• D R Spahn, W C Hu, L R Smith, and B J Leone.
• Department of Anesthesiology, Duke University Medical Center, Durham, NC 27710.
• J. Cardiothorac. Vasc. Anesth. 1993 Dec 1;7(6):696-704.

AbstractThe mechanisms leading to left ventricular (LV) asynchronies are incompletely understood, and reports on the functional significance of asynchronies for the affected segments are conflicting. To characterize LV asynchronies, 16 anesthetized dogs with critical stenosis of the left anterior descending coronary artery (LAD) were instrumented to measure subendocardial contractile function (sonomicrometry) and the ECG in the LAD territory. The subendocardial ECG was also recorded from the anterior basal LV territory. Time of regional S wave arrival (TS) and time of onset of segment shortening were determined. The animals underwent atrial pacing with increasing frequencies until systolic LAD territory contractile dysfunction and eventual LV asynchronies were observed. Six animals without LAD stenosis served as controls to define the normal response (mean +/- 2.SD) to increasing pacing rates of systolic shortening and onset time of segment shortening (time difference between TS and onset of segment shortening). LAD contractile dysfunction was considered as a systolic shortening below the normal range, and LV asynchronies as an onset time of segment shortening above the normal range. When LV asynchronies occurred, onset time of segment shortening in the LAD territory was 80.1 +/- 4.9 ms versus 14.8 +/- 3.7 ms at control (P < 0.01); the time difference between S wave arrival in the LAD and circumflex territories, however, was unchanged. LV asynchronies were associated with marked LAD territory contractile dysfunction (systolic shortening of 9.6 +/- 0.8% v 21.0 +/- 1.9% at control, after systolic shortening of 31.3 +/- 3.8% v 9.0 +/- 2.6% at control; P < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

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