Myocardial presynaptic and postsynaptic autonomic dysfunction in hypertrophic cardiomyopathy

Michael Schäfers, David Dutka, Christopher G. Rhodes, Adriaan A. Lammertsma, Flemming Hermansen, Otmar Schober, Paolo G. Camici

Research output: Contribution to journalArticlepeer-review


Although hypertrophic cardiomyopathy (HCM) is genetically determined, several other factors, including autonomic dysfunction, may play a role in the phenotypic expression. A recent study using positron emission tomography with [11C]CGP 12177 ([11C]CGP) demonstrated that β-adrenoceptor (βAR) density is reduced in HCM and is correlated with disease progression. This present study tested the hypothesis that this downregulation is associated with reduced catecholamine reuptake (uptake 1) by myocardial sympathetic nerve terminals leading to increased local norepinephrine concentration. Myocardial presynaptic catecholamine reuptake was assessed by measuring the volume of distribution (V(d)) of the catecholamine analogue [11C]hydroxyephedrine ([11C]HED) in 9 unrelated HCM patients aged 45 ± 15 years. The maximum number of binding sites (B(max)) for myocardial βAR density was measured in 13 unrelated HCM patients aged 40 ± 12 years using the nonselective β blocker [11C]CGP. Six patients were studied with both [11C]HED and [11C]CGP. Comparison was made with two groups of healthy control subjects for each ligand ([11C]HED, n=10, aged 35 ± 8 years; [11C]CGP, n= 19, aged 44 ± 16 years). Myocardial V(d) of [11C]HED (33.4 ± 4.3 mL/g tissue) and βAR density (7.3 ± 2.6 pmol/g tissue) were significantly reduced in HCM patients compared with control subjects (71.0±18.8 mL/g tissue, P

Original languageEnglish
Pages (from-to)57-62
Number of pages6
JournalCirculation Research
Issue number1
Publication statusPublished - 1998


  • Autonomic dysfunction
  • Beta adrenoceptors
  • Cardiomyopathy, hypertrophic
  • Catecholamines
  • Positron emission tomography

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine


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