocardial Edema on T2-Weighted MRI

Abstract

Although the advances in revascularization therapy have drastically decreased the mortality after ST-segment-elevation myo-cardial infarction (STEMI), the number of patients who develop heart failure after the reperfusion therapy continues to increase. More than 30% of the patients who survive STEMI develop heart failure long-term. 1 Clinical studies have demonstrated that the larger infarct size (IS) and the resultant left ventricular dysfunc-tion at the time of initial treatment significantly correlate with the likelihood of future adverse ventricular remodeling and ar-rhythmia. 2 Thus, the efforts to minimize the IS by prompt reper-fusion therapy is the primary rational in the treatment of STEMI in preventing heart failure and catastrophic cardiovascular events. Myocardial salvage determined by the initial perfusion defect, that is, myocardium at risk (MaR) and the final IS, is a surro-gate marker of a successful reperfusion therapy to predict clinical outcome. 3 Despite significant technological advances in the reperfusion therapy, myocardial reperfusion injury substantially decreases the myocardial salvage and increases the final tissue injury, which may account for ≤50% of the final IS. 4 Even though various pre-or post-conditioning strategies, including stress (re-versible ischemia, exercise, and hypothermia) and pharmaceutical intervention, may help to protect the heart from the ischemia/ reperfusion (I/R) injury, the efficacy of these treatments has not been sufficiently demonstrated in clinical studies. Thus, a robust imaging modality to assess the I/R injury and predict future car-diovascular events addresses a critical unmet clinical need. Article, see p 439 In ischemic heart disease, myocardial edema detected by magnetic resonance imaging (MRI) as high signal intensity on T2-weighted imaging (T2-WI) is a phenomenon associated with reperfusion. It is known that a permanent occlusion of the coronary artery leads to minimal myocardial edema. 5 The restoration of coronary blood flow increases the swelling of individual car-diomyocytes and exacerbates the interstitial edema secondary to reactive hyperemia and leakage from damaged capillaries. 5 At revascularization, the cellular debris from the ruptured athero-sclerotic culprit lesion(s) and the released soluble vasoconstric-tive, thrombogenic, and inflammatory substrates contribute to microvascular flow impairment. 4 In addition, the myocardial I/R impairs microcirculation directly as demonstrated in the experimental occlusion and reperfusion of nonatherosclerotic coronary arteries in the preclinical animal models. 2 These studies demonstrated that the swelling of the endothelial cells, obstruction of the capillary bed by platelet aggregation, and compression of the vasculature by interstitial edema result in microvascular obstruction (MVO) or no-reflow phenomenon. 2 Furthermore, advanced capillary destruction leads to intramyocardial hemorrhage (IMH). At the end of this complex post-injury physiology, MVO and IMH emerge in an anatomically dependent location. Using late gadolinium enhancement and T2-WI MRI, these lesions are delineated reliably as contrast void and low signal intensity, respectively, with excellent histological correlation. 6 Most importantly, these I/R injury-associated MRI findings predict the major adverse cardiac events (MACE). 7 Although the current standard methods to detect and evaluate the severity of the I/R injury include electrocardiographic evidence of persistent ST-segment elevation, angiographic finding of no-reflow or poor TIMI (thrombolysis in myocardial in-farction) blush grade, and poor myocardial salvage on SPECT (single-photon emission computed tomography), the integrative ability of cardiac MRI has also been recognized. This imaging technique combines T1-WI to identify the myocardial edema to delineate the MaR and late gadolinium enhancement to assess the IS, MVO, and IMH. Myocardial edema appearing in the early stages of the reperfused STEMI corresponds well with the histo-logical IS in an animal model. 8 Myocardial salvage index evaluated by cardiac MRI is reported to be a useful predictor of MACE. 9 However, careful attention must be paid in evaluating the MaR and IS by cardiac MRI because they undergo dynamic changes, especially, during the first week of myocardial infarc-tion. The extent of myocardial edema affected by the several clinical or pathological factors, including ischemic duration, concomitant diseases, and reperfusion injury, may confound the evaluation of MaR. In a clinical study, MaR by T2-WI obtained at 5 to 7 days post-intervention corresponded well with the initial perfusion defect on SPECT. However, in an individual case-by-case review, T2-WI showed a significantly different size of MaR compared with SPECT depending on the occlusion time and presence of spontaneous reperfusion. 10 Thus, the measurement of myocardial edema on T2-WI may evaluate the extent of I/R injury more reliably and provide a more accurate prediction of MACE in this highly vulnerable patient population.