Regional blood flow correlates of @entity308 in XXXX -induced myocardial ischemia.

@entity308 @entity301 @entity235 @entity1347 @entity63 @entity591 @entity15496
@entity591 produces @entity63 and @entity1347 after @entity301 . To determine whether a quantitative relationship exists between these ST shifts and transmural blood flow, 19 @entity235 were studied. Coronary obstruction was produced by ameroid @entity15496 of the left circumflex artery, and @entity591 was generated by atrial pacing at 90 to 210 beats/min. ST shifts were studied by body surface isopotential mapping with an 84-electrode torso grid, and blood flow was quantitated by serial radiolabeled microsphere injections. Isopotential maps at each paced rate, 40 msec into the ST segment, were classified as normal or @entity63 based on spatial patterns of voltages. Pacing after 3 weeks of ameroid @entity15496 reduced endocardial/epicardial flow ratios in 11 @entity235 from 1.16 +/- 0.22 at rest to 0.41 +/- 0.18 at 210 beats/min. @entity308 developed in these @entity235 at a rate of 184.0 +/- 16.5 beats/min. Endocardial/epicardial ratios with ST @entity308 (0.45 +/- 0.15) were lower than at those without ST @entity308 (1.05 +/- 0.19; p less than .01). Logistic regression analysis demonstrated that ST @entity308 corresponded to an endocardial/epicardial ratio of 0.67 or less (p less than .01). With this model, 95.5% of data sets were correctly classified. Neither heart rate nor perfusion bed size were significant independent predictors of an @entity63 electrocardiographic response. The magnitude of abnormal ST segment shift was significantly correlated (r = .87) with the transmural flow ratio. Thus development of electrocardiographic changes indicative of @entity63 corresponds to a predictable degree of flow redistribution and the magnitude of the ST shift is correlated with the intensity of the flow abnormality.
