title: Activation of electrical triggers of atrial fibrillation in hyperthyroidism.
abstract: BACKGROUND
  A shortening of the atrial refractory period has been considered as the main mechanism for the increased risk of atrial fibrillation in hyperthyroidism. However, other important factors may be involved.
  
  
  OBJECTIVE
  Our objective was to determine the activity of abnormal supraventricular electrical depolarizations in response to elevated thyroid hormones in patients without structural heart disease.
  
  
  METHODS
  Twenty-eight patients (25 females, three males, mean age 43+/-11 yr) with newly diagnosed and untreated hyperthyroidism were enrolled in a prospective trial after exclusion of heart disease. Patients were followed up for 16 +/- 6 months and studied at baseline and 6 months after normalization of serum TSH levels.
  
  
  METHODS
  The incidence of abnormal premature supraventricular depolarizations (SVPD) and the number of episodes of supraventricular tachycardia was defined as primary outcome measurements before the start of the study. In addition, heart rate oscillations (turbulence) after premature depolarizations and heart rate variability were compared at baseline and follow-up.
  
  
  RESULTS
  SVPDs decreased from 59 +/- 29 to 21 +/- 8 per 24 h (P = 0.003), very early SVPDs (so called P on T) decreased from 36 +/- 24 to 3 +/- 1 per 24 h (P < 0.0001), respectively, and nonsustained supraventricular tachycardias decreased from 22 +/- 11 to 0.5 +/- 0.2 per 24 h (P = 0.01) after normalization of serum thyrotropin levels. The hyperthyroid phase was characterized by an increased heart rate (93 +/- 14 vs. 79 +/- 8 beats/min, P < 0.0001) and a decreased turbulence slope (3.6 vs. 9.2, P = 0.003), consistent with decreased vagal tone. This was confirmed by a significant decrease of heart rate variability.
  
  
  CONCLUSIONS
  Hyperthyroidism is associated with an increased supraventricular ectopic activity in patients with normal hearts. The activation of these arrhythmogenic foci by elevated thyroid hormones may be an important causal link between hyperthyroidism and atrial fibrillation.
authors: Department of Cardiovascular Medicine, Swiss Cardiovascular Center Bern, University Hospital, CH-3010 Bern, Switzerland.
authors: K
authors: K
authors: Wustmann
authors: J P
authors: JP
authors: Kucera
authors: A
authors: A
authors: Zanchi
authors: A
authors: A
authors: Burow
authors: T
authors: T
authors: Stuber
authors: B
authors: B
authors: Chappuis
authors: P
authors: P
authors: Diem
authors: E
authors: E
authors: Delacrétaz
mesh_terms: D000200:Action Potentials / Q000502:physiology*; D000328:Adult; D013956:Antithyroid Agents / Q000627:therapeutic use; D001281:Atrial Fibrillation / Q000209:etiology* / Q000503:physiopathology; D002231:Carbimazole / Q000627:therapeutic use; D004452:Echocardiography; D004558:Electric Stimulation; D005260:Female; D006339:Heart Rate / Q000187:drug effects / Q000502:physiology; D006801:Humans; D006980:Hyperthyroidism / Q000150:complications* / Q000188:drug therapy / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D011441:Propylthiouracil / Q000627:therapeutic use; D013617:Tachycardia, Supraventricular / Q000209:etiology
chemical_list: D013956:Antithyroid Agents; D011441:Propylthiouracil; D002231:Carbimazole