Circulation, Vol 70, 102-112, Copyright © 1984 by American Heart Association
AE Weyman, TD Franklin Jr, RD Hogan, LD Gillam, PS Wiske, J Newell, EF Gibbons and RA Foale
A number of recent two-dimensional echocardiographic studies have attempted
to relate quantitative changes in short-axis left ventricular radial wall
motion to underlying myocardial ischemia/infarction. The significance of
temporal variation in the contraction sequence within these ischemic
regions in the overall evaluation of segmental left ventricular
dysfunction, however, remains undefined. To assess this, we examined the
motion of 192 individual radii that intersected known ischemic segments at
16.7 msec intervals from end-diastole to end- systole. The studies were
performed in 13 dogs 1 hr after acute coronary ligation (six of the left
anterior descending and seven of the circumflex coronary artery). Zones of
infarction were confirmed by triphenyltetrazolium chloride staining at the
termination of the experiment and by a corresponding decrease of more than
75% in myocardial perfusion at the 1 hr sampling period. Dyskinesis
(defined for each radius as negative or outward excursion relative to the
end- diastolic reference on two consecutive fields) was noted along 168 of
192 radii (88%) at some point in the contraction sequence. The maximal
outward or dyskinetic motion occurred most commonly in the fourth decile of
the normalized contraction sequence. In 147 of the 168 dyskinetic radii
(88%) the maximal outward motion occurred during the first half of systole
while in only two radii in one animal was the maximal outward motion noted
at end-systole. The total number of radii showing dyskinetic motion at any
given point in the contraction sequence likewise varied with time. Although
again the greatest number of radii showed abnormal motion during the fourth
decile of the normalized contraction sequence, only 66 of 168 or 39%
remained dyskinetic to end-systole. No relationship was observed between
the point of maximal dyskinesis (time-weighted average of all dyskinetic
radii for a given animal) and (1) the total number of radii showing
dyskinesis, (2) the total number of radii within the infarct zone, or (3)
the infarct area expressed as a percent of the slice area. The major factor
determining persistence of dyskinesis to end-systole for any radius was the
maximal outward motion of the endocardial segment at the point of maximal
dyskinesis. Therefore, simple measurement of endocardial excursion from
end-diastole to end-systole may fail to detect important wall motion
abnormalities and, in some cases, may miss dyskinetic segments completely.
ARTICLES
Importance of temporal heterogeneity in assessing the contraction abnormalities associated with acute myocardial ischemia
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