Vagus nerve stimulation reduces ventricular arrhythmias and increases ventricular electrical stability.

BACKGROUND: Transcutaneous stimulation of the auricular branch of the vagus nerve (AB-VNS) is a potentially noninvasive, inexpensive, and safe approach for vagus nerve stimulation that suppresses the induction and duration of atrial fibrillation and reduces sympathetic nerve outflow in healthy humans. Researchers have not determined whether AB-VNS affects ventricular arrhythmias. OBJECTIVE: To evaluate the antiarrhythmic effects of noninvasive AB-VNS on ventricular arrhythmias induced by myocardial infarction (MI). METHODS AND RESULTS: Twelve beagle dogs were randomly divided into the following two groups: a AB-VNS group (coronary artery occlusion and noninvasive AB-VNS) and a control group (coronary artery occlusion but without AB-VNS). We examined spontaneous ventricular arrhythmias, ventricular electrophysiological properties, and cardiac function in conscious dogs. Morphology, fibrosis, and ultrastructures were also assessed. AB-VNS significantly reduced the occurrence of spontaneous ventricular arrhythmias, including isolated premature ventricular complexes, ventricular couplets, ventricular bigeminy, ventricular trigeminy, and ventricular tachycardia. AB-VNS effectively increased ventricular electrical stability, including significantly prolonged ventricular effective refractory periods, decreased the dispersion of effective refractory period, enhanced the ventricular fibrillation threshold, and decreased the maximum slope of the monophasic action potential duration restitution curve. AB-VNS treatments alleviate ventricular interstitial fibrosis after MI. However, cardiac function was not improved, and MI-induced ultrastructural changes in the myocardium were not reversed by 4 weeks of AB-VNS. In addition, AB-VNS for 4 weeks resulted in mild mitochondrial swelling within the neuronal axons of the auricular vagus fiber. CONCLUSIONS: Noninvasive AB-VNS reduces the occurrence of spontaneous ventricular arrhythmias in conscious dogs with MI. AB-VNS increases ventricular electrical stability and alleviates ventricular interstitial fibrosis induced by MI.

Real-World Effectiveness of Ivabradine in Chinese Patients with Chronic Heart Failure: Interim Analysis of the POSITIVE Study.

BACKGROUND: Ivabradine improves cardiac function and clinical outcomes in chronic heart failure (HF) by reducing heart rate (HR), but there is a lack of real-world data on its effectiveness and safety in Chinese patients. METHODS: We designed a prospective, multicenter, observational study of Chinese adults with HF and left ventricular systolic dysfunction, resting HR ≥ 75 beats per minute (bpm), and an indication for ivabradine treatment. An interim analysis was performed using a cut-off date of 31 October 2019. The primary outcome was change in HR at 6 months after the initiation of ivabradine. Secondary endpoints included change in New York Heart Association (NYHA) functional class; quality of life (QoL), measured using the Kansas City Cardiomyopathy Questionnaire (KCCQ); and adverse events (AEs). RESULTS: Overall, 655 subjects were included in the interim analysis. Mean reduction in HR from baseline was 13.2 (95% confidence interval [CI] 11.2-15.2) bpm at Month 1, and 14.5 (95% CI 11.8-17.2) bpm at Month 6 (p < 0.001 for both changes). NYHA functional class and KCCQ scores improved significantly over time (p < 0.001 for all comparisons with baseline), indicating amelioration of symptoms and better QoL, respectively. Forty-four subjects (6.7%) reported a total of 60 ivabradine-related AEs, most frequently phosphenes and bradycardia (both n = 6, 0.9%). CONCLUSION: Treatment with ivabradine for 6 months effectively reduced HR and improved functional class and QoL in Chinese patients with chronic HF. Treatment was well tolerated. CLINICAL TRIAL REGISTRATION: ISRCTN11703380; registered on 8 November 2016.

Association between KCNE1 (G38S) genetic polymorphism and non-valvular atrial fibrillation in an Uygur population.

BACKGROUND: The relationship between KCNE1 G38S genetic polymorphism and non-valvular atrial fibrillation is different among different populations. The study explored the KCNE1 G38S to understand if the KCNE1 G38S is associated with the Uygur atrial fibrillation patients. METHODS: KCNE1 G38S genetic polymorphism was determined between 237 non-valvular atrial fibrillation cases and 237 control subjects using PCR-RFLP. RESULTS: In univariate analyses, there was a statistical difference in genotype distribution between the patients and controls, and a significant difference in allele frequency of KCNE1 G38S was observed between the two groups (62.6 vs 52.7 %, p = 0.003). In multivariate analyses, the KCNE1 38G variant was independently associated with a significant predisposing effect on AF after adjusting for related risk factors, and the odds ratio for patients was 1.634 (95 % CI: 1.192-2.240, p = 0.002). CONCLUSION: The KCNE1 38G is a risk factor for incident AF in an Uygur population. The KCNE1 G38S might have different impact on AF in different ethnicities.