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Circulation, Vol 88, 2596-2606, Copyright © 1993 by American Heart Association
FS Villanueva, WP Glasheen, J Sklenar and S Kaul
BACKGROUND. Since myocardial blood flow changes dynamically after
reperfusion and since both hyperemia and impairment in microvascular
function 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 relating these
to microsphere-derived blood flow; (2) differentiating viable from
infarcted tissue during different periods of reflow; and (3) defining
spatial perfusion patterns within the infarct bed in response to
exogenously induced maximal vasodilation and relating these to infarct size
and extent of myocardial salvage. METHODS AND RESULTS. Twenty-one dogs with
3 hours of left anterior descending coronary artery occlusion 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 dipyridamole. Radiolabeled
microsphere- derived blood flow was measured at 15 minutes and 2 and 3
hours after reflow and during dipyridamole effect. Infarct size was
measured at the end of the experiment by use of triphenyl tetrazolium
chloride. MCE data were processed with color-coding schemes that
highlighted differences in myocardial videointensities in proportion to the
concentration of microbubbles within the microvasculature. There was
significant variability in MCE-defined perfusion patterns after reflow,
with contrast defects noted mainly within the endocardium. There were 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 minutes after reflow, MCE defect size
underestimated infarct size by 50%. In comparison, in the presence of
dipyridamole, MCE defect size correlated strongly (r = .87, P < .001)
with infarct size and reasonably well with normalized transmural blood flow
(r = -.62, P = .04). Moreover, the topography of the MCE perfusion defect
reflected the topography of the infarct. CONCLUSIONS. MCE revealed striking
temporal heterogeneity in the spatial distribution of myocardial perfusion
during postischemia reflow and either significantly underestimated or did
not correlate with infarct size during reperfusion. Because of
abnormalities in coronary vascular reserve specific to infarcted tissue,
MCE in conjunction with intravenous dipyridamole depicted, in vivo, the
actual topography of the infarct with remarkable accuracy.
ARTICLES
Characterization of spatial patterns of flow within the reperfused myocardium by myocardial contrast echocardiography. Implications in determining extent of myocardial salvage
Cardiovascular Division, University of Virginia School of Medicine, Charlottesville 22908.
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