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Thyrotoxicosis-Induced Acute Myocardial Infarction Due to Painless Thyroiditis

Authors
Kim, Hee JinJung, Tae SikHahm, Jong RyealHwang, Seok-JaeLee, Sang MinJung, Jung HwaKim, Soo KyoungIl Chung, Soon
Issue Date
Oct-2011
Publisher
MARY ANN LIEBERT, INC
Citation
THYROID, v.21, no.10, pp 1149 - 1151
Pages
3
Indexed
SCI
SCIE
SCOPUS
Journal Title
THYROID
Volume
21
Number
10
Start Page
1149
End Page
1151
URI
https://scholarworks.gnu.ac.kr/handle/sw.gnu/23555
DOI
10.1089/thy.2010.0428
ISSN
1050-7256
1557-9077
Abstract
Background: Thyrotoxicosis influences cardiovascular hemodynamics and can induce coronary vasospasm. Patients with thyrotoxicosis-induced acute myocardial infarction (AMI) are unusual and almost all reported cases have been associated with Graves' disease. Patients with painless thyroiditis show a thyrotoxic phase during the early stages. Here we describe a very rare case of thyrotoxicosis with painless thyroiditis-induced AMI. Summary: A 35-year-old Korean man visited the emergency room for a 2-hour duration of typical AMI chest pain. The patient did not have any coronary artery disease (CAD) risk factors. The electrocardiogram showed 3 mm of ST-segment elevation in leads II, III, and aVF, which is consistent with inferior AMI. We immediately treated the patient with aspirin, clopidogrel, and nitroglycerine and performed emergent coronary angiography. Coronary angiography showed normal coronary arteries without any stenotic lesions. Consistent with AMI, cardiac enzyme levels of serum creatine kinase (CK), CK-MB, and troponin-I were also elevated. Laboratory findings showed thyrotoxicosis without any thyroid autoantibodies. A 99m-technetium scintigraphy showed markedly decreased thyroid uptake compatible with thyroiditis. We treated the patient with calcium channel blockers and nitrates. The patient spontaneously recovered normal thyroid function after 6 weeks of observation and did not complain of chest pain. Conclusion: Thyrotoxicosis due to painless thyroiditis provoked AMI in a young man who had no atherosclerotic coronary lesions and no CAD risk factors.
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