Importance of temporal heterogeneity in assessing the contraction abnormalities associated with acute myocardial ischemia.

Abstract

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. Circulation 70, No. 1, 102-112, 1984. A NUMBER of recent two-dimensional echocardiographic studies have attempted to quantitate the changes in regional wall motion and wall thickening that occur after acute coronary ligation and to relate these changes to infarct location and density.' -2 In most instances, wall motion and thickening have been

Perfusion Versus Function: The Ischemic Cascade in Demand Ischemia

“…Consequently, although tardokinesia and mild forms of hypokinesia can be detected with this technique, they can be missed when only end-diastolic and end-systolic frames are used. 20,21 Furthermore, we compared WT in every bed to that of the normally perfused bed at each dose of dobutamine. Thus, a unique threshold for abnormality was used separately for each dog at each dobutamine dose, which allowed detection of subtle WT abnormalities that were not readily observed visually.…”

“…Using the resting transstenotic pressure gradient (mm Hg), the stenosis stages were divided into mild, 10 -14 moderate, [15][16][17][18][19][20] and severe (Ͼ20 mm). For each stenosis level, a standard dobutamine stress protocol was performed with a baseline and up to four incremental 3-minute dobutamine stages (10 to 40 g/kg Ϫ1 · min Ϫ1 infused intravenously).…”

Overestimation of infarct size by quantitative two-dimensional echocardiography: the role of tethering and of analytic procedures.

“…First, the studies done to date have all required precise retrospective matching and aligning of the two-dimensional echocardiographic section with the pathologic section, a process that relies on internal landmarks that are distorted by the postmortem processing. 19 Second, Armstrong et al,20 in a preliminary report, found that at least some portion of this overestimation of ischemic region size was caused by inherent limitations of the two-dimensional echocardiographic analysis procedures used to evaluate regional left ventricular function. These procedures analyze thickening on a radial coordinate plot emanating from a floating center of mass and express extent of dysfunction as a percentage of the diastolic left ventricular circumference.…”

Echocardiographically detected dyskinesis, myocardial infarct size, and coronary risk region relationships in reperfused canine myocardium.

“…We chose a strict criterion because many studies in both animals and humans have found that there is heterogeneity of contraction in normal myocardium." [25][26][27][28] Another factor affecting the risk region-infarct size relationship is the duration of coronary occlusion before reperfusion. In our study the infarct size was almost twice as large in the animals subjected to 2 hr coronary occlusions compared with that in animals subjected to 1 hr occlusions.…”