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a Medizinische Klinik
II, Medizinische Universität zu Lübeck, Ratzeburger Allee 160, D-23538 Lübeck, Germany, b 1. Medizinische Klinik, Klinikum rechts der
Isar, TU München, München, Germany, c Nuklearmedizinische Klinik und
Poliklinik, Klinikum rechts der Isar, TU München, München, Germany
Correspondence to: Dr Hartmann. email: hartmann{at}medinf.muluebeck.de
Accepted for publication 13 October 1998
OBJECTIVE
To
assess presynaptic function of cardiac autonomic innervation in
patients with advanced congestive heart failure using positron emission
tomography (PET) and the recently developed radiolabelled catecholamine
analogue carbon-11 hydroxyephedrine (HED) as a marker for neuronal
catecholamine uptake function.
DESIGN AND PATIENTS29
patients suffering from dilated cardiomyopathy with moderate to severe
heart failure were compared with eight healthy controls. Perfusion scan
was followed by HED dynamic PET imaging of cardiac sympathetic
innervation. The scintigraphic results were compared with markers of
disease severity and the degree of sympathetic dysfunction assessed by
means of heart rate variability.
RESULTSIn contrast to
nearly normal perfusions, mean (SD) HED retention in dilated
cardiomyopathy patients was abnormal in 64 (32)% of the left
ventricle. Absolute myocardial HED retention was 10.7 (1.0)%/min in
controls v 6.2 (1.6)%/min in dilated
cardiomyopathy patients (p < 0.001). Moreover, significant regional
reduction of HED retention was demonstrated in apical and inferoapical
segments. HED retention was significantly correlated with New York
Heart Association functional class
(r = 
0.55, p = 0.002) and ejection fraction (r = 0.63, p < 0.001), but
not, however, with plasma noradrenaline concentrations as well as
parameters of heart rate variability.
CONCLUSIONSIn this
study, using PET in combination with HED in patients with dilated
cardiomyopathy, not only global reduction but also regional
abnormalities of cardiac sympathetic tracer uptake were demonstrated.
The degree of abnormality was positively correlated to markers of
severity of heart failure. The pathogenetic mechanisms leading to the
regional differences of neuronal damage as well as the prognostic
significance of these findings remain to be defined.
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