Association between alcohol consumption and incidence of type 2 diabetes mellitus in Japanese men: a secondary analysis of a Retrospective Cohort Study.

BACKGROUND: Alcohol consumption is known to be associated with an increased risk of type 2 diabetes (T2DM). However, the effect of alcohol intake on the incidence of T2DM remains controversial due to inconsistent results across studies. This study aimed to bridge the gap among available literature in order to better define the association between alcohol consumption and incidence of T2DM. METHODS: We performed a secondary analysis using open-access data from a retrospective Japanese cohort of 15,464 participants who underwent regular medical examinations at Murakami Memorial Hospital. All participants underwent an initial exam including a questionnaire survey, physical examination, and blood biochemical testing to establish a at baseline. The primary outcome was new-onset T2DM during the follow-up exam. Statistical analysis was conducted using Cox regression and Kaplan-Meier methods to assess the risk of alcohol consumption on T2DM. RESULTS: During a median follow-up time of 5.39 years, 373 new-onset T2DM events were observed. The cumulative risk of T2DM incidence was higher in the heavy alcohol consumption group vs. the other three groups: none/minimal, light, and moderate consumption (log-rank test, P = 0.0002). Multivariate Cox regression analysis indicated incidental T2DM was independently associated with alcohol consumption. The adjusted hazard ratio relative to the none/minimal consumption group was as follows: 1.02 (95% confidence interval: 0.71, 1.48) for light consumption, 1.06 (0.71, 1.57) for moderate consumption, and 2.06 (1.30, 3.24) for heavy consumption (P value = 0.024). Subsequent subgroup analysis confirmed the association between alcohol consumption and T2DM incidence in men, but not in women. CONCLUSION: Heavy alcohol consumption was independently associated with an increased risk of new-onset T2DM in Japanese men.

Eliciting α7-nAChR exerts cardioprotective effects on ischemic cardiomyopathy via activation of AMPK signalling.

Our previous studies have reported that agonist of α7 nicotinic acetylcholine receptors prevented electrophysiological dysfunction of rats with ischaemic cardiomyopathy (ICM) by eliciting the cholinergic anti-inflammatory pathway (CAP). Adenosine monophosphate-activated protein kinase (AMPK) signalling is widely recognized exerting cardioprotective effect in various cardiomyopathy. Here, we aimed to investigate whether the protective effects of the CAP are associated with AMPK signalling in ICM. In vivo, coronary artery of rats was ligated for 4 weeks to induce the ICM and then treated with PNU-282987 (CAP agonist) and BML-275 dihydrochloride (AMPK antagonist) for 4 weeks. In vitro, primary macrophages harvested from rats were induced inflammation by Lipopolysaccharide (LPS) treatment and then treated with PNU-282987 and BML-275 dihydrochloride. In vivo, exciting CAP by PUN-282987 elicited an activation of AMPK signalling, alleviated ventricular remodeling, modified the cardiac electrophysiological function, reduced the cardiac expression of collagens and inflammatory cytokines and maintained the integrity of ultrastructure in the ischemic heart. However, the benefits of CAP excitation were blunted by AMPK signaling antagonization. In vitro, excitation of the CAP was observed inhibiting the nuclear transfer of NF-κB p65 of macrophages and promoting the transformation of Ly-6Chigh macrophages into Ly-6Clow macrophages. However, inhibiting AMPK signalling by BML-275 dihydrochloride reversed the CAP effect on LPS-treated macrophages. Finally, our findings suggest that eliciting the CAP modulates the inflammatory response in ICM through regulating AMPK signalling.

Radiofrequency catheter ablation of ventricular arrhythmias arising from the region above pulmonary valve.

BACKGROUND: Ventricular arrhythmias (VAs) arising from the origin above pulmonary valve lack comprehensive investigation. This study aimed to disclose the characteristics and radiofrequency catheter ablation (RFCA) outcomes for those VAs. METHODS: One hundred six VAs arising from the region above pulmonary valve treated with RFCA were included in this study. RESULTS: Seventy-five cases were identified in the pulmonary sinus cusps (PSCs, 32 in left sinus cusp (PLC), 15 in right (PRC), 28 in anterior (PAC)) and 31 cases were in the main stem of pulmonary artery (MSPA, 18 above PLC (LMSPA), 3 above PRC (RMSPA), 10 above PAC (AMSPA)). Compared with PSCs VAs, MSPA VAs exhibited a higher R wave amplitude in the inferior leads, a total inferior R amplitude > 5.1 mV predicting MSPA origins. LMSPA, RMSPA and AMSPA VAs resembled PLC, PRC and PAC VAs in electrocardiographic characteristics respectively. No electrophysiological differences were found between PSCs and MSPA VAs. The irrigated-up catheter and R0 Swartz long sheath were more utilized for ablation of PSCs VAs than for MSPA VAs. All these VAs were successfully eliminated by RFCA. CONCLUSION: VAs arising from the origin above pulmonary valve were common. Based on certain electrocardiographic characteristics, they could be roughly located, which contributed to an effective RFCA.

Case presentation: implantation of cardiac resynchronization therapy pacemaker via the coronary sinus in a patient with triple valve replacement.

