Higher baseline adiponectin concentrations were associated with an increased risk of cardiovascular events in patients with manifest coronary artery disease (HR 1.02; 95% CI 1.0-1.04; P=0.012).
Cohort (n=1,890)
Effect estimate: HR 1.02 (95% CI 1.0-1.04)
p-value: p=0.012
AIMS: In primary prevention, the adipocytokine adiponectin seems to be protective against diabetes mellitus and cardiovascular disease. Data in patients with manifest coronary artery disease (CAD) are scant stimulating the investigation of the association of adiponectin concentrations and cardiovascular outcome in a prospective CAD cohort. METHODS AND RESULTS: In 1890 consecutive patients with documented CAD 1130 with stable angina (SAP) and 760 with acute coronary syndrome (ACS) baseline concentrations of adiponectin were measured by enzyme-linked immuno assay. During a median follow-up of 2.5 years cardiovascular events were registered (cardiovascular deaths 70; non-fatal myocardial infarction 46). Baseline adiponectin concentrations were similar in patients presenting with SAP 9.03 microg/mL (6.7, 13.45) or ACS 9.19 microg/mL (6.72, 13.15), P = 0.779. Kaplan-Meier survival analysis showed a stepwise decrease in event-free survival across quartiles of adiponectin baseline concentration (P log rank = 0.0188). A similar pattern was observed in both subgroups of patients (SAP P = 0.075 and ACS P = 0.254). In univariate analyses, continuous adiponectin concentration was related to event-free survival in all patients HR 1.02 (95% confidence interval 1.0-1.04), P = 0.012 as well as in the subgroup of SAP subjects 1.03 (1.01-1.05), P = 0.012. The relation was less strong in the subgroup presenting with ACS 1.014 (0.99-1.04), P = 0.280. A correlation of adiponectin with high density cholesterol (r = 0.39) and a negative relation to triglyceride levels (r = -0.22) could be described. An increase of one interquartile distance in adiponectin concentration was associated with a 1.17-fold risk for future cardiovascular events (P = 0.013), in B-type natriuretic peptide (BNP) it meant a 1.13-fold risk (P < 0.001). In the overall patient group, this risk association remained robust after the adjustment for classical risk factors, clinical presentation and cardiac medication. Only after adjustment for BNP adiponectin lost its independent predictive value. CONCLUSION: In contrast to studies including initially healthy individuals, the current prospective study demonstrates that adiponectin is associated with adverse cardiovascular outcome in patients with manifest CAD.
Schnabel et al. (Sun,) conducted a cohort in Coronary artery disease (n=1,890). Adiponectin concentration was evaluated on Cardiovascular events (cardiovascular deaths and non-fatal myocardial infarction) (HR 1.02, 95% CI 1.0-1.04, p=0.012). Higher baseline adiponectin concentrations were associated with an increased risk of cardiovascular events in patients with manifest coronary artery disease (HR 1.02; 95% CI 1.0-1.04; P=0.012).
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