Cardiac sympathetic innervation in patients with idiopathic right ventricular outflow tract tachycardi

Objectives. This study investigated the neuronal reuptake of norepinephrine (uptake-1) and the beta-adrenoceptor density in patients with idiopathic right ventricular outflow tract tachycardi (RVO-VT). Background. Clinical findings, such as the inducibility of ventricular tachycardi by stress or catecholamine infusion, and the therapeutic efficacy of antiarrhythmic drugs with antiadrenergic properties suggest abnormalities of cardiac sympathetic innervation in patients with idiopathic RVO-VT. Methods. Eight patients with idiopathic RVO-VT and total of 29 age-matched control subjects were investigated by positron emission tomography using [11C]hydroxyephedrine (HED) (volume of distribution of [11C]HED) to assess presynaptic norepinephrine reuptake; [11C]CGP 12177 (maximal binding capacity of [11C]CGP 12177) to measure postsynaptic beta-adrenoceptor density; and oxygen-15–labeled water for quantification of myocardial blood flow (MBF). Results. Both myocardial catecholamine reuptake and beta-adrenoceptor density were significantly reduced in patients with idiopathic RVO-VT. The volume of distribution of [11C]HED in patients with RVO-VT was (mean ± SD) 41.0 ± 13.5 versus 71.0 ± 18.8 ml/g in control subjects (p < 0.002). The maximal binding capacity of the beta-adrenoceptor antagonist [11C]CGP 12177 was 6.8 ± 1.2 pmol/g in patients with RVO-VT versus 10.2 ± 2.9 pmol/g in control subjects (p < 0.004). There were no significant differences in MBF at rest (0.98 ± 0.14 vs. 0.97 ± 0.24 ml/min per g, p = NS) between patients with RVO-VT and control subjects. Conclusions. The findings of the present study suggest that myocardial beta-adrenoceptor downregulation in patients with RVO-VT occurs subsequently to increased local synaptic catecholamine levels caused by impaired catecholamine reuptake.