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Objective: Assessment of tissue salvage after myocardial infarction (MI) requires accurate quantification of the ischemic area at risk (AAR). Although the AAR is typically measured retrospectively within one week after reperfusion, dynamic changes in tissue composition may affect the precision of this approach. Given recent cardiac MRI data demonstrating a transient reduction in myocardial edema 24 hours after reperfused MI, we tested the hypothesis that this is an optimal timepoint for accurate retrospective AAR assessment. Methods: Swine (n=27) were subjected to a 1 hour LAD occlusion, during which the AAR was assessed by contrast enhanced CT-derived quantification of the myocardial perfusion defect. Phthalocyanine blue was administered at the end of occlusion (n=7) or during re-occlusion of the LAD 3 hours (n=5), 24 hours (n=5) or 7 days (n=10) after reperfusion for pathologic determination of the AAR. Serial echocardiography was performed in the 24 hour reperfusion group to assess end diastolic wall thickness (EDWT) as a surrogate index of post-MI edema. Results: When assessed before reperfusion, the AAR was similar by CT and postmortem pathology ( Table ). However, AAR measurements 3 hours, 24 hours, and 7 days after reperfusion overestimated CT AAR mass by 38±7 %, 31±10 %, and 37±5%, respectively. Echocardiography showed a marked increase in EDWT 1 and 3 hours after reperfusion, followed by a decrease at 24 hours that remained significantly higher than pre-ischemia values. Conclusion: Despite partial resolution of edema 24 hours after reperfusion, AAR measurement at this time does not provide an accurate assessment of the AAR obtained during the initial coronary occlusion.

We read with great interest the recent article by Fernandez-Jimenez et al,1 in which 16 ST-segment elevation myocardial infarction (STEMI) patients each underwent 5 cardiovascular magnetic resonance (CMR) scans following primary percutaneous coronary intervention. They concluded that myocardial edema detected by T2 followed a bimodal pattern, with the first phase appearing at 3 hours and dissipating by 24 hours, and the second phase reappearing thereafter. The authors should be congratulated for completing such a challenging study. However, whether the observed bimodal pattern in edema detected by T2-short tau inversion recovery in their study was actually due to the presence of intramyocardial hemorrhage (IMH) attenuating the T2-signal at 24 hours cannot be excluded. O’Regan et al2 previously reported that …

Cardiac magnetic resonance (CMR) imaging in survivors of acute ST-segment–elevation myocardial infarction (STEMI) provides accurate and precise measurements of left ventricular dimensions, and infarct pathologies are uniquely characterized. Acute coronary artery occlusion initiates a wavefront phenomenon of ischemia1 commencing from the endocardial layer and propagating radially toward the epicardium, and typically, myocardial infarction will supervene unless coronary reperfusion is achieved in a timely manner. The myocardial area at risk is the jeopardized perfusion territory of the culprit artery. See Article by Nordlund et al Ischemia results in an increase in myocardial water content manifesting as myocardial edema, and the local changes in T1 and T2 relaxation times (milliseconds) can be revealed by CMR.2 Myocardial salvage is calculated by subtracting the infarct size on contrast-enhanced CMR from the myocardial area at risk, revealed by T1- or T2-weighted CMR, and predicts the likelihood of functional recovery.2 On the contrary, edema imaging has limitations because the area at risk diminishes in size from ≈5 days post reperfusion,3,4 and T2 relaxation times within the ischemic zone vary as infarct pathologies evolve.5,6 Several CMR methods are now available for imaging myocardial edema7; the most established of which is the T2-weighted short tau inversion recovery (T2-STIR) black blood technique. This method has the advantage of being generically available across all major vendors. However, image quality may be limited when using T2-STIR CMR because of low contrast-to-noise ratio between normal and abnormal myocardium and a propensity for subendocardial bright rim …

