Asynchrony of ventricular activation affects magnitude and timing of fiber stretch in late-activated regions of the canine heart

Abnormal electrical activation of the left ventricle results in mechanical dyssynchrony, which is in part characterized by early stretch of late-activated myofibers. To describe the pattern of deformation during "prestretch" and gain insight into its causes and sequelae, we implanted midwall and transmural arrays of radiopaque markers into the left ventricular anterolateral wall of open-chest, isoflurane-anesthetized, adult mongrel dogs. Biplane cineradiography (125 Hz) was used to determine the time course of two- and three-dimensional strains while pacing from a remote, posterior wall site. Strain maps were generated as a function of time. Electrical activation was assessed with bipolar electrodes. Posterior wall pacing generated prestretch at the measurement site, which peaked 44 ms after local electrical activation. Overall magnitudes and transmural gradients of strain were reduced when compared with passive inflation. Fiber stretch was larger at aortic valve opening compared with end diastole (P < 0.05). Fiber stretch at aortic valve opening was weakly but significantly correlated with local activation time (r(2) = 0.319, P < 0.001). With a short atrioventricular delay, fiber lengths were not significantly different at the time of aortic valve opening during ventricular pacing compared with atrial pacing. However, ejection strain did significantly increase (P < 0.05). We conclude that the majority of fiber stretch occurs after local electrical activation and mitral valve closure and is different from passive inflation. The increased shortening of these regions appears to be because of a reduced afterload rather than an effect of length-dependent activation in this preparation.