Ivabradine could not decrease mitral regurgitation triggered atrial fibrosis and fibrillation compared with carvedilol

doi:10.1002/ehf2.14577

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Title:	Ivabradine could not decrease mitral regurgitation triggered atrial fibrosis and fibrillation compared with carvedilol
Authors:	Lee, Wei-Chieh Lin, Yu-Wen Shih, Jhih-Yuan Chen, Zhih-Cherng Wu, Nan-Chun Chang, Wei-Ting
Contributors:	Natl Sun Yat Sen Univ, Coll Med, Sch Med Chi Mei Med Ctr, Dept Internal Med, Div Cardiol Natl Cheng Kung Univ, Coll Med, Inst Clin Med Chi Mei Med Ctr, Dept Surg, Div Cardiovasc Surg Chia Nan Univ Pharm & Sci, Dept Hosp & Hlth Care Adm Natl Sun Yat Sen Univ, Sch Med Natl Sun Yat Sen Univ, Coll Med, Doctoral Program Clin & Expt Med Natl Sun Yat Sen Univ, Ctr Excellence Metab Associated Fatty Liver Dis Chi Mei Med Ctr, Div Cardiovasc Med
Keywords:	Apoptosis Atrial fibrillation Carvedilol Ivabradine Mitral regurgitation
Date:	2024
Issue Date:	2024-12-25 11:05:12 (UTC+8)
Publisher:	WILEY PERIODICALS, INC
Abstract:	Background Ivabradine, a medical treatment for heart failure (HF), reduces heart rate (HR) and prolongs diastolic perfusion time. It is frequently prescribed to patients with HF who have a suboptimal response or intolerance to beta-blockers. Degenerative mitral regurgitation (MR) is a valvular heart disease often associated with the development of HF and atrial fibrillation (AF). However, studies comparing the effects of ivabradine and beta-blockers on MR are lacking. Therefore, this study aimed to explore the potential therapeutic effects of ivabradine and carvedilol on MR using a rat model.Methods and results Using a novel echo-guided mini-invasive surgery, MR was created in 12-weeks-old Sprague-Dawley rats. After 2 weeks, the rats were randomized to receive either ivabradine or carvedilol for 4 weeks. Echocardiography was performed at baseline and at two-week intervals. Following haemodynamic studies, postmortem tissues were analysed. Notably, the MR-induced myocardial dysfunction did not improve considerably after treatment with ivabradine or carvedilol. However, in haemodynamic studies, pharmacological therapies, particularly carvedilol, mitigated MR-induced chamber dilatation (end-systolic volume and end-diastolic volume; MR vs. MR + Carvedilol; P < 0.05) and decreased compliance (end-systolic pressure-volume relationship; MR vs. MR + Carvedilol; P < 0.05). Compared with ivabradine, a shorter duration (MR vs. MR + Carvedilol; P < 0.05) and reduced inducibility (MR vs. MR + Carvedilol and MR vs. MR + Ivabradine; P < 0.05) of AF were observed in MR rats treated with carvedilol. Similarly, reduced cardiac fibrosis and apoptosis were observed in the MR rat model in the treatment groups, especially in those treated with carvedilol (MR vs. MR + Carvedilol; P < 0.01).Conclusions Although both ivabradine and carvedilol, at least in part, mitigated MR-induced chamber dilatation and decreased compliance, carvedilol had a better effect on reversing MR-induced cardiac fibrosis, apoptosis, and arrhythmogenesis than ivabradine. When compared with Ivabradine, MR rats treated with carvedilol exhibited a shorter duration and reduced inducibility of AF, thus providing more effective suppression of HCN4. Further investigations are required to validate our findings.
Relation:	Esc Heart Failure, v.11, n.1, pp.251-260
Appears in Collections:	[Offices] 456

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