The relation between the sequence of electrical (E) and mechanical (M) activation was studied at the LV anterior wall of open-chest dogs (n = 11). M activation was defined as the onset of epicardial fibre shortening, as measured with a recently developed video technique. E activation was determined with a brush of extracellular electrodes. The delay between activation of basal and apical regions was consistently larger for M activation than for E activation: during spontaneous beating: 20.5 +/- 7.30 ms vs 8.8 +/- 3.31 ms, during right ventricular outflow tract pacing: 50.3 +/- 7.69 ms vs 39.0 +/- 5.31 ms and during left ventricular apex pacing 40.1 +/- 10.03 ms vs 25.4 +/- 9.30 ms, respectively (P less than 0.05 in all cases). The E-M time interval was consistently shorter in early than in late activated regions: 32 +/- 10 vs 41 +/- 8 ms during RV outflow tract pacing (P = 0.09) and 24 +/- 30 vs 40 +/- 24 ms during LV apex pacing (P less than 0.05). Electrical asynchronies larger than 40 ms resulted in decreases of systolic blood pressure and stroke volume. This study shows that the asynchrony of cardiac motion exceeds that of electrical activation because the time interval between electrical activation and onset of fibre shortening is larger the later a particular region is activated. Possible explanations for this phenomenon are discussed.
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