Oral Abstract: Understanding the physio-pathology of myocardial mechanics * Friday 9 December 2011, 14:00-15:30 * Location: Kaposvar

Abstract

Purpose: To evaluate the relationship between atrial contraction, mitral valve closure (MVC) and left ventricular isovolumic contraction. The horse is an ideal model to investigate this mechanism because of the low resting heart rate (25–45 bpm) and long atrioventricular (AV) interval. Methods: Five unsedated horses instrumented with pacing leads in the right atrium and right ventricle were evaluated during sinus rhythm (SR), ventricular pacing without preceding atrial contraction (VP) and dual-chamber pacing at AV delays ranging from 150 to 350 ms, programmed in a random sequence at a constant rate of 40 bpm. Color Doppler myocardial imaging was performed at high frame rates (>100 fps). Modified right parasternal four-chamber views were recorded for simultaneous measurements of MVC by anatomical M-mode and tissue Doppler-based left ventricular pre-ejectional peak velocity spikes and their timing. Results: During SR (AV interval 330–520 ms) and long AV intervals (300 and 350 ms), MVC occurred 12±37 ms after the onset of QRS. Two positive pre-ejectional velocity peaks were present. The first peak was identified as recoil of the left ventricle during atrial relaxation. This peak (2.5±1.1 cm/s) consistently preceded MVC (linear mixed model; P=0.84) by 44±18 ms. The second peak (4.8±1.3 cm/s) was called left ventricular isovolumic contraction and occurred after MVC. This suggests MVC caused by atrial contraction, followed by a true isovolumic contraction. However, during short AV intervals (150 and 200 ms) and VP, MVC occurred significantly later (P=0.002) at 125±5 ms after the onset of QRS. Only one pre-ejectional peak was present and the end of this peak coincided with MVC (linear mixed model; P=0.76). Peak velocity (9.2±2.4 cm/s) was remarkably higher than during SR and long AV intervals (P=0.009). These findings suggest MVC caused by left ventricular myocardial motion, resulting in a high pre-ejectional velocity peak as this contraction is not isovolumic. Conclusions: This study demonstrates the important influence of the atrioventricular interaction on mitral valve closure and pre-ejectional myocardial motion. Depending on the atrioventricular delay, mitral valve closure can be atrio- or ventriculogenic, resulting in high pre-ejectional velocities if the left ventricle is not in a true isovolumic state.