Effects of ventricular pacing on regional left ventricular performance in the dog

Abstract

Changes in regional left ventricular (LV) performance induced by ventricular pacing were studied in two groups of open-chest anesthetized dogs. In the first group of five dogs, local function at the LV anterior base, anterior apex, and posterior apex was assessed by ultrasonic crystal pairs with atrial, right ventricular, LV apical, and LV base pacing. Ventricular pacing produced asynchrony of contraction and marked changes in the shortening pattern at each site, as well as an average 27% reduction in peak systolic pressure and peak dP/dt compared to atrial pacing. Moreover, the extent of shortening during LV ejection was reduced or unchanged at all sites measured during ventricular pacing. In the second group of five dogs, function of the septum and opposing LV lateral wall was studied with atrial and LV lateral wall pacing. Lateral function was assessed with a crystal pair and septal function by cineradiography of a lead bead implanted in the septum. Ventricular pacing produced reciprocal interaction between the two walls, with early lateral shortening inducing septal bulging and late septal shortening inducing lateral wall systolic lengthening. We conclude that ventricular pacing produces significant changes in regional myocardial function, likely induced by reciprocal interaction of opposing myocardial regions. Furthermore, such interaction appears deleterious to global ventricular function, presumably because volume is sequestered and pressure is dissipated into relatively inactive segments that are out of phase with the bulk of contracting myocardium.

Relation between regional electrical activation time and subepicardial fiber strain in the canine left ventricle

“…In general, compared with other open-thorax studies [6,9,11], left ventricular peak systolic pressure and maximum dplv/dt during both synchronous and asynchronous electrical activation were relatively low. This might be ascribed to the use of pentobarbital -known for its negative inotropic effect [19] -as anesthetic.…”

“…During a normal cardiac beat, elecxtrical activation of the left ventricle is initiated from the atrium. Once the electrical impulse enters the bundle of His, which merges into the Purkinje fibers, transmission becomes very rapid, providing a relatively synchronous activation of the ventricular myocardium [6,28]. This moment is indicated by the center of the QRS complex.…”

“…Normally, electrical activation of the left ventricular wall is quite synchronous [6,28]. Because contraction of muscle fibers follows electrical activation with a nearly fixed delay [10,13,15], contraction occurs nearly simultaneously too [26].…”

“…When electrical activation is clearly asynchronous, the situation changes considerably [6,25,29]. If the ventricles are directly stimulated large differences in fiber strain may occur [6,25].…”

“…If the ventricles are directly stimulated large differences in fiber strain may occur [6,25]. Early-activated muscle fibers contract early and with a high shortening velocity, thus stretching the serially connected, as yet non-activated fibers.…”