BACKGROUND: In patients with triple valve replacement developing third-degree atrioventricular block (AVB), the most appropriate approach for permanent pacemaker implantation remains questionable. CASE PRESENTATION: In this case presentation, we first described the approach of implantation of the cardiac resynchronization therapy pacemaker (CRT-P) via one bipolar pacing lead in middle cardiac vein (MCV) and one quadripolar pacing lead in anterior interventricular vein (AIV) in a patient developing complete AVB, who had been previously diagnosed with rheumatic valvular heart disease with triple valve replaced. After the CRT-P implantation, the two pacing leads in coronary sinus (CS) provided a dual-site ventricular pacing from the anterior septum and posterior septum, which resulted in a narrow QRS complex and an increased ventricular synchrony. During the long-term follow-up, no deterioration of heart function was documented and pacing parameters remained good. CONCLUSION: In this patient developing complete AVB with triple valve replaced, our approach of CRT-P implantation provides an effective and reliable ventricular pacing, and is an alternative option when transvenous right ventricular pacing, transseptal left ventricular pacing and transpericardial epicardium pacing are not possible. Further prospective randomized trials are required to confirm the efficiency of our approach of dual-site ventricular pacing by CRT-P in this kind patients.

Catheter Ablation of Ventricular Arrhythmias Originating From the Region of DGCV-AIV via a Swartz Sheath Support Approach.

Aims: This study aimed to investigate an appropriate catheter manipulation approach for ventricular arrhythmias (VAs) originating from the left ventricular epicardium adjacent to the transitional area from the great cardiac vein to the anterior interventricular vein (DGCV-AIV). Methods: A total of 123 patients with DGCV-AIV VAs were retrospectively analyzed. All these patients underwent routine mapping and ablation by conventional approach [Non-Swartz sheath support (NS) approach] firstly. In the situation of the distal portion of the coronary venous system (CVS) not being accessed or a good target site not being obtained, the Swartz sheath support (SS) approach was attempted alternatively. If this still failed, the hydrophilic coated guidewire and left coronary angiographic catheter-guided deep engagement of Swartz sheath in GCV to support ablation catheter was performed. Results: A total of 103 VAs (103/123, 83.74%) were successfully eliminated in DGCV-AIV. By NS approach, the tip of the catheter reached DGCV in 39.84% VAs (49/123), reached target sites in 35.87% VAs (44/123), and achieved successful ablation in 30.89% VAs (38/123), which was significantly lower than by SS approach (88.61% (70/79), 84.81 % (67/79), and 75.95% (60/79), P < 0.05). There were no significant differences in complication occurrence between the NS approach and the SS approach (4/123, 3.25% vs. 7/79, 8.86%, p > 0.05). The angle between DGCV and AIV <83° indicated an inaccessible AIV by catheter tip with a predictive value of 94.5%. Width/height of coronary venous system>0.69 more favored a SS approach with a predictive value of 87%. Conclusion: For radiofrequency catheter ablation (RFCA) of VAs arising from DGCV-AIV, the SS approach facilitates the catheter tip to achieve target sites and contributes to a successful ablation.

Sodium Houttuyfonate Alleviates Post-infarct Remodeling in Rats via AMP-Activated Protein Kinase Pathway.

With the chronic ischemia persisting after acute myocardial infarction, the accompanying low-degree inflammation and subsequent fibrosis result in progression of cardiac remodeling and heart failure. Recently, Sodium Houttuyfonate (SH), a pure compound extracted from Houttuynia cordata, has been confirmed exerting anti-inflammatory and anti-fibrotic effects under diseased situations. Here, we aimed to investigate whether SH could reverse the cardiac remodeling post-myocardial infarction by alleviating cardiac inflammation and fibrosis. Left anterior descending coronary artery of adult male Sprague-Dawley rats was ligated to elicit myocardial infarction. Low and high dose of SH was administered by oral gavage for four consecutive weeks post-myocardial infarction. Long-term SH treatment decreased heart rate, heart weight/ body weight (HW/BW), and left ventricle weight/body weight (LVW/BW), reduced cardiac expression of brain natriuretic peptide (BNP), improved left ventricular heart function, and ameliorated the histopathological changes caused by myocardial infarction. Western blotting revealed the expression of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), transforming growth factor-ß (TGF-ß), collagen I, and collagen III of the infarcted ventricle were reduced by SH treatment. Meanwhile, we found that SH treatment post-myocardial infarction activated AMP-activated protein kinase (AMPK) and suppressed nuclear factor-κB p65 (NF-κB p65). Furthermore, on H9C2 cells induced hypoxic injury with cobalt chloride (CoCl2), the reduction of inflammatory cytokines (IL-6, TNF-α, and TGF-ß), activation of AMPK, and suppression of NF-κB p65 were also observed by SH treatment. However, transfection of H9C2 with AMPKα siRNA blunted the suppression of NF-κB p65 and inflammatory cytokines (IL-6, TNF-α, and TGF-ß) by SH post-hypoxia. Taken together, these findings suggested that long-term administration of SH post-myocardial infarction reduced cardiac inflammatory and fibrotic responses, and reversed cardiac remodeling process. The underlying mechanism may be activating AMPK and suppressing NF-κB pathway.