Introduction: In acute coronary syndromes, the extent of myocardial injury can be substantially greater than the infarct zone. Existing imaging methods identify the infarct zone but do not assess “global myocardial injury” (GMI), which measures the total area of myocardium that sustained injuries including and beyond the infarct zone per se. Hypothesis: GMI can be detected based on changes in cellular membrane organization as a surrogate marker, using Tc-99m-duramycin. Methods: Balloon angioplasty was used for coronary occlusion in a pig model of myocardial ischemia and reperfusion (n = 9). Tc-99m-duramycin scans were acquired on a SPECT/CT scanner on day 1. On day 2, the infarct zone was assessed with Tc-99m-tetrofosmin. In an open-chest pig model of myocardial ischemia/reperfusion (n = 4) we used Evans Blue dye to facilitate the measurement of area-at-risk (AAR). Tc-99m-duramycin uptake was measured by gamma counting after tetrazolium (TTC) staining and physically dissecting the AAR, infarct zone and the noninfarcted-but-ischemically-damaged tissues. Histopathology was used to document cellular damages. Results: Quantitatively, Tc-99m-duramycin uptake delineated an area of myocardium that included but was substantially more extensive than the infarct zone. Under the current experimental condition, this area accounted for 81.0 ± 9.6% of the AAR, whereas the infarct zone was 25.5 ± 14.0% of the AAR. This was consistent with in vivo imaging, where the size of Tc-99m-duramycin positive tissue was visually larger than the perfusion defect in the Tc-99m-tetrofosmin scan. By histopathology, the noninfarcted-but-ischemically-damaged tissues contained features associated with cellular damages, and a heterogeneous mix of viable and dead cells. Conclusions: Tc-99m-duramycin has significant uptake in infarcted as well as noninfarcted-but-ischemically-damaged myocardium, thus reflecting global myocardial injury. The data support GMI as a new criterion independent of infarct size and AAR. The noninfarcted-but-ischemically-damaged myocardium is pathologically heterogeneous, thus a potential substrate for ventricular arrhythmias. The ability to detect such tissues may have important diagnostic and prognostic value.

We agree with Abdellaoui et al that the area at risk may explain up to 50% of infarct size, as this has been shown in experimental trials. In our randomized trial of intracoronary versus intravenous abciximab bolus administration, we did not assess the area at risk, which might be a limitation.1 However, because this was a randomized trial, differences in area at risk are extremely unlikely given that all …

The purpose of this study was to develop a clinically applicable system for quantifying premortem myocardial area at risk. Coronary artery occlusion was performed in 18 closed-chest dogs (11 left anterior descending and seven circumflex). 99mTc (15 mCi)-labeled macroaggregated albumin was then injected through an angiographic catheter into the left main coronary artery. Gated nuclear images were obtained in the left anterior oblique view in dogs with left anterior descending occlusions and in right anterior oblique views in dogs with circumflex artery occlusions. The corresponding end-diastolic images were analyzed. The percent area at risk was determined as the planimetric ratio between the hypoperfused area and that of the total left ventricular myocardium. At the completion of the study the heart was excised and the autoradiographic area at risk for the left ventricle was determined. The theoretic advantage of the use of gated acquisition for determination of area at risk over the use of nongated acquisition was assessed. For each study a time-integrated nongated image was produced by summating all frames of the gated study. The area at risk on this composite image was analyzed in the same manner as for the gated study and compared with the postmortem area at risk. Studies in five control dogs in which concomitant left atrial and intracoronary injection of different radioactive-labeled macroaggregates were used revealed no false-positive defects and similar and relatively homogenous radionuclide distribution. Postmortem autoradiographic area at risk ranged from 3.8% to 36.3% of the left ventricular mass. End-diastolic areas at risk in vivo correlated well with those determined by the postmortem autoradiographic method (r = .95, y = 0.86x + 2.7). The regression equations relating interobserver and intraobserver variance for analysis of the end-diastolic image areas at risk were small (r = .98, y = 1.06x - 0.66 and r = .96, y = 1.06x - 0.50, respectively). The interobserver and intraobserver differences for determinations of autoradiographic area at risk were represented by r = .99, y = 1.04x - 0.54 and r = .95, y = 0.88x + 2.79. Finally, comparison of the area at risk in vivo for the nongated image with the postmortem area at risk yielded a correlation of r = .79, y = 0.80x - 2.2. Nongated imaging was less sensitive and accurate than gated imaging and resulted in three false-negative studies, as well as a poorer correlation with results of postmortem autoradiography.(ABSTRACT TRUNCATED AT 400 WORDS)

Testing drugs on their efficacy in limiting infarct size is difficult in the experimental setting because of the considerable variation in the sizes of infarcts produced in control animals, mainly in dogs. This variation in infarct size in the canine model is theoretically related to variations in the size of the ischemic bed or area at risk, in pre-existing collateral blood flow, and in myocardial metabolic demand. In this study, we identified the determinants of infarct size after different periods of coronary artery occlusion in unconscious dogs and constructed a mathematical model based on these determinants using stepwise logistic regression analysis. Eighty-nine percent of the variability in infarct size is accounted for by variations in the size of the ischemic bed and coronary collateral blood flow. Using this model, we were able to predict infarct size and to make valid comparisons between treated and control groups.