Abstract 1577: Transmural Dyssynchrony of Myofiber Shortening is Determined by Depolarization Sequence within Myocardial Layers
The delay in myofiber shortening (MS) onset between the endocardial and epicardial layers is greater than the electrical activation delay during sinus rhythm (SR) and decreases at the location of the pacing site during epicardial pacing (EP). The goal of this study is to demonstrate that increased transmural mechanical delay during SR is determined by the electrical activation sequence within the myocardial layers, rather than the transmural activation pattern. We employed a novel 3D anatomically-accurate electromechanical model of the rabbit ventricles that incorporated a detailed model of cardiac myofilament dynamics. MS was calculated throughout the ventricular volume during SR and for EP at the left ventricular anterior wall. Onset of MS followed the direction of electrical activation for both SR and EP, as shown in Figure⇓. However, transmural delay in MS onset was greater during SR, consistent with experiments (28ms-SR vs. 19ms-EP). Difference in the MS delay could not be explained by changes in transmural electrical activation delay (19ms-SR vs. 25ms-EP). Examination of the mechanisms revealed a longer apex-to-base electrical activation delay on the epicardium as compared to that on the endocardium during SR. “Prestretching” of the late-activated epicardial myofibers at the base by the shortening of the early-activated apical region increased MS delay. No prestretching was observed following EP. This finding indicates that transmural MS delay strongly depends on the electrical and mechanical activation sequence within the myocardial layers.
This research has received full or partial funding support from the American Heart Association, AHA Mid-Atlantic Affiliate (Maryland, North Carolina, South Carolina, Virginia & Washington, DC).