title: Hyperthyroidism is associated with lengthening of ventricular repolarization.
abstract: OBJECTIVE
  Lengthened ventricular repolarization, as assessed by the QT interval on electrocardiogram (ECG), can predispose to an increased risk of cardiac dysrhythmias; no data are available on QT corrected for heart rate (QTc) in hyperthyroidism in vivo.
  
  
  METHODS
  QT and RR intervals from 24 h ambulatory ECG Holter recording were measured in patients with hyperthyroidism and again following pharmacological achievement of stable euthyroidism for at least 2 months.
  
  
  METHODS
  We enrolled a total of 16 hyperthyroid patients with Graves' disease, six males and 10 females (mean age 47 +/- 4 years, mean +/- SEM); 13 healthy age- and sex-matched subjects were utilized as a control group.
  
  
  METHODS
  The QT analysis was carried out by a computerized algorithm (QTc was corrected by the heart rate by Bazett's formula). Serum total T4, total T3, free T4, free T3 and TSH concentrations were measured by a fully automated immunoenzymometric assay; plasma norepinephrine by automatized high-pressure liquid chromatography, potassium and chloride by a potentiometric method, magnesium and calcium by a colourimetric method.
  
  
  RESULTS
  The 24-h average QTc in the hyperthyroid patients was significantly prolonged compared to controls (458 +/- 7 vs. 431 +/- 6 ms, P = 0.01) and it returned to normal after treatment of thyrotoxicosis (432 +/- 6 ms, P < 0.05 vs. time H, NS vs. controls). QTc positively correlated with FT3 (r = 0.63, P < 0.001) and with FT4 (r = 0.481, P < 0.02). Conversely, QTc did not correlate with plasma basal norepinephrine levels, nor with electrolytes.
  
  
  CONCLUSIONS
  Hyperthyroidism is associated with prolonged QTc that normalizes once the patient becomes euthyroid. The strong positive correlation between FT3 and QTc supports the hypothesis of an important role of thyroid hormone on modulation of QTc lengthening.
authors.affiliation: Cardiovascular Neuroendocrine Unit, CNR Institute of Clinical Physiology, Via P. Savi, I-56126 Pisa, Italy.
authors.forename: R M
authors.initials: RM
authors.lastname: Colzani
authors.forename: M
authors.initials: M
authors.lastname: Emdin
authors.forename: F
authors.initials: F
authors.lastname: Conforti
authors.forename: C
authors.initials: C
authors.lastname: Passino
authors.forename: M
authors.initials: M
authors.lastname: Scarlattini
authors.forename: G
authors.initials: G
authors.lastname: Iervasi
mesh_terms: D000319:Adrenergic beta-Antagonists / Q000627:therapeutic use; D000328:Adult; D015716:Electrocardiography, Ambulatory; D004573:Electrolytes / Q000097:blood; D005260:Female; D005500:Follow-Up Studies; D006111:Graves Disease / Q000150:complications* / Q000188:drug therapy / Q000503:physiopathology; D006339:Heart Rate / Q000502:physiology; D006801:Humans; D008133:Long QT Syndrome / Q000097:blood / Q000188:drug therapy / Q000209:etiology*; D008297:Male; D008875:Middle Aged; D009638:Norepinephrine / Q000097:blood; D011433:Propranolol / Q000627:therapeutic use; D013961:Thyroid Gland / Q000503:physiopathology; D013972:Thyrotropin / Q000097:blood; D013974:Thyroxine / Q000097:blood; D014284:Triiodothyronine / Q000097:blood
chemical_list: D000319:Adrenergic beta-Antagonists; D004573:Electrolytes; D014284:Triiodothyronine; D013972:Thyrotropin; D011433:Propranolol; D013974:Thyroxine; D009638:Norepinephrine