PDF(Pubmed)
Abstract：
BACKGROUND: Amiodarone-induced thyroid dysfunction (AIT) is a side-effect associated with the use of Amiodarone for the treatment of refractory arrythmias. Resulting hyperthyroidism can precipitate cardiac complications, including cardiac ischemia and myocardial infarction, although this has only been described in a few case reports.
METHODS: We present here a clinical scenario involving a 66-year-old male Caucasian patient under Amiodarone for atrial fibrillation, who developed AIT. In the presence of dyspnea, multiple cardiovascular risk factors and ECG abnormalities, a transthoracic echocardiogram was performed, showing inferobasal hypokinesia. This led to further investigations through a cardiac PET-CT, where cardiac ischemia was suspected. Ultimately, the coronary angiography revealed no abnormalities. Nonetheless, these extensive cardiologic investigations led to a delay in initiating an emergency endovascular revascularization for acute-on-chronic left limb ischemia. Although initial treatment using Carbimazole was not successful after three weeks, the patient reached euthyroidism after completion of the treatment with Prednisone so that eventually thyroidectomy was not performed. Endovascular revascularization was finally performed after more than one month.
CONCLUSIONS: We discuss here cardiac abnormalities in patients with AIT, which may be due to relative ischemia secondary to increased metabolic demand during hyperthyroidism. Improvement of cardiac complications is expected through an optimal AIT therapy including medical therapy as the primary approach and, when necessary, thyroidectomy. Cardiac investigations in the context of AIT should be carefully considered and may not justify delaying other crucial interventions. If considered mandatory, diagnostic procedures such as coronary angiography should be preferred to functional testing.
METHODS: We present here a clinical scenario involving a 66-year-old male Caucasian patient under Amiodarone for atrial fibrillation, who developed AIT. In the presence of dyspnea, multiple cardiovascular risk factors and ECG abnormalities, a transthoracic echocardiogram was performed, showing inferobasal hypokinesia. This led to further investigations through a cardiac PET-CT, where cardiac ischemia was suspected. Ultimately, the coronary angiography revealed no abnormalities. Nonetheless, these extensive cardiologic investigations led to a delay in initiating an emergency endovascular revascularization for acute-on-chronic left limb ischemia. Although initial treatment using Carbimazole was not successful after three weeks, the patient reached euthyroidism after completion of the treatment with Prednisone so that eventually thyroidectomy was not performed. Endovascular revascularization was finally performed after more than one month.
CONCLUSIONS: We discuss here cardiac abnormalities in patients with AIT, which may be due to relative ischemia secondary to increased metabolic demand during hyperthyroidism. Improvement of cardiac complications is expected through an optimal AIT therapy including medical therapy as the primary approach and, when necessary, thyroidectomy. Cardiac investigations in the context of AIT should be carefully considered and may not justify delaying other crucial interventions. If considered mandatory, diagnostic procedures such as coronary angiography should be preferred to functional testing.
摘要：
背景：胺碘酮诱导的甲状腺功能障碍（AIT）是与使用胺碘酮治疗难治性心律失常相关的副作用。导致的甲状腺功能亢进可以引起心脏并发症，包括心肌缺血和心肌梗死,尽管仅在少数病例报告中对此进行了描述。
方法：我们在此介绍一个涉及一名66岁男性高加索患者服用胺碘酮治疗心房颤动的临床情景，谁开发了AIT。在呼吸困难的情况下，多种心血管危险因素和心电图异常，进行了经胸超声心动图检查,表现为垂体运动功能减退.这导致通过心脏PET-CT进行进一步的研究，怀疑心脏缺血。最终,冠状动脉造影未发现异常.尽管如此，这些广泛的心脏检查导致急性-慢性左肢体缺血的急诊血管内血运重建延迟.尽管使用卡比咪唑的初始治疗在三周后没有成功，患者在完成泼尼松治疗后达到甲状腺功能正常,因此最终未进行甲状腺切除术.超过1个月后终于进行了血管内血运重建。
结论：我们在这里讨论AIT患者的心脏异常，这可能是由于甲状腺功能亢进期间代谢需求增加继发的相对缺血。心脏并发症的改善有望通过最佳的AIT治疗，包括药物治疗作为主要方法，必要时,甲状腺切除术.应仔细考虑AIT背景下的心脏调查，并且可能无法证明延迟其他关键干预措施是合理的。如果被认为是强制性的，冠状动脉造影等诊断程序应优于功能测试.
方法：我们在此介绍一个涉及一名66岁男性高加索患者服用胺碘酮治疗心房颤动的临床情景，谁开发了AIT。在呼吸困难的情况下，多种心血管危险因素和心电图异常，进行了经胸超声心动图检查,表现为垂体运动功能减退.这导致通过心脏PET-CT进行进一步的研究，怀疑心脏缺血。最终,冠状动脉造影未发现异常.尽管如此，这些广泛的心脏检查导致急性-慢性左肢体缺血的急诊血管内血运重建延迟.尽管使用卡比咪唑的初始治疗在三周后没有成功，患者在完成泼尼松治疗后达到甲状腺功能正常,因此最终未进行甲状腺切除术.超过1个月后终于进行了血管内血运重建。
结论：我们在这里讨论AIT患者的心脏异常，这可能是由于甲状腺功能亢进期间代谢需求增加继发的相对缺血。心脏并发症的改善有望通过最佳的AIT治疗，包括药物治疗作为主要方法，必要时,甲状腺切除术.应仔细考虑AIT背景下的心脏调查，并且可能无法证明延迟其他关键干预措施是合理的。如果被认为是强制性的，冠状动脉造影等诊断程序应优于功能测试.
