Abnormality of the left ventricular sympathetic nervous function assessed by I-123 metaiodobenzylguanidine imaging in pediatric patients with neurocardiogenic syncope

Olgunturk R., Turan L., Tunaoglu F., Gokcora N., Karabacak N., Azizoglu F., ...Daha Fazla

PACE-PACING AND CLINICAL ELECTROPHYSIOLOGY, cilt.26, sa.10, ss.1926-1930, 2003 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 26 Sayı: 10
  • Basım Tarihi: 2003
  • Doi Numarası: 10.1046/j.1460-9592.2003.00297.x
  • Dergi Adı: PACE-PACING AND CLINICAL ELECTROPHYSIOLOGY
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.1926-1930
  • Anahtar Kelimeler: I-123 MIBG, neurocardiogenic syncope, head-up tilt test, beta-blocking agents, HEAD-UP TILT, NOREPINEPHRINE, CATECHOLAMINES
  • Gazi Üniversitesi Adresli: Evet

Özet

The purpose of this study was to assess the left ventricular sympathetic nervous system function in the patients with neurocardiogenic syncope (NCS) using I-123 metaiodobenzylguanidine (MIBG) imaging of the heart, and to compare the plasma noradrenaline (NA) and MIBG results of tilt positive and tilt negative patients following a head-up tilt test (HUT). The study included 30 patients. Their physical and laboratory examinations did not show a pathology that may be the cause of their syncope. HUT test was positive in 13 patients and negative in 17 patients. Plasma NA concentrations were higher in the HUT positive than the HUT negative group at the beginning and at the 10(th) minute of the test. Specific I-123 MIBG uptake assessed as the cardiac to mediastinal activity ratio in the delayed image was significantly higher in HUT positive group. The higher levels of MIBG uptake and plasma NA observed in HUT positive patients may reflect the greater capacity of NA storage in cardiac adrenergic neuronal tissue in patients with NCS. The results of this study support the critical role of autonomic nervous system in the pathophysiology of NCS and the excessive sympathetic nervous stimulation as the trigger of paradox reflex.