Myocarditis as a Possible Underlying Cause for Mid-Ventricular Takotsubo Cardiomyopathy: A Case Report

Our case report characterizes a rare presentation of mid-ventricular Takotsubo cardiomyopathy (TTC) in a patient with suspected myocarditis as an underlying cause. Mid-ventricular TTC is a rare variant of TTC presenting with overlapping symptoms and physical exam findings of acute coronary syndrome, which often leads to misdiagnosis as myocardial infarction. Our case is of a 77-year-old female patient with a history of hyperlipidemia, right breast ductal carcinoma in situ, and diverticular disease who presented to the emergency department for evaluation of chest pain radiating to the jaw with associated nausea and vomiting. She had a similar event eight months earlier and was diagnosed with ischemia with non-obstructive coronary arteries (INOCA) based on cardiac catheterization findings. Family history was notable for myocardial infarction in the patient's father and paternal grandfather. At presentation, the patient had elevated blood pressure, elevated troponins (initially 1058 ng/L with a repeat level of 11,421 ng/L), and electrocardiogram (ECG) findings of sinus bradycardia without ischemic changes. Cardiac MRI (CMR) revealed sub-epicardial delayed enhancement suggestive of possible myocarditis and diffuse hypokinesis involving the inferolateral left ventricular wall, sparing the basal and apical segments. Left ventricular function was mildly decreased (ejection fraction of 49%) and improved prior to discharge with ejection fraction (55-60%). There were no wall motion abnormalities or significant valve disease. This case presentation exemplifies a rare manifestation of mid-ventricular TTC that occurred in the setting of underlying myocarditis. Given the patient's history, elevated troponins, and CMR results suggestive of myocarditis, we hypothesize that underlying myocarditis may have incited the development of mid-ventricular TTC. The absence of identifiable triggers in conjunction with the inferolateral ventricular wall hypokinesis and late gadolinium enhancement on CMR supports our hypothesis. The variability in clinical presentations between the present case and other reported cases of mid-ventricular TTC emphasizes the need for a deeper understanding of this condition, its triggers, and the associated clinical features to reduce the risk of future misdiagnoses. This case report highlights the significance of thorough imaging assessments for patients presenting with INOCA. Further investigations are warranted to determine underlying causes for hemodynamic instability and unique aspects of the mid-ventricular manifestation of TTC, with an emphasis on the potential association of myocarditis as an inciting factor.