Summary: Aims: This systematic review and meta‐analysis evaluated the associations between shift work patterns and risks of specific types of obesity.Methods: PubMed was searched until March 2017 for observational studies that examined the relationships between shift work patterns and obesity. Odds ratio for obesity was extracted using a fixed‐effects or random‐effects model. Subgroup meta‐analyses were carried out for study design, specific obesity types and characteristics of shift work pattern.Results: A total of 28 studies were included in this meta‐analysis. The overall odds ratio of night shift work was 1.23 (95% confidence interval = 1.17–1.29) for risk of obesity/overweight. Cross‐sectional studies showed a higher risk of 1.26 than those with the cohort design (risk ratio = 1.10). Shift workers had a higher frequency of developing abdominal obesity (odds ratio = 1.35) than other obesity types. Permanent night workers demonstrated a 29% higher risk than rotating shift workers (odds ratio 1.43 vs. 1.14).Conclusion: This meta‐analysis confirmed the risks of night shift work for the development of overweight and obesity with a potential gradient association suggested, especially for abdominal obesity. Modification of working schedules is recommended, particularly for prolonged permanent night work. More accurate and detailed measurements on shift work patterns should be conducted in future research.

Background: Diabetes mellitus is an important risk factor for atrial fibrillation (AF) development. Sodium–glucose co-transporter-2 (SGLT-2) inhibitors are used for the treatment of type 2 diabetes mellitus (T2DM). Their cardioprotective effects have been reported but whether they prevent AF in T2DM patients are less well-explored. We tested the hypothesis that the SGLT-2 inhibitor, empagliflozin, can prevent atrial remodeling in a diabetic rat model. Methods: High-fat diet and low-dose streptozotocin (STZ) treatment were used to induce T2DM. A total of 96 rats were randomized into the following four groups: (i) control (ii) T2DM, (iii) low-dose empagliflozin (10 mg/kg/day)/T2DM; and (iv) high-dose empagliflozin (30 mg/kg/day)/T2DM by the intragastric route for 8 weeks. Results: Compared with the control group, left atrial diameter, interstitial fibrosis and the incidence of AF inducibility were significantly increased in the DM group. Moreover, atrial mitochondrial respiratory function, mitochondrial membrane potential, and mitochondrial biogenesis were impaired. Empagliflozin treatment significantly prevented the development of these abnormalities in DM rats, likely via the peroxisome proliferator-activated receptor-c coactivator 1α (PGC-1α)/nuclear respiratory factor-1 (NRF-1)/mitochondrial transcription factor A (Tfam) signaling pathway. Conclusions: Empagliflozin can ameliorate atrial structural and electrical remodeling as well as improve mitochondrial function and mitochondrial biogenesis in T2DM, hence may be potentially used in the prevention of T2DM-related atrial fibrillation.

Blood circulation is the result of the beating of the heart, which provides the mechanical force to pump oxygenated blood to, and deoxygenated blood away from, the peripheral tissues. This depends critically on the preceding electrical activation. Disruptions in the orderly pattern of this propagating cardiac excitation wave can lead to arrhythmias. Understanding of the mechanisms underlying their generation and maintenance requires knowledge of the ionic contributions to the cardiac action potential, which is discussed in the first part of this review. A brief outline of the different classification systems for arrhythmogenesis is then provided, followed by a detailed discussion for each mechanism in turn, highlighting recent advances in this area.

Atrial fibrillation (AF) has different underlying substrates. Atrial remodeling involves electrophysiological and structural abnormalities that promote the development and perpetuation of AF. Experimental and clinical data indicate that inflammation is implicated in the pathophysiology of atrial remodeling. The mechanistic links between atrial remodeling and inflammation are complex while diverse underlying diseases and conditions may affect these pathways. Inflammatory markers have also been associated with AF development, recurrence, perpetuation, total AF burden as well as with thromboembolic complications. The development of specific anti‐inflammatory interventions in this setting seems to be challenging and complicated. Several agents with pleiotropic properties, including anti‐inflammatory, have been tested in experimental and clinical settings with variable results. This updated review provides a concise overview of all available data regarding the role of inflammation in AF including the predictive role of inflammatory markers. Also, current knowledge and future directions on anti‐inflammatory strategies are critically discussed.

Sudden cardiac death, frequently due to ventricular arrhythmias, is a significant problem globally. Most affected individuals do not arrive at hospital in time for medical treatment. Therefore, there is an urgent need to identify the most-at-risk patients for insertion of prophylactic implantable cardioverter defibrillators. Clinical risk markers derived from electrocardiography are important for this purpose. They can be based on repolarization, including corrected QT (QT_c) interval, QT dispersion (QT_D), interval from the peak to the end of the T-wave (T_peak – T_end), (T_peak – T_end)/QT, T-wave alternans (TWA), and microvolt TWA. Abnormal repolarization properties can increase the risk of triggered activity and re-entrant arrhythmias. Other risk markers are based solely on conduction, such as QRS duration (QRS_d), which is a surrogate marker of conduction velocity (CV) and QRS dispersion (QRS_D) reflecting CV dispersion. Conduction abnormalities in the form of reduced CV, unidirectional block, together with a functional or a structural obstacle, are conditions required for circus-type or spiral wave re-entry. Conduction and repolarization can be represented by a single parameter, excitation wavelength (λ = CV × effective refractory period). λ is an important determinant of arrhythmogenesis in different settings. Novel conduction–repolarization markers incorporating λ include Lu et al.' index of cardiac electrophysiological balance (iCEB: QT/QRS_d), [QRS_D× (T_peak − T_end)/QRS_d] and [QRS_D × (T_peak − T_end)/(QRS_d × QT)] recently proposed by Tse and Yan. The aim of this review is to provide up to date information on traditional and novel markers and discuss their utility and downfalls for risk stratification.