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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.

We used a canine preparation of experimental infarction to study the natural course of echocardiographically defined regional wall motion abnormalities in the 6 weeks after acute coronary ligation. Eight dogs underwent serial short-axis echocardiographic evaluation and microsphere blood flow determinations at control, and 30 min, 48 hr, 1 week, 3 weeks, and 6 weeks after acute coronary artery ligation. Wall motion analysis and blood flow calculations were applied to 10 degree radial segments of the left ventricle (short axis) and correlated to the size and extent of infarction as defined histologically at 6 weeks. All animals had at least 50% transmural histologic infarction. The ratio of flow in infarcted tissue vs noninfarcted myocardium fell to 0.40 +/- 0.13 for endocardium and 0.56 +/- 0.13 for epicardium at 30 min after ligation, but recovered to 0.83 +/- 0.15 for endocardium and 1.12 +/- 0.11 for epicardium by 6 weeks. The maximum circumferential extent of abnormal regional wall motion was observed at 48 hr after infarction (mean circumferential extent = 51%), but was resolved to a significant extent by 6 weeks (circumferential extent = 21%, p less than .001). Four animals had virtually normal wall motion by 6 weeks after infarction. Segment-by-segment regional dysfunction correlated highly with the regional transmural reduction in blood flow of 20% )r = .89, p = .0001) for the experiment as a whole, but the echocardiogram tended to underestimate the size of the histologic infarct at 6 weeks.(ABSTRACT TRUNCATED AT 250 WORDS)