Circulation, Vol 71, 1206-1214, Copyright © 1985 by American Heart Association
DM Mirvis, L Ingram, MK Holly, JL Wilson and KB Ramanathan
Clinical and experimental data have documented the ability of nontransmural
myocardial infarction 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 dogs were studied before
and after occlusion-reperfusion (26 dogs) or latex embolization (four dogs)
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 infarction.
Infarct size was quantitated by computer analysis of heart slices stained
with triphenyl tetrazolium chloride. Six dogs did not develop infarction.
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 dogs with nontransmural and those with transmural lesions.
Infarct size (expressed as a percentage of the left ventricle infarcted),
the percentage of endocardium subjacent to infarction, the average depth of
necrosis, 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 dogs 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)
ARTICLES
Electrocardiographic effects of experimental nontransmural myocardial infarction