Myocardial contrast two-dimensional echocardiography(MC-2DE) has been known to have the real time capabilities for repeat in vivo assessment of ischemic risk areas and for evaluation of the myocardial perfusion. The aims of this investigation are (1) to evaluate the feasibility of MC-2DE for the delineation and quantitation of the area at risk. (2) to determine the relationship between the extent of the echocontrast defect area(EDA) during reperfusion and the size of myocardial infarction as determined by post-mortem tissue examination, and (3) to observe serial changes in the time echo-intensity characteristics of MC-2DE during coronary occlusion and reperfusion.

Myocardial contrast echocardiographic images were made by injecting bolus 5mL of two-syringe-agitated mixture of sodium meglumine ioxaglate(Hexabrix®) and normal saline(2 : 3 by volume) into the aortic root before and during coronary occlusion of the left anterior descending coronary artery, distal to the first diagonal branch and during reperfusion on eight open-chest dogs. Two-dimensional echocardiographic short axis views were obtained at four anatomic levels : the apex, the low papillary muscle, the high papillary muscle and the mitral valve. The changes in EDA and echo-intensity with its wash-out half time(WHT) at the high papillary muscle level during coronary occlusion and reperfusion were measured every 15 minutes. The total EDA was measured by planimetry at 3 minutes after coronary occlusion and at 60 minutes after reperfusion. Evans blue or methylene blue were used for the measurement of the anatomic area at risk and triphenyl-tetrazolium chloride(TTC) for the measurement of the infarct area.

The EDA measured 30 minutes after coronary occlusion(19.6%) was smaller than that at 3 minutes after coronary occlusion(24.0%, p<0.01). Then EDA at 3 minutes occlusion was strongly predictive of the anatomic extent of area at risk(EDA=0.48 Area at risk+16.95, r=0.84, p<0.05). The EDA at 60 minutes after reperfusion, which showed an irregular margin and was located within the subendocardium of the area at risk, also correlated well with the infarct area(IA)(EDA=0.78 IA+3.32, r=0.82, p=0.09). The peak echo-intensity in the ischemic area during coronary occlusion was significantly low(14.2±6.5 vs 73.8±31.7 in the non-ischemic area, p<0.01) and the WHT was delayed more in the ischemic area than in the non-ischemic area(23.2±2.8 sec vs 8.1±3.3sec, p<0.01). During the period of reperfusion, WHT in the previously ischemic area was markedly delayed compared to that in the non-ischemic area (p<0.01), although the peak echo-intensity in the ischemic area at 3 minutes after reperfusion increased modestly compared to that in the non-ischemic area(80.9±22.8 vs 72.7±8.4), suggesting the impairment in the transit of microbubbles is probably due to microvascular damage after reperfusion. There were no adverse hemodynamic or electrocardiographic effects after injection of the contrast agent.

These findings suggest that myocardial contrast echocardiography was useful as a non-invasive technique, first, to delineate the area at risk in vivo during coronary occlusion and, after reperfusion, the infarct area, and secondly, to evaluate indirectly the state of myocardial perfusion during coronary occlusion and reperfusion.