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We thank Dr Ferrante et al.1 for their interest in our work. By enrolling consecutive cath lab patients in the AtheroGene cohort, we had the opportunity to evaluate adiponcetin concentrations across the entire range of coronary artery disease (CAD) patients. This may be seen as an advantage, but also implies heterogeneity of the cohort which we addressed by presenting our data in the more homogenous subgroups of patients with stable angina (SAP) and acute coronary syndrome (ACS). In ACS, we observe a similar magnitude and direction of association. Especially in the categorical analysis, it becomes obvious that high concentrations of adiponectin may be related to higher cardiovascular event rates that can be viewed as confirmatory.2 For survival analysis, we do provide the number of events, which shows, as expected, a higher event rate for ACS patients. These hypothesis generating results need to be prospectively confirmed in ACS cohorts.3

We did not exclude participants on the basis of B-type natriuretic peptide (BNP) concentrations. In Model 2 of the statistical regression analysis, adjusting for ACS, adiponectin concentrations remain related to outcome at the 0.05 level. Only after additional adjustment for BNP in the last model, the association becomes borderline when based on the statistical cut-off of 0.05. The effect size and direction remain approximately the same. Two reasons may, in part, account for this: (i) we did not have BNP measurements in all participants, which reduces the power to achieve a statistical threshold, (ii) a positive correlation between adiponectin and BNP is known,4 which often weakens the effect in a regression analysis.

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