Efficacy of radiofrequency catheter ablation for premature ventricular contractions in children.

PURPOSE: This study evaluated the efficacy and safety of transcatheter radiofrequency ablation (RFCA) in treating ventricular premature contractions (PVCs) in children, summarized the countermeasures during intraoperative ventricular fibrillation (VF), and improved the safety of ventricular premature treatment. METHODS: A retrospective analysis was conducted on 75 children with PVCs who received RFCA in the Second Affiliated Hospital of Wenzhou Medical University from January 2010 to April 2019. Data including age, sex, body weight, ejection fraction, left ventricular end diastolic diameter, burden and number of PVCs/24 h, origin of PVCs, and its complications were collected. Paired t test was used to compare changes in cardiac function before and after surgery. RESULTS: Among the 75 cases treated with RFCA, 68 were successfully ablated, giving a success rate of 90.67%. After ablation, the left ventricular ejection fraction (LVEF) of the children was 69.13 ± 3.81%, which was significantly higher than that before surgery (69.13 ± 3.81% vs. 66.21 ± 3.22%, P = 0.012). One of the patients experienced VF during the operation, with no other complications. The initial locus of origin was the anterior septum of the right ventricular outflow tract, but VF occurred during the ablation process. Mean follow-up time was 39 ± 33 months, with two recurrent cases (2.94%). CONCLUSIONS: Performing RFCA in children is safe and effective, with a low recurrence rate and few complications. VF is not an indication to cease surgery; the key to eliminating complications is repositioning the catheter and finding a more accurate origin point.

Neuroprotective Effects of Adenosine A1 Receptor Signaling on Cognitive Impairment Induced by Chronic Intermittent Hypoxia in Mice.

Obstructive sleep apnea-hypopnea syndrome (OSAHS) is a breathing disorder associated with cognitive impairment. However, the mechanisms leading to cognitive deficits in OSAHS remain uncertain. In this study, a mouse model of chronic intermittent hypoxia (CIH) exposures were applied for simulating the deoxygenation-reoxygenation events occurring in OSAHS. The conventional adenosine A1 receptor gene (A1R) knockout mice and the A1R agonist CCPA- or antagonist DPCPX-administrated mice were utilized to determine the precise function of A1R signaling in the process of OSAHS-relevant cognitive impairment. We demonstrated that CIH induced morphological changes and apoptosis in hippocampal neurons. Further, CIH blunted hippocampal long-term potentiation (LTP) and resulted in learning/memory impairment. Disruption of adenosine A1R exacerbated morphological, cellular, and functional damage induced by CIH. In contrast, activation of adenosine A1R signaling reduced morphological changes and apoptosis of hippocampal neurons, promoted LTP, and enhanced learning and memory. A1Rs may up-regulate protein kinase C (PKC) and its subtype PKC-ζ through the activation of Gα(i) improve spatial learning and memory disorder induced by CIH in mice. Taken together, A1R signaling plays a neuroprotective role in CIH-induced cognitive dysfunction and pathological changes in the hippocampus.