doi: 10.1161/CIRCULATIONAHA.106.671289
(Circulation. 2007;115:e323.)
© 2007 American Heart Association, Inc.
Correspondence |
Response to Letter Regarding Article, "Adiponectin and Coronary Heart Disease: A Prospective Study and Meta-Analysis"
University Department of Vascular Biochemistry, Glasgow, Scotland
Department of Primary Care and Population Sciences, Royal Free UCL Medical School, London, England
Department of Public Health and Primary Care, University of Cambridge, Cambridge, England
Division of Community Health Sciences, St George’s, University of London, London, England
We thank Dr Pischon and colleagues for their interest in our work.1 We have reported the largest single prospective population-based study of adiponectin levels and coronary heart disease thus far, reinforced by a meta-analysis of 6 previous studies totaling 1313 incident cases.1 Overall, the adjusted risk ratio for coronary heart disease was 0.84 (95% CI: 0.70 to 1.01) in a comparison of individuals in the top third with those in the bottom third of baseline adiponectin concentrations, and there was no evidence of heterogeneity among the 7 reports (
2=8.4; P=0.21; I2=29% [95% CI: 0% to 69%]). We analyzed the new data using different cut points, such as comparisons of extreme fifths (adjusted odds ratio: 1.12; 95% CI: 0.75 to 1.66) and per 50% increase in loge adiponectin levels (adjusted odds ratio: 1.02; 95% CI: 0.93 to 1.12). Although the available evidence suggests that adiponectin levels are less strongly associated with coronary heart disease risk than was previously suspected, we have stated that further data are needed.
Pischon et al draw attention to potential underestimation of effects due to prolonged storage of serum samples at –20°C. We have acknowledged this possibility, but we also have noted that it was unlikely to be a major factor because (1) adiponectin concentrations (and correlations with several risk markers) in our study were comparable with those previously reported,2–4 and (2) adiponectin concentrations were reasonably stable for a 4-year duration in paired measurements (self-correlation coefficient: 0.58; 95% CI: 0.49 to 0.66), reflecting our study’s reasonably robust sample storage and assay methods. There are no data suggesting that adiponectin is influenced by delayed measurement, prolonged storage, or repeated freeze–thaw cycles, but we agree that such considerations merit further study. The assay method attributed to the study of Zoccali et al5 in Table 4 of our report was incorrectly stated as the assay by Linco (St Charles, Mo); it was an in-house ELISA (leptin levels in this study were measured with the radioimmunoassay adiponectin assay kit described). The study of Wolk et al6 did use the radioimmunoassay adiponectin assay kit by Linco, but on frozen rather than fresh blood samples. Five of the 6 principal investigators of previous studies (including Wolk,6 who have published on leptin levels) have provided standard comparisons of odds ratios for coronary heart disease adjusted for at least age, sex, smoking, blood pressure, and lipids (the majority involving further adjustment for markers of adiposity). This information enabled reasonable consistency of data analysis in our literature-based review, but, as implied by Pischon et al3, more detailed pooling of available data (such as on the basis of individual-participant meta-analysis) would be required to achieve even greater consistency.
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Acknowledgments |
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Disclosures
None.
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References |
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