Basic Res Cardiol 96: 91 – 97 (2001) © Steinkopff Verlag 2001 ORIGINAL CONTRIBUTION Michael A. Schäfers Thomas Wichter Klaus P. Schäfers Shakil Rahman Christopher G. Rhodes Adriaan A. Lammertsma Hartmut Lerch Markus Knickmeier Flemming Hermansen Otmar Schober Paolo G. Camici Günter Breithardt Pulmonary  adrenoceptor density in arrhythmogenic right ventricular cardiomyopathy and idiopathic tachycardia  Abstract Objective. In recent in vivo studies using positron emission tomo- graphy (PET) our group demonstrated that the myocardial  adrenoceptor (AR) density is reduced in arrhythmogenic right ventricular cardiomyopathy (ARVC) and idiopathic right ventricular outflow tract tachycardia (RVO-VT) associated with an increased presynaptic catecholamine washout. It was hypoth- esised that the reduction of myocardial AR density is secondary to an increase of local catecholamines in the myocardium resulting from the presynaptic dys- function since circulating plasma catecholamines were demonstrated to be unchanged in these conditions. To further prove this hypothesis of an organ-lim- ited adrenergic nervous dysfunction of the heart, this study aimed to investigate AR density in another thoracic organ, the lung. Methods. Pulmonary and myocardial AR density was measured in 7 ARVC patients, 8 RVO-VT patients and in a group of healthy controls (n = 13) using the non-selective -blocker [ 11 C]-CGP 12177 and PET. Results. Pulmonary AR density was similar in con- trols (12.4 ± 1.7 pmol/g tissue), ARVC (11.6 ± 1.7 pmol/g tissue, p = ns) and RVO- VT (12.8 ± 2.0 pmol/g tissue, p = ns), whereas myocardial AR density was sig- nificantly reduced in ARVC (6.3 ± 1.1 pmol/g tissue, p = 0.006) and RVO-VT (6.8 ± 1.2 pmol/g tissue, p=0.02) as compared to controls (8.8±1.5 pmol/g tissue). Conclusion. The unchanged pulmonary AR density in the presence of a previ- ously described significant reduction in myocardial AR density in the same patient principally supports our pathophysiological hypothesis that the myocar- dial AR density may be reduced in ARVC and RVO-VT because of an increase in local synaptic catecholamine levels due to an organ-limited presynaptic adrenergic dysfunction of the heart. Since in the present study only pulmonary AR density was measured, future functional studies excluding pulmonary AR desensitisation are required to finally prove the unchanged pulmonary sympa- thetic innervation in ARVC and RVO-VT.  Key words Autonomic nervous system – adrenergic – receptors – ventricular arrhythmias – positron emission tomography BRC 239 Prof. Dr. M. A. Schäfers () K. P. Schäfers · H. Lerch · M. Knickmeier O. Schober FESC Department of Nuclear Medicine Münster University Albert-Schweizer-Str. 33 48129 Münster, Germany E-mail: schafmi@uni-muenster.de T. Wichter · G. Breithardt Department of Cardiology and Angiology Münster University S. Rahman · C. G. Rhodes A. A. Lammertsma · F. Hermansen P. G. Camici FESC FACC FRCP MRC Cyclotron Unit Imperial College School of Medicine Hammersmith Hospital London, UK Current addresses Adriaan A. Lammertsmaa Academisch Ziekenhuis Vrije Universiteit Klinisch PET-centrum De Boelelaan 1117, Amsterdam, The Netherlands Flemming Hermansen Aarhus University Hospitals Pet Center Noerrebrogade 44, 8000 Aarhus, Denmark Hartmut Lerch Nuklearmedizin Klinikum Wuppertal Heusnerstr. 40, 42283 Wuppertal, Germany Received: 22 May 2000 Returned for 1. revision: 19 June 2000 1. Revision received: 5 July 2000 Returned for 2. revision: 2 August 2000 2. Revision received: 7 August 2000 Accepted: 9 August 2000