Relationship among neuropeptide Y, catecholamines and haemodynamics in congestive heart failure

The relationship among neuropeptide Y (NPY), catecholamines and haemodynamics was assessed both at baseline and during inotropic intervention in patients with congestive heart failure. Eighteen patients with idiopathic dilated cardiomyopathy (left ventricular ejection fraction (LVEF) = 26± 10%) underwent both right and left catheterization. Haemodynamicparameters were recorded at baseline and during dobutamine infusion. To measure norepinephrine (NE), epinephrine (E) (nmol. l−1: radioenzymatic assay) and NPY (pmol. l−1: immunoradiometric assay) plasma concentrations, blood samples were drawn from the femoral artery and from the coronary sinus, both at baseline and during dobutamine infusion. At baseline, NPY concentration were 2·15±0·97pmol.l−1 in the femoral artery and 1 ·97 ±0·63 pmol. l−1 in the coronary sinus. Peripheral concentrations of NPY were, however, no different from those of patients without congestive heart failure: 2·4±2·7pmol. l−1. Peripheral NE concentration was correlated to haemodynamic parameters: L VEF (r= — 0·65; P<0·01), cardiac index (r = — 0·54; P < 0·05), L Vend-diastolic pressure (r= +0-59; P<005), while peripheral N PY and E concentrations were not. Dobutamine improved haemodynamics, since cardiac index increased by 30% and LV end-diastolic pressure decreased by 40% (P<0·01). Peripheral NE concentration decreased from 6·48 + 4·5 to 482 ±2·69 nmol. l−1(P<0·05) but there was no change in E (0·99±0·61 vs 1·04 + 0·74 nmol .l−1) or NPY concentrations (2·41 + 0·99pmol. l−1). In the coronary sinus, neither NE nor NPY concentrations changed during dobutamine infusion. Thus, low levels of peripheral and coronary sinus NPY concentrations may not render the action of circulating NP Y deleterious to failing hearts. NE but not NP Y is related to haemodynamic parameters. When sympathetic tone decreases, NE and NPY seem to have different patterns of release. However, NPY's local role in neurotransmission in the pathogenesis of congestive heart failure should not be ruled out.