OBJECTIVE Lengthened ventricular repolarization, as assessed by the QT inte
rval on electrocardiogram (ECG), can predispose to an increased risk of car
diac dysrhythmias; no data are available on QT corrected for heart rate (QT
c) in hyperthyroidism in vivo.
DESIGN QT and RR intervals from 24 h ambulatory ECG Holter recording were m
easured in patients with hyperthyroidism and again following pharmacologica
l achievement of stable euthyroidism for at least 2 months.
PATIENTS We enrolled a total of 16 hyperthyroid patients with Graves' disea
se, six males and 10 females (mean age 47 +/- 4 years, mean +/- SEM); 13 he
althy age- and sex-matched subjects were utilized as a control group.
MEASUREMENTS The QT analysis was carried out by a computerized algorithm (Q
Tc was corrected by the heart rate by Bazett's formula). Serum total T4, to
tal T3, free T4, free T3 and TSH concentrations were measured by a fully au
tomated 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 no
t correlate with plasma basal norepinephrine levels, nor with electrolytes.
CONCLUSIONS Hyperthyroidism is associated with prolonged QTc that normalize
s once the patient becomes euthyroid. The strong positive correlation betwe
en FT3 and QTc supports the hypothesis of an important role of thyroid horm
one on modulation of QTc lengthening.