Adiponectin and risk for future CHD/stroke
RESULTS Selection of studies evaluating the risk of adiponectin on coronary heart disease After selection of 6,143 potentially relevant articles, 129 articles were evaluated in detail. Twenty articles (19,20,24–41) were considered eligible for meta-analyses as they met the inclusion criteria. Of these articles, four publications (36–39) were additionally excluded since results based upon the same data were published elsewhere (25,28,30). For duplicate publications, only the first published manuscript was included in analyses. Two articles (40,41) provided insufficient data, leaving a final number of 14 articles which were used for meta-analyses as is shown in Figure 1. Of these 14 included articles, two articles were based upon data derived from the same cohort (33,35). Both studies were included as they were used for separate analyses. Study characteristics of all 14 included studies are displayed in Table 1. Descriptions of the study outcomes and effect estimates are presented in Tables 2 and 3, respectively. Included articles were published in the period 2004– 2012 and were either nested casecontrol studies (18,19,24–26,30–33,35) or cohort studies (27–29,34). In total, data of 21,272 patients with valid adiponectin measurements were available in which 5,790 CHD outcome events occurred. The mean age varied from 53 to 75 years and patients originated from various (mostly Western) countries. Risk of adiponectin on coronary heart disease events No statistically significant associations between adiponectin concentration and incident CHD were found as 1 SD increase in log-transformed adiponectin was accompanied by a RR of 0.97 (95% CI 0.87–1.09) for CHD (Figure 2). The I2 was 64%, indicating moderate to substantial between study heterogeneity. With regard to this heterogeneity, stratified analyses were performed, which did not identify specific effect modifiers (Table 4). All studies were considered of high quality as they scored _6 on the Newcastle- Ottawa Scale. The funnel plot was symmetrically shaped (Figure not shown), and neither the Begg test (P = 0.25) nor the Egger test (P = 0.35) suggested publication bias. Using GLS, including the data of eight studies (18, 19,25,26,28,30,31,35), which led to 10 data points, comprising 3,184 CHD events among 11,452 patients, 10 µg mL-1 adiponectin increase effectuated a RR of 0.91 (95% CI 0.80–1.03). The corresponding forest plot is displayed in Figure 3. The Begg adjusted rank correlation test (P = 0.93) nor Egger regression test (P = 0.76) suggested publication bias. Sensitivity analyses for the relation between adiponectin and coronary heart disease risk In sensitivity analyses, none of the individual studies substantially altered the pooled RRs, which varied from 0.94 (95%C I 0.84–1.06) to 1.01 (95% CI 0.91–1.11) per 1 SD increase in log-transformed adiponectin. The sensitivity analyses were done by omitting one study at a time in a stepwise procedure and calculating the pooled RR for the remainder of the studies. In addition, a fixed-effects model instead of a random-effects model resulted comparable pooled RRs for CHD (RR 1.01; 95% CI 0.95–1.06 vs. RR 0.97;
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