Author + information
- Li Yaodong,
- Yutong Ji,
- Xianhui Zhou,
- Qiang Xing,
- Yanmei Lu,
- Jianghua Zhang and
- Baopeng Tang
Atrial fibrillation is one of the most common tachyarrhythmia with relatively high incidence rate. Previous studies have shown that increased expression of HCN channel in the pulmonary vein and atrial tissues could increase the risk of developing AF. Ivabradine is an ion channel inhibitor that could inhibit the transmembrane velocity of funny current (If) and the expression of HCN channel, and thus present potential antiarrhythmic effects. To evaluate the effects of Ivabradine on the expression of HCN2 and HCN4 channel proteins and mRNA levels in the pulmonary vein and atrial tissues of the dogs with age-related AF, and explore the mechanisms involved.
Twelve aged dogs were selected as the subjects. Rapid atrial pacing was performed for two months to induce age-related AF model. The dogs were then randomly divided into Ivabradine group and age-related AF group, and the multi-channel electrophysiological instrument was used to detect the induction rate and the duration of AF two months later. The pulmonary vein and atrial tissues of the dogs in both groups were collected, and PCR and Western blot were used to measure the expression of HCN2 and HCN4 channel mRNA and protein.
Ivabradine significantly reduced the duration (71.50±16.87 s vs. 155.83±9.32 s; P=0.001) and induction rate (28% vs. 57%, P=0.001) of AF. Comparing with the age-related AF group, the expression of HCN2 and HCN4 mRNA and protein decreased significantly in the pulmonary vein and left atrial tissues in the Ivabradine group (P<0.05).
Ivabradine could prevent age-related AF by down-regulating the expression of HCN channel mRNAs and proteins in the pulmonary vein and atrial tissues of dogs with age-related AF.