Coronary reserve abnormalities in the infarcted myocardium : Assessment of myocardial viability immediately versus late after reflow by contrast echocardiography

The aim of this study was to determine whether myocardial contrast echocardiography (MCE) during exogenous vasodilation can accurately delineate infarct size, and hence the extent of myocardial viability, both immediately (15 minutes) and late (3 hours) after reperfusion when postreflow coronary hyp...

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Bibliographic Details
Published in:Circulation (New York, N.Y.) N.Y.), 1996-08, Vol.94 (4), p.748-754
Main Authors: VILLANUEVA, F. S, CAMARANO, G, ISMAIL, S, GOODMAN, N. C, SKLENAR, J, KAUL, S
Format: Article
Language:English
Subjects:
Adenosine - pharmacology
Animals
Biological and medical sciences
Cardiology. Vascular system
Coronary Circulation
Coronary heart disease
Dipyridamole - pharmacology
Dogs
Echocardiography
Heart
Heart - drug effects
Heart - physiopathology
Medical sciences
Myocardial Infarction - diagnostic imaging
Myocardial Infarction - pathology
Myocardial Infarction - physiopathology
Myocardial Reperfusion
Myocardium - pathology
Regression Analysis
Time Factors
Vasodilation
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Summary:The aim of this study was to determine whether myocardial contrast echocardiography (MCE) during exogenous vasodilation can accurately delineate infarct size, and hence the extent of myocardial viability, both immediately (15 minutes) and late (3 hours) after reperfusion when postreflow coronary hyperema is still present. Twenty-one open-chest anesthetized dogs underwent 3 to 6 hours of coronary occlusion followed by reperfusion. MCE was performed 15 minutes after reflow before and during infusion of 0.2 mg.kg-1.min-1 adenosine i.v.. In 12 dogs, infarct size was measured at this time. In the remaining 9 dogs, reperfusion was continued for 3 hours, when MCE was repeated before and after an infusion of 0.56 mg.kg-1.min-1 dipyridamole i.v. and infarct size was measured. In the absence of adenosine, MCE perfusion defect at 15 minutes underestimated infarct sizes at both 15 minutes and 3 hours, whereas in the presence of adenosine, the estimate of infarct size was more accurate. Similarly, in the absence of dipyridamole, although MCE perfusion defect underestimated infarct size (both measured 3 hours after reflow), in the presence of dipyridamole, the estimate of infarct size was more accurate. By unmasking abnormalities in flow reserve within the infarct bed, MCE in conjunction with coronary vasodilators can accurately predict infarct size both 15 minutes and 3 hours after reperfusion. Thus, MCE can be used for assessing the extent of myocardial viability both immediately and late after reperfusion when postreflow coronary hyperemia is still present.
ISSN:0009-7322
1524-4539
DOI:10.1161/01.CIR.94.4.748