Abstract 3605: Adiponectin is Released from the Heart in Patients with Non-Ischemic Heart Failure
Plasma adiponectin (AdP) levels are decreased in ischemic heart disease (IHD), and low AdP levels predict a worse prognosis in IHD patients. However, recent studies reported that AdP levels are increased in heart failure (HF), and that high levels of AdP predict a worse prognosis in HF patients. We and others recently reported that AdP is produced and secreted from cultured cardiomyocytes. Therefore, we hypothesized that AdP may be released from the heart in HF patients, which may explain increased plasma AdP levels in HF.
Methods and Results: AdP levels in plasma from the aorta (AO), the coronary sinus (CS), and a peripheral vein (PV) were measured by ELISA in 77 consecutive HF patients with systolic left ventricular dysfunction (LV ejection fraction < 40%). They included 43 non-ischemic and 34 ischemic HF patients. Patients with renal failure (serum creatinine levels > 2.5mg/dl) were excluded. The LV ejection fraction and BNP levels were comparable between the 2 patient groups. AdP levels were also measured in 40 age- and sex-matched normal subjects. AdP levels in the PV were 2-fold higher in non-ischemic HF than ischemic HF and normals, and the levels were comparable between ischemic HF and normals (22.8 ± 2.0 μg/ml in non-ischemic HF*, 10.6 ± 0.7 μg/ml in ischemic HF, 9.9 ±0.9 ±g/ml in normals, *p < 0.01 vs. ischemic HF and normals by ANOVA). There was a significant step-up of AdP levels in the CS compared with levels in the AO in non-ischemic HF (26.1 ± 2.2 vs. 22.1 ± 1.8 μg/ml, respectively, p < 0.01) but not in ischemic HF (10.8 ± 0.8 vs. 11.1 ± 0.9 μg/ml, ns) and normals (9.7 ± 1.1 vs. 11.1 ±0.8 μg/ml, ns). The CS - AO difference in AdP levels, reflecting cardiac release of AdP, was positively correlated with the PV levels in non-ischemic HF (r = 0.63, p < 0.01) but not ischemic HF (r = − 0.20, ns). The CS - AO difference in AdP levels was positively correlated with PV levels of BNP (r = 0.49, p < 0.01) and inversely with LV ejection fraction (r =− 0.46, p < 0.01) in non-ischemic HF, while no significant correlations were observed in ischemic HF.
Conclusions: AdP is released from the heart into the peripheral circulation in proportion to the extent of LV dysfunction in non-ischemic HF but not in ischemic HF. The pathophysiological role of AdP may be different between non-ischemic and ischemic HF.