Diabetes mellitus (DM) is one of the most important risk factors for atrial fibrillation (AF) and is a predictor of stroke and thromboembolism. DM may increase the incidence of AF, and when it is combined with other risk factors, the incidence of stroke and thromboembolism may also be higher; furthermore, hospitalization due to heart failure appears to increase. Maintenance of well-controlled blood glucose and low levels of HbA1c in accordance with guidelines may decrease the incidence of AF. The mechanisms of AF associated with DM are autonomic remodeling, electrical remodeling, structural remodeling, and insulin resistance. Inhibition of the renin-angiotensin system is suggested to be an upstream therapy for this type of AF. Studies have indicated that catheter ablation may be effective for AF associated with DM, restoring sinus rhythm and improving prognosis. Catheter ablation combined with hypoglycemic agents may further increase the rate of maintenance of sinus rhythm and reduce the need for reablation.

Background. Rapid atrial pacing (RAP) can induce electrical and autonomic remodeling and facilitate atrial fibrillation (AF). Recent reports showed that low-level vagosympathetic nerve stimulation (LLVNS) can suppress AF, as an antiarrhythmic effect. We hypothesized that LLVNS can reverse substrate heterogeneity induced by RAP. Methods and Results. Mongrel dogs were divided into (LLVNS+RAP) and RAP groups. Electrode catheters were sutured to multiple atrial sites, and LLVNS was applied to cervical vagosympathetic trunks with voltage 50% below the threshold slowing sinus rate by ⩽30 msec. RAP induced a significant decrease in effective refractory period (ERP) and increase in the window of vulnerability at all sites, characterized by descending and elevated gradient differences towards the ganglionic plexi (GP) sites, respectively. The ERP dispersion was obviously enlarged by RAP and more significant when the ERP of GP-related sites was considered. Recovery time from AF was also prolonged significantly as a result of RAP. LLVNS could reverse all these changes induced by RAP and recover the heterogeneous substrate to baseline. Conclusions. LLVNS can reverse the electrical and autonomic remodeling and abolish the GP-central gradient differences induced by RAP, and thus it can recover the homogeneous substrate, which may be the underlying mechanism of its antiarrhythmic effect.

AimsPermanent pacemaker implantation (PPI) combined with hypertension leads to a higher risk of new-onset atrial fibrillation (NOAF) for patients. Hence, it is essential to study how to reduce this risk. Currently, the effects of the two common anti-hypertensive drugs, angiotensin-converting enzyme inhibitors (ACEI)/angiotensin receptor blockers (ARB) and calcium channel blockers (CCB), on the risk of NOAF for such patients remain unknown. This study aimed to investigate this association.MethodsThis single-center retrospective study included hypertensive patients with PPI and without prior history of AF/atrial flutter, heart valve disease, hyperthyroidism, etc. Patients were classified into ACEI/ARB group and CCB group based on their exposure drug information. The primary outcome was NOAF events that occurred within 12 months after PPI. The secondary efficacy assessments were the changes from baseline to follow-up in blood pressure and transthoracic echocardiography (TTE) parameters. A multivariate logistic regression model was used to verify our aim.ResultsA total of 69 patients were finally included (51 on ACEI/ARB and 18 on CCB). Both univariate analysis [odds ratio (OR) 0.241, 95% confidence interval (CI) 0.078–0.745] and multivariate analysis (OR: 0.246, 95% CI: 0.077–0.792) demonstrated that ACEI/ARB were associated with a lower risk of NOAF compared to CCB. The mean reduction in left atrial diameter (LAD) from baseline was greater in ACEI/ARB group than in CCB group (P = 0.034). There was no statistical difference between groups in blood pressure and other TTE parameters after treatment.ConclusionFor patients with PPI combined with hypertension, ACEI/ARB may be superior to CCB in selecting anti-hypertensive drugs, as ACEI/ARB further reduces the risk of NOAF. One reason for this may be that ACEI/ARB improves left atrial remodelling such as LAD better.

Key Clinical MessageThe case is a 52‐year‐old male admitted to cardiology department with chest tightness. Admission ECG showed nontypical T‐wave changes in V2–V4 leads in pain peroids, and increasing severe narrowing of proximal LAD. Cardiac enzymes were abnormal. Emergency coronary angiography showed severe stenosis (99%) in proximal LAD.

Abstract:Objective To observe the abnormal expression of IL-1βin hippocampus after bilateral common carotid artery ligation and to evaluate its effects on memory impairment induced by chronic cerebral ischemia. Methods Bilateral common carotid artery ligation (2-vessel occlusion, 2VO) was performed in wild type (Wild Type WT) and interleukin -1 receptor knock-out (IL-1 Resept Knock Out, IL-1R KO) C57 mice (male) to produce chronic cerebral ischemia mouse models. After the operation, their memory was detected with eight-arm radial maze test and the novel object recognition test, and the level of IL-1β and BDNF in hippocampus was detected with Western Blot. Results The average number of working memory errors of the KO-2VO mice was significantly decreased (P<0.05), and the recognition index was significantly increased (P<0.05) compared with those of the WT-2VO mice. Dramatic decrease in IL-1β in hippocampus (P<0.05) and substantial increase in BDNF (P<0.05) were observed in the KO-2VO mice. In the behavioral experiment and Western Blot, there was no significant difference between the KO-sham mice and the WT-sham controls. Conclusion Increase in the level of the IL-1β in hippocampus after bilateral common carotid artery ligation can lead to decrease in the level of the BDNF, which may cause memory impairment.