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CLINICAL STUDIES

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

Michael Schäfers, MD^* , Hartmut Lerch, MD^*, Thomas Wichter, MD^*, Christopher G. Rhodes, MSc, Adriaan A. Lammertsma, PhD, Martin Borggrefe, MD^*, Flemming Hermansen, MD, Otmar Schober, MD, PhD^*, G.ünter Breithardt, MD, FESC, FACC^* and Paolo G. Camici, MD, FESC, FACC, FRCP

^* Department of Nuclear Medicine and Department of Cardiology and Angiology and Institute for Arteriosclerosis Research, Westfälische Wilhelms University, Munster, Germany
Medical Research Council–Cyclotron Unit and Imperial College School of Medicine, Hammersmith Hospital, London, England, United Kingdom

Manuscript received October 8, 1997; revised manuscript received March 27, 1998, accepted April 9, 1998.

Address for correspondence: Dr. Paolo G. Camici, Medical Research Council–Cyclotron Unit, Hammersmith Hospital, Ducane Road, W12 ONN, London, England, United Kingdom
paolo{at}cu.rpms.ac.uk

Objectives. This study investigated the neuronal reuptake of norepinephrine (uptake-1) and the beta-adrenoceptor density in patients with idiopathic right ventricular outflow tract tachycardia (RVO-VT).

Background. Clinical findings, such as the inducibility of ventricular tachycardia 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 a 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.

Abbreviations and Acronyms   Bmax = maximal binding capacity   BGO = bismuth germanate   [11C]HED = [11C]hydroxyephedrine   MBF = myocardial blood flow   [123I]MIBG = [123I]meta-iodo-benzylguanidine   PET = positron emission tomography (tomographic)   ROI = region of interest   RVO-VT = right ventricular outflow tract tachycardia   Vd = volume of distribution

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