Sequential deformation and physiological considerations in unipolar right or left ventricular pacing.
OBJECTIVE
To determine the effects of ventricular pacing on the normal contraction sequence of the helical ventricular myocardial band, and its' impact on left ventricular function.


METHODS
Ten pigs (25-68 kg) underwent analysis of percent segmental shortening (%SS) by sonomicrometry, with crystals placed along the fiber orientation of the ascending and descending segments, and posterior LV wall of the geometry of the helical heart. Unipolar pacing electrodes stimulated either the right atrium (RA), right ventricular apex (RVA) and outflow tract (RVOT), or posterior LV wall. Systemic hemodynamics, QRS-interval, cardiac index (CI), systolic and diastolic LV function and pressure-dimension (P-D) loops were analyzed and cardiac motion was monitored by video analysis.


RESULTS
Normal sinus heart rate (NSR) was elevated from 84+/-15 beats/min to 113+/-22 beats/min by pacing (p<0.05). The variables of NSR were not changed by atrial pacing. Conversely, compared with NSR, ventricular pacing (RVA, RVOT, LV) significantly (p<0.05) prolonged the QRS-interval (94-111 ms vs 52+/-7 ms, p<0.05) decreased mean arterial pressure (46-47 mmHg vs 62+/-11 mmHg), CI (2.7-3.4 L/(min m2) vs 4.9+/-0.9L/(min m2)) and systolic LV pressure (56-61 mmHg vs 92+/-10 mmHg). Furthermore, ventricular pacing decreased peak +dP/dt and -dP/dt (p<0.05) and lowered PRSW to 59-77%, with most profound change after RVA pacing (p<0.05). Each ventricular pacing intervention decreased SS% significantly in the descending, ascending, and posterior LV segments compared with NSR. Disruption of the normal NSR sequence of shortening (progression from descending to posterior to ascending regions) followed each pacing intervention. Changes were characterized by premature stimulation of the segment adjacent to the pacer stimulus, with associated (1) decrease of pressure-dimension loop area, (2) desynchronization of P-D loops and (3) consistent loss of the twisting pattern of visible cardiac motion.


CONCLUSIONS
Ventricular pacing disrupts the natural sequence of shortening along the myocardial band, and the resultant dyssynchrony impairs LV function.
Liakopoulos
Oliver J
OJ
Department of Surgery, Division of Cardiothoracic Surgery, David Geffen School of Medicine at University of California Los Angeles, 10833 Le Conte Avenue, 62-258 CHS, Los Angeles, CA 90095-1741, USA.
Tomioka
Hideyuki
H
Buckberg
Gerald D
GD
Tan
Zhongtuo
Z
Hristov
Nikola
N
Trummer
George
G
D000818:Animals; D001794:Blood Pressure / Q000502:physiology; D002302:Cardiac Output / Q000502:physiology; D002304:Cardiac Pacing, Artificial / Q000379:methods*; D004562:Electrocardiography / Q000379:methods; D006339:Heart Rate / Q000502:physiology; D009068:Movement / Q000502:physiology; D009200:Myocardial Contraction / Q000502:physiology*; D013552:Swine; D016276:Ventricular Function; D016277:Ventricular Function, Left / Q000502:physiology*