Insomnia symptoms have been suggested to be associated with the risk of cardio-cerebral events. However, the results of previous studies have been inconsistent. Therefore, we conducted a meta-analysis to examine whether there were associations between cardio-cerebral vascular events and insomnia symptoms, including difficulty initiating sleep, difficulty maintaining sleep, early-morning awakening or non-restorative sleep. A meta-analysis of prospective cohort studies. PubMed, Web of science and the Cochrane Library were searched without language restriction. Prospective cohort studies of adults with at least a 2-year follow-up duration were included. Random effect models were used in order to pool the results for each insomnia symptom. Subgroup and sensitivity analyses were conducted in order to assess potential heterogeneity, and funnel plots and Egger’s tests were used in order to assess publication bias. Fifteen studies (23 cohorts) were included. Positive associations were observed between difficulty initiating sleep, difficulty maintaining sleep and non-restorative sleep with risk of cardio-cerebral vascular events. The pooled relative risks and 95% confidence intervals were 1.27 (1.15–1.40), 1.11 (1.04–1.19) and 1.18 (1.05–1.33), respectively. However, less evidence existed to support the conclusions about the association between early-morning awakening and cardio-cerebral vascular events. Our meta-analysis demonstrated that insomnia symptoms of difficulty initiating sleep, difficulty maintaining sleep and non-restorative sleep were associated with an increased risk of future cardio-cerebral vascular events.

Background: Although several studies have explored the genetic polymorphisms of apolipoprotein E (APOE) and their impact on premature coronary artery disease (PCAD), there is still some controversy regarding the significance of their association. Our aim is to estimate the association between APOE polymorphisms and PCAD via meta-analysis. Methods: All relevant case-control studies and cohort studies published in Chinese or English prior to March 2016 were searched for in electronic databases. Detailed information concerning each piece of literature was independently extracted by two researchers. We used STATA11.0 to process all data and to determine the pooled odds ratio (OR). Altogether, four genetic models were applied to calculate OR and 95% confidence interval (CI): (1) ε2 allele vs. ε3 allele; (2) ε2 carriers vs. ε3/3; (3) ε4 allele vs. ε3 allele; (4) ε4 carriers vs. ε3/3. Results: Eighteen studies concerning APOE polymorphisms and their impact on PCAD were included in the final analysis. The pooled analysis displayed that the ε2 allele and ε2 carriers increased the risk of PCAD significantly among Asians (OR 1.54; 95% CI, 1.09–2.17; OR 1.65; 1.10–2.47), while they showed protective effects on PCAD in Caucasians (OR 0.77; 95% CI, 0.62–0.95; OR 0.69; 0.54–0.89). Subjects with the ε4 allele and ε4 carriers showed significant associations with PCAD (OR 1.62; 95% CI, 1.27–2.06; OR 1.65; 1.27–2.15). Conclusions: Our investigation supported the fact that the ε2 allele in APOE may appear as a risk factor for PCAD in Asians while a protective factor in Caucasians and that the ε4 allele acted as a genetic risk factor for PCAD.

A number of studies had reported the association between tumor necrosis factor-alpha (TNF-α) gene polymorphisms and ischemic heart disease (IHD) risk. However, the results remained controversial. Therefore, we performed a systematic review with multiple meta-analyses to provide the more precise estimations of the relationship. We systematically searched electronic databases (PubMed, the Web of Science, EMBASE, Medline, Chinese National Knowledge Infrastructure, WanFang and ChongQing VIP Database) for relevant studies published up to February 2017. The odds ratios (ORs) and 95% confidence intervals (CIs) were estimated for assessing the association. The present meta-analysis was performed using STATA 12.0 software. In total, 45 articles with 17,375 cases and 15,375 controls involved were included. Pooled ORs revealed a significant association between TNF-α −308G/A gene polymorphism and IHD (A vs. G: OR = 1.22, 95% CI = 1.10–1.35; (AA + GA) vs. GG: OR = 1.18, 95% CI = 1.03–1.36; (AA vs. (GA+GG): OR = 1.37, 95% CI = 1.08–1.75)), indicating that the TNF-α −308A allele might be an important risk factor for IHD. No association between other TNF-α gene polymorphisms and susceptibility to IHD were observed. No publication bias were found. Sensitivity analyses indicated that our results were stable. The present study indicated a possible association between the TNF-α −308G/A gene polymorphism and IHD risk. However, evidence was limited to confirm the role of TNF-α −238G/A, −857C/T, −863C/A, −1031T/C and other TNF-α gene polymorphisms in the risk of IHD.

Prognostic role of copeptin with all-cause mortality after heart failure: a systematic review and meta-analysis Peng Zhang, Xiaomei Wu, Guangxiao Li, Hao Sun, Jingpu Shi Department of Clinical Epidemiology, Center of Evidence-Based Medicine, Institute of Cardiovascular Disease, The First Hospital of China Medical University, Shenyang, People’s Republic of China Background: As the C-terminal section of vasopressin precursor, copeptin has been recently suggested as a new prognostic biomarker after heart failure (HF). Thus, the aim of this study was to evaluate the prognostic value of plasma copeptin level with all-cause mortality in patients with HF.Methods: Comprehensive strategies were used to search relevant studies from electronic databases. Pooled hazard ratios (HRs) and standardized mean differences (SMDs) together with their 95% confidence intervals (CIs) were calculated. Subgroup analysis and sensitivity analysis were performed to find the potential sources of heterogeneity.Results: A total of 5,989 participants from 17 prospective studies were included in this meta-analysis. A significant association was observed between circulating copeptin levels and risk of all-cause mortality in patients with HF (categorical copeptin: HR =1.69, 95% CI =1.42–2.01; per unit copeptin: HR =1.03, 95% CI =1.00–1.07; log unit copeptin: HR =3.26, 95% CI =0.95–11.25). Pooled SMD showed that copeptin levels were significantly higher in patients with HF who died during the follow-up period than in survivors (SMD =1.19, 95% CI =0.81–1.57). Subgroup analyses also confirmed this significant association, while sensitivity analyses indicated that the overall results were stable.Conclusion: This study demonstrated that circulating copeptin seemed to be a novel biomarker to provide better prediction of all-cause mortality in patients with HF. Keywords: heart failure, copeptin, all-cause mortality, meta-analysis