CHARACTERIZATION OF SPATIAL PATTERNS OF FLOW WITHIN THE REPERFUSED MYOCARDIUM BY MYOCARDIAL CONTRAST ECHOCARDIOGRAPHY - IMPLICATIONS IN DETERMINING EXTENT OF MYOCARDIAL SALVAGE

Background. Since myocardial blood flow changes dynamically after repe rfusion and since both hyperemia and impairment in microvascular funct ion exist within the acutely reperfused bed, we sought to investigate the role of myocardial contrast echocardiography (MCE) in (1) defining the temporal variability in perfusion patterns after reflow and relat ing these to microsphere-derived blood flow; (2) differentiating viabl e from infarcted tissue during different periods of reflow; and (3) di fining spatial perfusion patterns within the infarct bed in response t o exogenously induced maximal vasodilation and relating these to infar ct size and extent of myocardial salvage. Methods and Results. Twenty- one dogs with 3 hours of left anterior descending coronary artery occl usion and 2 to 3 hours of reflow were studied. MCE was performed at 15 and 45 minutes and 2 and 3 hours after reflow. It was also performed at either 2 or 3 hours after reflow in the presence of 0.56 mg/kg of d ipyridamole. Radiolabeled microsphere-derived blood flow was measured at 15 minutes and 2 and 3 hours after reflow and during dipyridamole e ffect Infarct size was measured at the end of the experiment by use of triphenyl tetrazolium chloride. MCE data were processed with color-co ding schemes that highlighted differences in myocardial videointensiti es in proportion to the concentration of microbubbles within the micro vasculature. There was significant variability in MCE-defined perfusio n patterns after reflow, with contrast defects noted mainly within the endocardium. There was fair and significant (P<.05) correlation (r=-. 73 to r=-55) between MCE defect size and normalized endocardial blood flow. Except at 15 minutes after reflow, there was poor correlation (r =.31 to r=.51) between MCE defect and infarct sizes. Even at 15 minute s after reflow, MCE defect size underestimated infarct size by 50%. In comparison, in the presence of dipyridamole, MCE defect size correlat ed strongly (r=.87, P<.001) with infarct size and reasonably well with normalized transmural blood flow (r=-.62, P=.04). Moreover, the topog raphy of the MCE perfusion defect reflected the topography of the infa rct. Conclusions. MCE revealed striking temporal heterogeneity in the spatial distribution of myocardial perfusion during postischemia reflo w and either significantly underestimated or did not correlate with in farct size during reperfusion. Because of abnormalities in coronary va scular reserve specific to infarcted tissue, MCE in conjunction with i ntravenous dipyridamole depicted, in vivo, the actual topography of th e infarct with remarkable accuracy.