Long-term follow-up of atrial function after cardioversion of atrial fibrillation in horses.

Atrial fibrillation (AF) causes atrial electrical and contractile remodelling in horses. The aim of this study was to quantify left atrial (LA) contractile function and its time course of recovery after cardioversion of naturally-occurring AF in horses. The study population included 42 AF horses which were successfully treated using transvenous electrical cardioversion TVEC (n=39) or quinidine sulfate (n=3), with trivial or mild mitral regurgitation present in 25 horses. Thirty-seven healthy horses were used as controls. AF duration was estimated based on the history and previous examinations. Echocardiography was performed during general anaesthesia after TVEC (day 0) and on days 1, 2, 6 and then 7 weeks after cardioversion. The two-dimensional (2D) echocardiographic measurements included LA diameter, area and ejection phase indices such as fractional shortening. Atrial TDI measurements included peak myocardial velocity during atrial contraction (A), time to onset A, time to peak A and duration of A. During follow-up after cardioversion, atrial contractile function measured by 2D echocardiography and TDI gradually improved. At 7 weeks following cardioversion, TDI-based myocardial velocities returned to reference values. However, AF horses still showed significantly larger atrial dimensions, lower 2D ejection phase indices and prolonged TDI-based conduction time compared to the control group. In conclusion, AF-induced atrial contractile dysfunction gradually improves in the weeks following cardioversion, but at 7 weeks post-cardioversion, significant differences remain compared to healthy controls.

Evaluation of tissue Doppler imaging for regional quantification of radial left ventricular wall motion in healthy horses.

OBJECTIVE: To compare the feasibility and repeatability of tissue Doppler imaging (TDI) for quantification of radial left ventricular (LV) velocity and deformation from different imaging planes and to correlate cardiac event timing data obtained by TDI to M-mode and pulsed-wave Doppler-derived time intervals in horses. ANIMALS: 10 healthy adult horses. PROCEDURES: Repeated echocardiography was performed by 2 observers from right and left parasternal short-axis views at papillary muscle and chordal levels. The TDI measurements of systolic and diastolic velocity, strain rate, strain peak values, and timing were performed in 8 LV wall segments (LV free wall and interventricular septum from right parasternal views; left and right region of LV wall from left parasternal views). The inter- and intraobserver within- and between-day variability and measurement variability were assessed. The correlation between TDI-based measurements and M-mode and pulsed-wave Doppler-based time measurements was calculated. RESULTS: TDI measurements of velocity, strain rate, and strain were feasible in each horse, although deformation could often not be measured in the LV free wall. Systolic and diastolic time intervals could be determined with low to moderate variability, whereas peak amplitude variability ranged from low to high. The TDI-based time measurements were significantly correlated to M-mode and pulsed-wave Doppler measurements. CONCLUSIONS AND CLINICAL RELEVANCE: TDI measurements of radial LV velocity and deformation were feasible with low to moderate variability in 8 LV segments. These measurements can be used for evaluating LV function in further clinical studies.

Influence of atrioventricular interaction on mitral valve closure and left ventricular isovolumic contraction measured by tissue Doppler imaging.

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.