# Stress-Induced Cardiomyopathy Mimicking Acute Coronary Syndrome in a High-Risk Female Patient: A Case Report

## TL;DR

A 55-year-old woman with heart risk factors developed chest pain after stress, mimicking a heart attack, but was diagnosed with stress-induced cardiomyopathy.

## Contribution

This case highlights the diagnostic challenge of stress-induced cardiomyopathy mimicking acute coronary syndrome in high-risk patients.

## Key findings

- The patient showed typical echocardiographic features of Takotsubo cardiomyopathy, including apical akinesis and basal hyperkinesis.
- The patient fully recovered left ventricular ejection fraction during hospitalization but had mild diastolic dysfunction at follow-up.
- The case emphasizes the need for careful imaging to distinguish stress-induced cardiomyopathy from acute coronary syndrome.

## Abstract

Takotsubo cardiomyopathy (TTC), also known as takotsubo syndrome, is a transient but potentially serious cardiac dysfunction that often mimics acute coronary syndrome (ACS) in the absence of obstructive coronary artery disease. It is typically associated with intense emotional or physical stress and presents predominantly in postmenopausal women, but can occur in other populations. We present a case of a 55-year-old postmenopausal woman with multiple cardiac risk factors, including uncontrolled diabetes, dyslipidemia, and smoking, who developed chest pain and dynamic troponin elevation (42 ng/L to 97 ng/L) following a severe emotional stressor. She was initially diagnosed with non-ST elevation myocardial infarction (NSTEMI) based on ischemic electrocardiographic changes and a rising troponin trend. Subsequent echocardiography revealed apical akinesis with basal hyperkinesis - features typical of TTC. The patient was initially managed as a case of NSTEMI, with treatment, including dual antiplatelet therapy (DAPT), statins, beta-blockers, angiotensin-converting enzyme (ACE) inhibitors, and insulin, with complete recovery of left ventricular ejection fraction (LVEF) during hospitalization. Mild diastolic dysfunction persisted at a five-month follow-up without clinical heart failure or the need for additional intervention. This case underscores the importance of maintaining clinical suspicion for non-ischemic causes such as stress-induced cardiomyopathy in patients presenting with ACS-like symptoms. This vigilance is crucial as standard ischemic evaluation is critical, and TTC is a diagnosis of exclusion. It requires careful assessment via imaging modalities, echocardiography, CT angiogram, and cardiac MRI to differentiate it from ACS or other cardiomyopathies, as management strategies differ significantly.