Profibrillatory Effects of Multiple Extrastimuli

Profibrillatory Effects of Extrastimuli . Multiple extrastimuli are known to cause ventricular Hhrillation in normal hearts. The mechanisms by which multiple extrastimuli facilitate induction of ventricular fibrillation were studied in 10 normal, anesthetized, open chest dogs. Strength‐interval curves and latency‐interval curves were measured following basic drive (S 1 S 1 ) and following captured single and double extrastimuli (S 2 and S 3 ). The zone of relative refractoriness was widened by closely coupled extrastimuli: 44 ± 8 msec after basic drive. 81 ± 19 msec after S 2 and 92 ± 15 msec after S 2 S 3 (P <0.001 compared to basic drive). The maximum latency between a test stimulus and its propagated response was prolonged by extrastimuli: 95 ± 6 msec after basic drive, 144 ± 11 msec after S 2 , and 162 ± 12 msec after S 3 (P <0.001). Extrastimuli that were not closely coupled (i.e., that were delivered 30 or 50 msec following the effective refractory period of the previous beat) had little effect on the zone of relative refractoriness or maximum latency of subsequent stimuli. Catbodal, anodal, and bipolar extrastimuli had similar effects on effective refractory period, zone of relative refractoriness, and latency. Extrastimuli did not cause decreases in threshold for capture and did not exaggerate early diastolic dips in strength‐interval curves. Forty episodes of ventricular fibrillation were induced in eight of ten dogs. Latency‐interval curves that induced VF had longer maximum latency (P <0.001) and wider zones of relative refractoriness (P <0.001) than did latency interval curves that did not result in ventricular fibrillation. Prolongation of the relative refractory period resulted in corresponding prolongation of latency with correlation coefficient of 0.97, however, both of these parameters correlated poorly with the coupling interval of The premature stimuli (R = 044 and 043). In conclusion, premature extrastimuli may facilitate induction of ventricular fibrillation by widening the relative refractory period and prolonging latency. However, premature stimuli initiated at coupling intervals of over 30 msec above the ERP of the previous propagated beat eliminate much of the relative refractory period and latency increase, and were not associated with ventricular flbrillation. ( J Cardiovasc Electrophysiol, Vol. I, No. 3, pp 197–208, June 1990 )