The effects of ivabradine on left atrial electromechanical function in patients with systolic heart failure
Serkan Ozturk1, Selçuk Öztürk2, Fatma Hizal Erdem2
1Faculty of Medicine, Department of Cardiology, Abant Izzet Baysal University, Golkoy, Bolu, 14280, Turkey. drserkan69@hotmail.com.
Insights
Ivabradine treatment in systolic heart failure patients significantly reduced heart rate and improved atrial electrical and mechanical functions. This study highlights ivabradine
Area of Science:
- Cardiology
- Electrophysiology
- Heart Failure Management
Background:
- Ivabradine is known to reduce heart rate (HR) and improve left ventricle filling in systolic heart failure (HF).
- The specific effects of ivabradine on atrial conduction time and mechanical function remain less understood.
Purpose of the Study:
- To evaluate the 3-month effects of ivabradine on atrial conduction time and mechanical functions in stable outpatients with systolic HF.
- To assess changes in left atrial (LA) volumes and function parameters.
Main Methods:
- Prospective evaluation of 43 HF patients treated with ivabradine.
- Comprehensive echocardiographic assessment including M-mode, 2D, Doppler, and tissue Doppler imaging (TDI).
- Measurement of LA volumes (Vmax, Vmin, Vp) and calculation of LA emptying fractions; assessment of interatrial and intra-atrial electromechanical delay.
Main Results:
- Ivabradine significantly reduced resting heart rate.
- Significant improvements were observed in atrial conduction times (PA lateral, septal, tricuspid durations) and electromechanical delays.
- Left atrial Vmax and Vp, as well as active emptying volume and fraction, were significantly decreased post-treatment.
Conclusions:
- Adding ivabradine to standard therapy in systolic HF patients effectively reduces HR.
- Ivabradine significantly improves both electrical and mechanical functions of the left atrium.
- These findings suggest a beneficial role for ivabradine in modulating atrial function in HF.
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.
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