Takotsubo syndrome with apical thrombosis associated with hyperthyroidism crisis: a case report from high-altitude...

Catecholamine surge is considered the primary trigger of Takotsubo syndrome(TTS), but its pathophysiological mechanisms remain incompletely understood. Cases of TTS with intracardiac thrombus induced by thyrotoxicosis in the setting of high-altitude hypoxia are particularly rare.

A 65-year-old woman living at 3,200 m was admitted with abdominal and chest pain. On admission, her BP was 108/68 mmHg, HR 135 bpm, Temp 37.8°C, and SpO₂ 95% on room air. Hemoglobin was 168 g/L, consistent with chronic high-altitude adaptation. Coronary angiography at the local hospital showed mild stenosis of the left anterior descending artery. She presented with tachycardia, marked ST-segment elevation, and elevated troponin T and B-type natriuretic peptide (BNP) levels. The ST-segment elevation gradually resolved during hospitalization, arguing against acute myocardial infarction. However, markedly elevated thyroid hormone and thyrotropin receptor antibody levels were indicative of a thyroid storm. Transthoracic echocardiography (TTE) revealed apical hypokinesia and ballooning accompanied by an apical thrombus. Myocardial contrast echocardiography (MCE) indicated delayed and sparse perfusion in the apical segment, while Magnetic resonance imaging (MRI) ruled out remote myocardial injury. Mildly elevated myocardial enzymes and rapid resolution of ST-segment elevation supported the diagnosis of Takotsubo cardiomyopathy. Thyrotoxicosis may have enhanced myocardial sensitivity to catecholamines, predisposing to stress-related injury. Chronic high-altitude hypoxia can further increase sympathetic activity and impair coronary microcirculation. The patient was treated with β-blockers, antithyroid agents, and anticoagulation, along with supportive therapy targeting oxidative stress, which was followed by regression of the apical thrombus and improvement in cardiac function.

The combined effects of severe thyrotoxicosis and chronic high-altitude hypoxia may induce TTS and its related complications by enhancing sympathetic activity and catecholamine responsiveness.