Aubry Yoann, Dosch Michel, Donath Marc Y
Clinic of Endocrinology, Diabetes and Metabolism, Hospital Delémont, Hôpital du Jura, Faubourg Des Capucins 30, 2800, Delémont, Switzerland.
Clinic of Endocrinology, Diabetes and Metabolism, University Hospital Basel, Basel, Switzerland.
J Med Case Rep. 2024 May 2;18(1):235. doi: 10.1186/s13256-024-04552-w.
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.
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.
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.
胺碘酮诱发的甲状腺功能障碍（AIT）是使用胺碘酮治疗难治性心律失常时的一种副作用。由此导致的甲状腺功能亢进可能会引发心脏并发症，包括心脏缺血和心肌梗死，不过这仅在少数病例报告中有描述。
我们在此呈现一个临床病例，一名66岁的白种男性患者因房颤正在服用胺碘酮，发生了AIT。在出现呼吸困难、多种心血管危险因素和心电图异常的情况下，进行了经胸超声心动图检查，显示下基底段运动减弱。这促使通过心脏PET-CT进行进一步检查，怀疑存在心脏缺血。最终，冠状动脉造影显示无异常。尽管如此，这些广泛的心脏检查导致了对慢性左下肢急性缺血进行紧急血管内血运重建的延迟。虽然最初使用卡比马唑治疗三周后未成功，但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。一个多月后最终进行了血管内血运重建。
我们在此讨论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导致的相对缺血。通过包括以药物治疗为主要方法并在必要时进行甲状腺切除术的最佳AIT治疗，有望改善心脏并发症。在AIT背景下的心脏检查应仔细考虑，可能无法为延迟其他关键干预措施提供理由。如果认为是必要的，冠状动脉造影等诊断程序应优先于功能测试。
