Pulmonary β adrenoceptor density in arrhythmogenic right ventricular cardiomyopathy and idiopathic tachycardia

M. A. Schäfers, T. Wichter, K. P. Schäfers, S. Rahman, C. G. Rhodes, A. A. Lammertsma, H. Lerch, M. Knickmeier, F. Hermansen, O. Schober, P. G. Camici, G. Breithardt

Research output: Contribution to journalArticlepeer-review


Objective. In recent in vivo studies using positron emission tomography (PET) our group demonstrated that the myocardial β adrenoceptor (βAR) 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 hypothesised that the reduction of myocardial βAR density is secondary to an increase of local catecholamines in the myocardium resulting from the presynaptic dysfunction since circulating plasma catecholamines were demonstrated to be unchanged in these conditions. To further prove this hypothesis of an organ-limited adrenergic nervous dysfunction of the heart, this study aimed to investigate βAR density in another thoracic organ, the lung. Methods. Pulmonary and myocardial βAR density was measured in 7 ARVC patients, 8 RVO-VT patients and in a group of healthy controls (n = 13) using the non-selective β-blocker [11C]-CGP 12177 and PET. Results. Pulmonary βAR density was similar in controls (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 βAR density was significantly 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 βAR density in the presence of a previously described significant reduction in myocardial βAR density in the same patient principally supports our pathophysiological hypothesis that the myocardial βAR 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 βAR density was measured, future functional studies excluding pulmonary βAR desensitisation are required to finally prove the unchanged pulmonary sympathetic innervation in ARVC and RVO-VT.

Original languageEnglish
Pages (from-to)91-97
Number of pages7
JournalBasic Research in Cardiology
Issue number1
Publication statusPublished - 2001


  • Adrenergic
  • Autonomic nervous system
  • Positron emission tomography
  • Receptors
  • Ventricular arrhythmias

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine


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