Amiodarone-induced thyrotoxicosis: left ventricular dysfunction is associated with increased mortality.
OBJECTIVE
Amiodarone-induced thyrotoxicosis (AIT) is a challenging management problem, since patients treated with amiodarone invariably have underlying heart disease. Consequently, thyrotoxicosis can significantly contribute to increased morbidity and mortality. The aim of this study was to compare the clinical outcome and hormone profiles of patients with AIT (n = 60) with those with Graves' thyrotoxicosis (n = 49) and toxic multinodular goitre (MNG, n = 40).


METHODS
A retrospective study of patients with AIT in a single institution was conducted.


METHODS
Data from patients with AIT over 12 years were collected.


RESULTS
Mean TSH levels were significantly suppressed in all three groups. However, there was no intergroup significant difference. Free thyroxine (T4) levels were significantly higher in AIT (45.6 +/- 3.5 pmol/l) and Graves' disease (44.6 +/- 4.0 pmol/l) compared with toxic MNG (31.5 +/- 5.1 pmol/l, P < 0.05). In contrast, free triiodothyronine (T3) levels were only significantly higher in Graves' disease (14.7 +/- 1.5 pmol/l, P = 0.002) compared with AIT (8.6 +/- 0.7 pmol/l) and toxic MNG (7.4 +/- 0.5 pmol/l). Six deaths occurred in the patients with AIT (10.0%, P < 0.01) and no deaths occurred in the other groups. Amiodarone treatment (P = 0.002) was the most significant predictor of death, whereas free T4, free T3 and age did not affect outcome. Within the amiodarone-treated group severe left ventricular dysfunction (P = 0.0001) was significantly associated with death.


CONCLUSIONS
(i) AIT differs from other forms of thyrotoxicosis, and (ii) severe left ventricular dysfunction is associated with increased mortality in AIT.
Department of Medicine and Endocrinology, St George Hospital and University of New South Wales, Kogarah, Sydney, Australia. A.OSullivan@unsw.edu.au
Anthony J
AJ
O'Sullivan
Mridula
M
Lewis
Terrance
T
Diamond
D000328:Adult; D000368:Aged; D000638:Amiodarone / Q000009:adverse effects*; D001145:Arrhythmias, Cardiac / Q000188:drug therapy; D005260:Female; D006044:Goiter, Nodular / Q000097:blood / Q000150:complications / Q000401:mortality; D006111:Graves Disease / Q000097:blood / Q000150:complications / Q000401:mortality; D006801:Humans; D008297:Male; D008875:Middle Aged; D012189:Retrospective Studies; D013971:Thyrotoxicosis / Q000139:chemically induced* / Q000401:mortality*; D013972:Thyrotropin / Q000097:blood; D013974:Thyroxine / Q000097:blood; D014284:Triiodothyronine / Q000097:blood; D018487:Ventricular Dysfunction, Left / Q000150:complications*
D014284:Triiodothyronine; D013972:Thyrotropin; D000638:Amiodarone; D013974:Thyroxine