BACKGROUND: The influence of atrioventricular (AV) interaction on mitral valve closure (MVC) and left ventricular (LV) isovolumic contraction is not fully clarified. We investigated the relationship among AV delay, MVC, and LV isovolumic contraction using a horse model because of the low heart rate and physiologically long AV delay. METHODS AND RESULTS: Six horses were evaluated during sinus rhythm, right ventricular pacing without preceding atrial contraction, and dual-chamber pacing at AV delays of 150 to 350 ms, programmed at a constant rate. Right parasternal 4-chamber views were recorded for simultaneous measurements of MVC from anatomic M-mode and radial tissue Doppler-based LV pre-ejection velocity and isovolumic acceleration. During sinus rhythm and long AV delays (≥300 ms), 2 positive pre-ejection velocity peaks were present. The first peak was identified as LV recoil during atrial relaxation and consistently preceded MVC by 33±17 ms. The second peak was related to LV isovolumic contraction, occurring after MVC. This suggests that MVC was caused by atrial relaxation and followed by true isovolumic contraction. During short AV delays (<300 ms) and right ventricular pacing, MVC occurred significantly later. Only 1 pre-ejection peak was present, of which the end coincided with MVC with a mean difference of -1.5±10 ms. This suggests that LV contraction caused MVC. Peak velocity and isovolumic acceleration were significantly higher (P<0.001) because the mitral valve was open at the onset of LV contraction. CONCLUSIONS: Depending on the AV delay, MVC can be atrio- or ventriculogenic, resulting in significant alterations of the LV peak pre-ejection velocity and isovolumic acceleration.
BACKGROUND: The influence of atrioventricular (AV) interaction on mitral valve closure (MVC) and left ventricular (LV) isovolumic contraction is not fully clarified. We investigated the relationship among AV delay, MVC, and LV isovolumic contraction using a horse model because of the low heart rate and physiologically long AV delay. METHODS AND RESULTS: Six horses were evaluated during sinus rhythm, right ventricular pacing without preceding atrial contraction, and dual-chamber pacing at AV delays of 150 to 350 ms, programmed at a constant rate. Right parasternal 4-chamber views were recorded for simultaneous measurements of MVC from anatomic M-mode and radial tissue Doppler-based LV pre-ejection velocity and isovolumic acceleration. During sinus rhythm and long AV delays (≥300 ms), 2 positive pre-ejection velocity peaks were present. The first peak was identified as LV recoil during atrial relaxation and consistently preceded MVC by 33±17 ms. The second peak was related to LV isovolumic contraction, occurring after MVC. This suggests that MVC was caused by atrial relaxation and followed by true isovolumic contraction. During short AV delays (<300 ms) and right ventricular pacing, MVC occurred significantly later. Only 1 pre-ejection peak was present, of which the end coincided with MVC with a mean difference of -1.5±10 ms. This suggests that LV contraction caused MVC. Peak velocity and isovolumic acceleration were significantly higher (P<0.001) because the mitral valve was open at the onset of LV contraction. CONCLUSIONS: Depending on the AV delay, MVC can be atrio- or ventriculogenic, resulting in significant alterations of the LV peak pre-ejection velocity and isovolumic acceleration.
Authors: Ahmad A Abdouni; Carlos M A Brandão; Carlos E Rochitte; Pablo M A Pomerantzeff; Elinthon T Veronese; Ariane B Pacheco; Antonio S Santis; Flávio Tarasoutchi; Fábio B Jatene Journal: Clinics (Sao Paulo) Date: 2020-11-27 Impact factor: 2.365