Electrocardiographic effects of experimental nontransmural XXXX .

@entity5045 @entity39 @entity235 @entity1188 @entity583
Clinical and experimental data have documented the ability of nontransmural @entity583 to produce abnormal Q waves on both the epicardial and body surfaces. We undertook this study to define the anatomic determinants of such Q wave development. Thirty @entity235 were studied before and after occlusion-reperfusion (26 @entity235 ) or latex embolization (four @entity235 ) of the left circumflex coronary artery. Occlusion was maintained for 60 to 240 min before reperfusion to produce nontransmural lesions of various sizes. Electrocardiographic data were registered from 84 torso electrodes by body surface mapping techniques before and 1 week after @entity1188 . @entity1188 size was quantitated by computer analysis of heart slices stained with @entity5045 . Six @entity235 did not develop @entity1188 . Of the remaining 24, 10 did and 14 did not develop significant changes in body surface Q wave duration and width. The incidence of Q wave changes was not different in @entity235 with nontransmural and those with transmural lesions. @entity1188 size (expressed as a percentage of the left ventricle infarcted), the percentage of endocardium subjacent to @entity1188 , the average depth of @entity39 , the percent of the four outer fifths of the ventricular wall infarcted, and the duration of occlusion were significantly (p less than .05) greater in @entity235 with than in those without Q wave changes. Logistic regression modeling demonstrated that only two anatomic parameters--percentage of left ventricle infarcted and average lesion depth--significantly and independently predicted Q wave development. A model including only these two variables accurately classified all 24 cases.(ABSTRACT TRUNCATED AT 250 WORDS)
