Hokkaido University · Medicine
Professor Masaya Watanabe's research lab focuses on the mechanisms underlying cardiac arrhythmias in diabetes and heart failure, with a particular emphasis on atrial fibrillation and ventricular arrhythmias. The lab investigates the role of metabolic and mitochondrial dysfunction, especially in the context of diabetes-induced cardiomyopathy, and explores the cardioprotective effects of SGLT2 inhibitors like empagliflozin on ion handling, oxidative stress, and structural remodeling. Using animal models, optical mapping, and clinical translational approaches—including studies on epicardial adipose tissue and postoperative atrial fibrillation—the lab aims to uncover novel therapeutic targets for cardiac rhythm disorders.
Figures are computed from collected data and may differ slightly.
Diabetes mellitus (DM) is an independent risk of atrial fibrillation. However, its arrhythmogenic substrates remain unclear. This study sought to examine the precise propagation and the spatiotemporal dispersion of the action potential (AP) in the diabetic atrium. DM was induced by streptozotocin (65 mg/kg) in 8-wk-old male Wister rats. Optical mapping and histological analysis were performed in the right atrium (RA) from control (n = 26) and DM (n = 27) rats after 16 wk. Rate-dependent alterati
These data suggest that empagliflozin has a cardioprotective effect, at least in part, by reducing mitochondrial ROS generation through AMPK signaling pathways in the atrium of diabetic rats. This suggests that empagliflozin might suppress the development of AF in T2DM.
Diabetic cardiomyopathy has been reported to increase the risk of fatal ventricular arrhythmia. The beneficial effects of the selective sodium-glucose cotransporter-2 inhibitor have not been fully examined in the context of antiarrhythmic therapy, especially its direct cardioprotective effects despite the negligible SGLT2 expression in cardiomyocytes. We aimed to examine the antiarrhythmic effects of empagliflozin (EMPA) treatment on diabetic cardiomyocytes, with a special focus on Ca<sup>2+</su
Anatomical re-entry in ventricular tissue can be manipulated by optogenetic induction of a local and reversible conduction block in the re-entrant pathway, allowing effective re-entry termination. These results provide distinctively new mechanistic insight into re-entry termination and a novel perspective for cardiac arrhythmia management.
Epicardial adipose tissue (EAT) is an active endocrine organ that is closely associated with occurrence of atrial fibrillation (AF). However, the role of EAT in the development of postoperative AF (POAF) remains unclear. We aimed to investigate the association between EAT profile and POAF occurrence in patients who underwent cardiovascular surgery. We obtained EAT samples from 53 patients to evaluate gene expression, histological changes, mitochondrial oxidative phosphorylation (OXPHOS) capacity
Two women (16-year-old, 54-year-old) of atrial septal defect with absence of right superior vena cava and persistent left superior vena cava were successfully operated on. Electrocardiographic findings show coronary sinus rhythm and atrial fibrillation. When we closed atrial septal defect cannulated to persistent left superior vena cava via the coronary sinus directly, sick sinus syndrome was not appeared postoperatively.
Electrical storm (ES), defined by 3 or more occurrences of ventricular arrhythmias within 24 hours, has been shown to be associated with an increased risk of mortality; however, detailed information remains lacking. We aimed to examine the incidence and determinants of ES and its impact on mortality in patients enrolled in the nationwide implantable cardioverter-defibrillator (ICD) registry.We studied 1,256 patients (age 65 ± 12 years) who had structural heart disease with an ICD. The patients w
Intraoperative ventricular tachycardia (VT) ablation targeting the epicardial substrate using three-dimensional electroanatomic mapping (EAM) was performed during left ventricular assist device (LVAD) implantation. We proved that EAM can be safely performed during LVAD implantation and that an ablation strategy based on electrophysiological information may reduce VT recurrence after LVAD implantation. A left ventricular assist device (LVAD) is a therapeutic option in advanced heart failure. Vent
Atrial fibrillation (AF) is associated with electrical remodeling processes that promote a substrate for the maintenance of AF. Although the small-conductance Ca<sup>2+</sup>-activated K<sup>+</sup> (SK) channel is a key factor in atrial electrical remodeling, the mechanism of its activation remains unclear. Regional nitric oxide (NO) production by neuronal nitric oxide synthase (nNOS) is involved in atrial electrical remodeling. In this study, atrial tachyarrhythmia (ATA) induction and optical
Long-term investigation of a male case of Landau-Kleffner syndrome with auditory, verbal and non-verbal agnosia was performed clinico-electroencephalographically and neuropsychologically. Atypical absences and secondarily generalized tonic-clonic seizures were observed. The spike-wave index of slow wave sleep from all-night EEG recordings was 96% in this case. It was impossible to differentiate this case from epilepsy with "continuous spikes and waves during slow wave sleep (CSWS)" except the pr
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