AIM: Heart rate (HR) reduction with ivabradine improves left ventricle filling by the prolongation of the diastolic time and increases stroke volume. But, it remains unclear what ivabradine's effect is on atrial conduction time and atrial mechanical functions. The aim of our study was to evaluate in stable outpatients with systolic heart failure (HF) the 3 months effect of ivabradine on atrial conduction time and mechanical functions. METHOD: We evaluated prospectively 43 (31 males, 12 females) patients with HF. Before and after treatment, all patients were evaluated by transthoracic M mode, two dimensional (2D), pulsed-wave (PW), continuous wave (CW), color flow and tissue Doppler imaging (TDI), and LA volumes were obtained apical four-chamber views by a disc's method. LA maximum volume (Vmax) at the end-systolic phase, LA minimum volume (Vmin) at the end-diastolic phase, and LA volume before atrial systole (Vp) were evaluated. The LA function parameters were calculated as follows: LA passive emptying volume = Vmax - Vp; LA passive emptying fraction = [(Vmax - Vp)/Vmax] × 100%, LA active emptying volume = Vp - Vmin; LA active emptying fraction = [(Vp - Vmin)/Vp] × 100%. RESULTS: Thirty men and 13 women with mean ± SD age of 63.9 ± 10.1 years were included in this study. Resting heart rate was significantly reduced after ivabradine treatment. There were no significantly difference in LVEF, and E/A before and after ivabradine treatment. LA diameter and Vmin were similar before and after ivabradine treatment (p = 0.793 and p = 0.284). However, Vmax and Vp were significantly decreased after ivabradine treatment (p = 0.040 and p = 0.012). Moreover, LA active emptying volume and LA active emptying fraction were significantly decreased after ivabradine treatment (p = 0.030 and p = 0.008). The PA lateral, septal, and tricuspid durations were significantly reduced after ivabradine treatment (p < 0.001, p < 0.001, and p = 0.002, respectively). Interatrial electromechanical delay and right intra-atrial electromechanical delay were significantly decreased after ivabradine treatment (33.7 ± 12.7 vs 26.2 ± 10.1, p = 0.001; and 14.1 ± 6.1 vs 9.2 ± 6.8, p < 0.001). CONCLUSIONS: The present study demonstrated that adding ivabradine to the standard therapy reduced HR and improves significantly LA electrical and mechanical functions in systolic HF patients.
AIM: Heart rate (HR) reduction with ivabradine improves left ventricle filling by the prolongation of the diastolic time and increases stroke volume. But, it remains unclear what ivabradine's effect is on atrial conduction time and atrial mechanical functions. The aim of our study was to evaluate in stable outpatients with systolic heart failure (HF) the 3 months effect of ivabradine on atrial conduction time and mechanical functions. METHOD: We evaluated prospectively 43 (31 males, 12 females) patients with HF. Before and after treatment, all patients were evaluated by transthoracic M mode, two dimensional (2D), pulsed-wave (PW), continuous wave (CW), color flow and tissue Doppler imaging (TDI), and LA volumes were obtained apical four-chamber views by a disc's method. LA maximum volume (Vmax) at the end-systolic phase, LA minimum volume (Vmin) at the end-diastolic phase, and LA volume before atrial systole (Vp) were evaluated. The LA function parameters were calculated as follows: LA passive emptying volume = Vmax - Vp; LA passive emptying fraction = [(Vmax - Vp)/Vmax] × 100%, LA active emptying volume = Vp - Vmin; LA active emptying fraction = [(Vp - Vmin)/Vp] × 100%. RESULTS: Thirty men and 13 women with mean ± SD age of 63.9 ± 10.1 years were included in this study. Resting heart rate was significantly reduced after ivabradine treatment. There were no significantly difference in LVEF, and E/A before and after ivabradine treatment. LA diameter and Vmin were similar before and after ivabradine treatment (p = 0.793 and p = 0.284). However, Vmax and Vp were significantly decreased after ivabradine treatment (p = 0.040 and p = 0.012). Moreover, LA active emptying volume and LA active emptying fraction were significantly decreased after ivabradine treatment (p = 0.030 and p = 0.008). The PA lateral, septal, and tricuspid durations were significantly reduced after ivabradine treatment (p < 0.001, p < 0.001, and p = 0.002, respectively). Interatrial electromechanical delay and right intra-atrial electromechanical delay were significantly decreased after ivabradine treatment (33.7 ± 12.7 vs 26.2 ± 10.1, p = 0.001; and 14.1 ± 6.1 vs 9.2 ± 6.8, p < 0.001). CONCLUSIONS: The present study demonstrated that adding ivabradine to the standard therapy reduced HR and improves significantly LA electrical and mechanical functions in systolic HFpatients.
Authors: Roberto M Lang; Michelle Bierig; Richard B Devereux; Frank A Flachskampf; Elyse Foster; Patricia A Pellikka; Michael H Picard; Mary J Roman; James Seward; Jack S Shanewise; Scott D Solomon; Kirk T Spencer; Martin St John Sutton; William J Stewart Journal: J Am Soc Echocardiogr Date: 2005-12 Impact factor: 5.251
Authors: L P Lai; M J Su; J L Lin; C H Tsai; F Y Lin; Y S Chen; J J Hwang; S K Huang; Y Z Tseng; W P Lien Journal: J Cardiovasc Electrophysiol Date: 1999-07