Mechanism of abnormal interventricular septal motion during delayed left ventricular activation.
To evaluate the mechanism of the abnormal motion of the interventricular septum (IVS) seen echocardiographically in some patients with relatively delayed ventricular activation, we simultaneously recorded high-fidelity left and right ventricular pressures and electrograms and echocardiograms of the IVS in nine open-chest dogs. During sinus rhythm and during left IVS pacing, the IVS was activated from left to right, preejection left ventricular pressure exceeded right ventricular pressure, and IVS motion was normal. During right ventricular pacing from the outflow tract, apex, free wall or right IVS was activated from right to left, right ventricular pressure increased before left ventricular pressure and simultaneously there was an abrupt posterior IVS motion. Simultaneous pacing from the right IVS and left ventricular free wall activated the IVS from right to left and produced a normal transseptal preejection pressure gradient and normal IVS motion. Simultaneous pacing from the left IVS and right ventricular free wall activated the IVS from left to right, and produced abrupt preejection posterior IVS motion coincident with an altered transseptal pressure gradient. During right ventricular pacing, IVS motion after the abrupt preejection posterior movement was variable. Anterior motion was associated with a greater asynchrony of right and left ventricular contraction than was normal posterior motion. We conclude that abrupt preejection posterior IVS motion seen with delayed left ventricular activation from right ventricular pacing is due to passive IVS displacement from an altered transseptal pressure gradient, and subsequent IVS motion depends on the degree of asynchrony between right and left ventricular contraction.
D000818:Animals; D001145:Arrhythmias, Cardiac / Q000503:physiopathology*; D002304:Cardiac Pacing, Artificial; D004285:Dogs; D004452:Echocardiography; D004562:Electrocardiography; D006346:Heart Septum / Q000503:physiopathology*; D006352:Heart Ventricles; D009200:Myocardial Contraction