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

Abstract Background The pathophysiological mechanism of Takotsubo syndrome (TTS) has not been clarified. Although it is associated with catecholamine storm, the occurrence of TTS with thrombus directly related to hyperthyroidism is rare. The patient resides in a high plateau, which is more susceptible to ischemia and hypoxia. Case Summary A 65-year-old female, residing at an altitude of 3200 meters, was admitted to the hospital presenting with abdominal and chest pain. She exhibited tachycardia along with extensive ST-segment elevation, and elevated levels of troponin T and B-natriuretic peptide. As her ST elevation gradually diminished during her hospitalization, the data did not align with a diagnosis of acute myocardial infarction. However, markedly increased levels of thyroid hormone and thyrotropin receptors suggested the possibility of a hyperthyroidism crisis. Transthoracic echocardiography (TTE) was conducted, revealing hypokinesia of the mid and apical segments of the left ventricle with characteristic apical ballooning. The left ventricular ejection fraction (LVEF) of 49% and an apical thrombus were detected. Myocardial contrast echocardiography (MCE) showed delayed and slightly sparse myocardial perfusion in the middle and apical segment of the left ventricle. Magnetic resonance imaging (MRI) confirmed the presence of an apical thrombus without enhancement, indicating no apparent abnormalities in the first perfusion and delayed enhancement, ruling out remote myocardial injury. Additionally, a slight increase in myocardial enzymes and a rapid decline in ST segment further supported the diagnosis of Takotsubo cardiomyopathy. Hence, treatment commenced with beta-blockers, antithyroxine synthesis inhibitors, anticoagulation therapy, and measures to improve oxidative stress. As a result, the thrombus decreased in size, and cardiac function improved. Conclusion In TTS, excessive thyroid hormone levels can upregulate adrenergic receptors, leading to increased myocardial chronotropy and a positive myocardial response to catecholamines. Furthermore, in Tibetan regions where ischemia and hypoxia are more prevalent, coronary microvascular vasoconstriction and dysfunction may contribute to myocardial dysfunction in TTS.