BACKGROUND: Physiologic pacing is claimed to be superior to ventricular pacing in as much as it entails lower risk of atrial fibrillation, stroke, and atrial remodeling. There are few data on the relation between atrioventricular (AV) synchrony and atrial clot formation. Utilizing transesophageal echocardiography (TEE), this study sought to evaluate the effect of AV synchrony loss on left atrial physiology, atrial stasis, and clot formation. METHODS: We conducted a cross-sectional study on patients with both AV and ventricular pacing with left ventricular ejection fraction (LVEF) >30%. TEE enabled us to explore atrial and pacing leads thrombi and measure left atrial appendage (LAA) flow velocity. RESULTS: A total 72 patients (mean age, 65 +/- 11.7) were enrolled in the study. The pacing mode was VVI in 53% and AV sequential in 47% of patients. LVEF (mean +/- SD; %) was 53.3 +/- 6.2% in ventricular pacing mode and 52.2 +/- 6.6 in physiologic pacing mode. Thrombus formation on pacing lead (<10 mm in 97% of patients) was observed in 32% of all the patients (23% in patients with AV sequential pacing mode and 39% with VVI mode). Left atrial appendage flow velocity (LAA-FV) was significantly higher among the patients with AV sequential pacing mode (49.44 +/- 18 cm/s vs 40.94 +/- 19.4 cm/s, P value = 0.02). LAA-FV >40 cm/s was detected in 60% of the patients, 60% of whom were in physiologic mode. Left atrial size was significantly larger among the patients with VVI pacing mode (42.3 +/- 2.3 mm vs 37.79 +/- 4.5 mm, P = 0.001). Multivariate analysis showed no relation between LAA-FV and age, hypertension, diabetes mellitus, left atrial size, and left ventricular function. Only one patient had right atrial clot. There was no thrombus in the ventricles and atrial appendage. CONCLUSION: Long-term loss of AV synchrony induced by VVI pacing is associated with the impairment of LAA contraction. Thrombus formation in the LAA is not increased by VVI pacing in patients with relatively good left ventricular (LV) function and sinus rhythm.
BACKGROUND: Physiologic pacing is claimed to be superior to ventricular pacing in as much as it entails lower risk of atrial fibrillation, stroke, and atrial remodeling. There are few data on the relation between atrioventricular (AV) synchrony and atrial clot formation. Utilizing transesophageal echocardiography (TEE), this study sought to evaluate the effect of AV synchrony loss on left atrial physiology, atrial stasis, and clot formation. METHODS: We conducted a cross-sectional study on patients with both AV and ventricular pacing with left ventricular ejection fraction (LVEF) >30%. TEE enabled us to explore atrial and pacing leads thrombi and measure left atrial appendage (LAA) flow velocity. RESULTS: A total 72 patients (mean age, 65 +/- 11.7) were enrolled in the study. The pacing mode was VVI in 53% and AV sequential in 47% of patients. LVEF (mean +/- SD; %) was 53.3 +/- 6.2% in ventricular pacing mode and 52.2 +/- 6.6 in physiologic pacing mode. Thrombus formation on pacing lead (<10 mm in 97% of patients) was observed in 32% of all the patients (23% in patients with AV sequential pacing mode and 39% with VVI mode). Left atrial appendage flow velocity (LAA-FV) was significantly higher among the patients with AV sequential pacing mode (49.44 +/- 18 cm/s vs 40.94 +/- 19.4 cm/s, P value = 0.02). LAA-FV >40 cm/s was detected in 60% of the patients, 60% of whom were in physiologic mode. Left atrial size was significantly larger among the patients with VVI pacing mode (42.3 +/- 2.3 mm vs 37.79 +/- 4.5 mm, P = 0.001). Multivariate analysis showed no relation between LAA-FV and age, hypertension, diabetes mellitus, left atrial size, and left ventricular function. Only one patient had right atrial clot. There was no thrombus in the ventricles and atrial appendage. CONCLUSION: Long-term loss of AV synchrony induced by VVI pacing is associated with the impairment of LAA contraction. Thrombus formation in the LAA is not increased by VVI pacing in patients with relatively good left ventricular (LV) function and sinus rhythm.
Authors: Vaibhav R Vaidya; Christopher V DeSimone; Samuel J Asirvatham; Vishnu M Chandra; Amit Noheria; David O Hodge; Joshua P Slusser; Alejandro A Rabinstein; Paul A Friedman Journal: J Interv Card Electrophysiol Date: 2014-04-27 Impact factor: 1.900