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J Am Coll Cardiol, 1989; 14:462-471
© 1989 by the American College of Cardiology Foundation
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Early identification with ultrasonic integrated backscatter of viable but stunned myocardium in dogs

MR Milunski, GA Mohr, KA Wear, BE Sobel, JG Miller, and SA Wickline

Cardiovascular Division, Washington University, St. Louis, Missouri 63110.

It has been shown that canine and human hearts exhibit a cardiac cycle-dependent variation of integrated backscatter (cyclic variation) that reflects intrinsic regional contractile performance. To determine whether ultrasound tissue characterization can identify viable though stunned myocardium before recovery of regional wall thickening, transient ischemic injury was produced in eight open chest dogs for 15 min followed by reperfusion for 2 h. Cyclic variation and wall thickening were measured before ischemia, at 15 min after the onset of ischemia and at selected intervals after the onset of reperfusion from multiple sites within the ischemic zone with a novel combined two-dimensional and M-mode acquisition system. Cyclic variation and wall thickening were computed from digitized M-mode integrated backscatter images with an algorithm developed and validated for this purpose. Magnitude and "delay" of cyclic variation and wall thickening were compared. Delay represents the degree of synchrony of regional cyclic variation or wall thickening with global ventricular mechanical systole. Baseline cyclic variation and wall thickening magnitudes were 3.8 +/- 0.2 dB and 37 +/- 1.4%, respectively. With ischemia, cyclic variation and wall thickening decreased to 1.7 +/- 0.2 dB and 17 +/- 2%, respectively (p less than 0.05, compared with baseline). Cyclic variation recovered to baseline levels within 20 min after reperfusion (3.3 +/- 0.4 dB, p = NS). Wall thickening remained depressed for 2 h after the onset of reperfusion (23 +/- 2%, p less than 0.05 compared with baseline). Delay of cyclic variation in a unitless ratio expressed as delay (in milliseconds) divided by the QT interval (in milliseconds) increased from 0.87 +/- 0.03 at baseline to 1.10 +/- 0.12 with ischemia, a change consistent with mild asynchrony, and returned to baseline (0.95 +/- 0.07, p = NS compared with baseline) within 20 min after reperfusion. Delay of wall thickening was 0.88 +/- 0.02 at baseline, increased to 1.23 +/- 0.09 with ischemia and remained significantly increased 2 h after reperfusion (1.07 +/- 0.05, p less than 0.05 compared with baseline). Recovery time constants for cyclic variation and wall thickening with reperfusion reflected earlier restoration of cyclic variation (8.1 min) than of wall thickening (420.5 min). Thus, cyclic variation recovers before wall thickening with reperfusion. Its analysis appears to provide a useful index of the presence of viable and potentially salvageable tissue in regions of stunned myocardium that is independent of wall thickening.


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