Mous outcome data from individual RP54476 manufacturer trials was analyzed using the risk
Mous outcome data from individual trials was analyzed using the risk ratio (RR) measure and its 95 confidence interval (CI) [19]. Overall effect was estimated using the Mantel-Haenszel method for RRs [20, 21]. Heterogeneity was evaluated using 2 tests and I2 statistics. Studies were considered statistically heterogeneous if I2 > 50 and p 0.05. If heterogeneity between studies were identified, a random-effects model was applied. Otherwise, a fixed-effects model was taken instead [22]. Publication bias was assessed with funnel plots and the Begg regression test [22]. In sensitivity analysis, we removed anyone of the study at a time and repeated the meta-analysis to ensure that no single study would be responsible for the significance of any result separately [22]. Meta-regression was conducted to explore the potential heterogeneity related to the participants (age, cause of HF, left ventricular ejection fraction, and follow-up weeks), the agent used (different types). P < 0.05 was PubMed ID:http://www.ncbi.nlm.nih.gov/pubmed/27488460 considered statistically significant [22].Tai et al. BMC Cardiovascular Disorders (2017) 17:Page 3 ofMeta-analysis was performed by the Review Manager software (Version 5.0. Copenhagen: The Nordic Cochrane Centre, the Cochrane Collaboration) and the Stata software (version 12.0; Stata Corporation, College Station, TX).ResultsEligible studies and baseline characteristicscomparator was active treatment [7, 8, 31?8]; and 9 arms (n = 20,406) compared ACEIs with PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/26104484 ARBs [9?2, 14, 39?2]). Two independent investigators (Y. X. and D. X.) assessed the quality of the studies included. There were 32 studies of good quality (Jadad score 3) with low risk of bias and six studies of low quality (Jadad score < 3) with high risk of bias.Initial search identified 1002 reference articles, of these 107 relevant articles were selected and reviewed. Then, several studies were further excluded because they were publications from the same trial (n = 7) or reported of the end points other than cardiovascular events or death (n = 15) or used RAAS inhibitors simultaneously in both trial arms (n = 7) or were not relevant (n = 40). Finally, 38 RCTs assessing the association of cardiovascular outcome or cardiovascular or total mortality with ACEIs or ARBs were included in the meta-analysis [2?4, 22?7]. As shown in Fig. 1, literature research process was summarized by a chart flow. Baseline characteristics of all selected studies are detailed in Table 1. A total of 47,662 subjects were included with a mean/median follow-up ranged from 12 weeks to 4.5 years. Of all 38 studies, six (n = 8404) trials compared ARBs with placebo [13, 43?7], while 32 trials (n = 39,254) compared ACEIs with various control therapies (13 arms (n = 10,134) compared ACEIs [2?, 23?0] with placebo treatment; 10 arms (n = 8714) in which theEffect of ACEIs and ARBs on all-cause mortalityThirty-two studies [2?2, 14, 23?2] reported the effect of ACEIs on all-cause mortality in a total of 39,254 HF patients with moderate heterogeneity in overall analysis (I2 = 44 , p = 0.005). ACEIs were associated with a statistically significant 11 reduction in all-cause mortality (RR: 0.89, 95 CI: 0.83?.96, p = 0.001, Fig. 2). Similar findings were observed when ACEIs were compared with placebo treatment (p < 0.001, Fig. 2). There was no evidence of publication bias (p = 0.833). Moreover, 15 studies [9?4, 39?7] reported the effect of ARBs on all-cause mortality in a total of 28,814 HF patients with no significant heterogeneity in overal.
