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

Michael Schäfers, Hartmut Lerch, Thomas Wichter, Christopher G. Rhodes, Adriaan A. Lammertsma, Martin Borggrefe, Flemming Hermansen, Otmar Schober, Günter Breithardt, Paolo G. Camici

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Abstract

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.

Original languageEnglish
Pages (from-to)181-186
Number of pages6
JournalJournal of the American College of Cardiology
Volume32
Issue number1
DOIs
Publication statusPublished - Jul 1998

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Tachycardia
Adrenergic Receptors
Catecholamines
Norepinephrine
Adrenergic Antagonists
Anti-Arrhythmia Agents
Ventricular Tachycardia
Positron-Emission Tomography
Down-Regulation
Oxygen
Water
CGP 12177

ASJC Scopus subject areas

  • Nursing(all)

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Cardiac sympathetic innervation in patients with idiopathic right ventricular outflow tract tachycardia. / Schäfers, Michael; Lerch, Hartmut; Wichter, Thomas; Rhodes, Christopher G.; Lammertsma, Adriaan A.; Borggrefe, Martin; Hermansen, Flemming; Schober, Otmar; Breithardt, Günter; Camici, Paolo G.

In: Journal of the American College of Cardiology, Vol. 32, No. 1, 07.1998, p. 181-186.

Research output: Contribution to journalArticle

Schäfers, M, Lerch, H, Wichter, T, Rhodes, CG, Lammertsma, AA, Borggrefe, M, Hermansen, F, Schober, O, Breithardt, G & Camici, PG 1998, 'Cardiac sympathetic innervation in patients with idiopathic right ventricular outflow tract tachycardia', Journal of the American College of Cardiology, vol. 32, no. 1, pp. 181-186. https://doi.org/10.1016/S0735-1097(98)00213-7
Schäfers, Michael ; Lerch, Hartmut ; Wichter, Thomas ; Rhodes, Christopher G. ; Lammertsma, Adriaan A. ; Borggrefe, Martin ; Hermansen, Flemming ; Schober, Otmar ; Breithardt, Günter ; Camici, Paolo G. / Cardiac sympathetic innervation in patients with idiopathic right ventricular outflow tract tachycardia. In: Journal of the American College of Cardiology. 1998 ; Vol. 32, No. 1. pp. 181-186.
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abstract = "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.",
author = "Michael Sch{\"a}fers and Hartmut Lerch and Thomas Wichter and Rhodes, {Christopher G.} and Lammertsma, {Adriaan A.} and Martin Borggrefe and Flemming Hermansen and Otmar Schober and G{\"u}nter Breithardt and Camici, {Paolo G.}",
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T1 - Cardiac sympathetic innervation in patients with idiopathic right ventricular outflow tract tachycardia

AU - Schäfers, Michael

AU - Lerch, Hartmut

AU - Wichter, Thomas

AU - Rhodes, Christopher G.

AU - Lammertsma, Adriaan A.

AU - Borggrefe, Martin

AU - Hermansen, Flemming

AU - Schober, Otmar

AU - Breithardt, Günter

AU - Camici, Paolo G.

PY - 1998/7

Y1 - 1998/7

N2 - 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.

AB - 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.

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