CARDIAC SYMPATHETIC INNERVATION IN PATIENTS WITH IDIOPATHIC RIGHT-VENTRICULAR OUTFLOW TRACT TACHYCARDIA

Objectives. This study investigated the neuronal reuptake of norepinep hrine (uptake-1) and the beta-adrenoceptor density in patients,vith id iopathic right ventricular outflow tract tachycardia (RVO-VT). Backgro und. Clinical findings, such as the inducibility of ventricular tachyc ardia by stress or catecholamine infusion, and the therapeutic efficac y of antiarrhythmic drugs with antiadrenergic properties suggest abnor malities of cardiac sympathetic innervation in patients,vith idiopathi c RVO-VT. Methods. Eight patients with idiopathic RVO-VT and a total o f 29 age-matched control subjects were investigated by positron emissi on tomography using [C-11] hydroxyephedrine (HED) (volume of distribut ion of [C-11]HED) to assess presynaptic norepinephrine reuptake; [C-11 ] CGP 12177 (maximal binding capacity of [C-11]CGP 12177) to measure p ostsynaptic beta-adrenoceptor density; and oxygen-15-labeled water for quantification of myocardial blood flow (MBF). Results. Both myocardi al catecholamine reuptake and beta adrenoceptor density were significa ntly reduced in patients with idiopathic RVO-VT. The volume of distrib ution of [C-11]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 ma ximal binding capacity of the beta-adrenoceptor antagonist [C-11] 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 d ifferences 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. Conclusi ons. The findings of the present study suggest that myocardial beta-ad renoceptor downregulation in patients with RVO-VT occurs subsequently to increased local synaptic catecholamine levels caused by impaired ca techolamine reuptake.