A Case Report of Recurrent Takotsubo Cardiomyopathy in a Patient during Myasthenia Crisis

Abstract

Introduction: Patients with myasthenia crisis can develop Takotsubo stress cardiomyopathy (SC) due to emotional or physical stress and high level of circulating catecholamines. We report a patient who developed recurrent Takotsubo cardiomyopathy during myasthenia crisis. Coexisting autoimmune disorders known to precipitate stress cardiomyopathy like Grave's disease need to be evaluated.

Case report: A 69-year-old female with seropositive myasthenia gravis (MG), Grave's disease, and coronary artery disease on monthly infusion of intravenous immunoglobulin (IVIG), prednisone, pyridostigmine, and methimazole presented with shortness of breath and chest pain. Electrocardiogram (ECG) showed ST elevation in anterolateral leads with troponemia. Coronary angiogram was unremarkable for occlusive coronary disease with left ventriculogram showing reduced wall motion with apical and mid left ventricle (LV) hypokinesis suggestive of Takotsubo stress cardiomyopathy. Her symptoms were attributed to MG crisis. Her symptoms, ECG, and echocardiographic findings resolved after five cycles of plasma exchange (PLEX). She had another similar episode one year later during myasthenia crisis with subsequent resolution in 10 days after PLEX.

Conclusion: Takotsubo cardiomyopathy can be one of the manifestations of myasthenia crisis with or without coexisting Grave's disease. These patients might benefit from meticulous fluid status and cardiac monitoring while administering rescue treatments like IVIG and PLEX.

Figure 1

ECG during first episode of Takotsubo stress cardiomyopathy with ST elevation V1–V6, Q waves in V1–V3.

Figure 2

Left ventriculogram in RAO projection in diastole (a) demonstrates normal cavity contour and in systole (b) preserved basal and apical contractility with akinesia of the mid ventricle consistent with Takotsubo stress cardiomyopathy.

Figure 3

ECG during second SC episode with deep symmetrical T inversions in leads V1–V6.

Figure 4

ECG 3 days later showing nonspecific ST-T wave changes only.