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Atypical Takotsubo Cardiomyopathy Presenting as ST-Elevation Myocardial Infarction
Atypical Takotsubo Cardiomyopathy Presenting as ST-Elevation Myocardial Infarction
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Atypical Takotsubo Cardiomyopathy Presenting as ST-Elevation Myocardial Infarction
Atypical Takotsubo Cardiomyopathy Presenting as ST-Elevation Myocardial Infarction
Journal Article

Atypical Takotsubo Cardiomyopathy Presenting as ST-Elevation Myocardial Infarction

2025
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Overview
A 64-year-old woman with a past medical history of diverticulosis and duodenal ulcer presented with classical features of ST-elevation myocardial infarction (STEMI), including cardiac sounding chest pain, ST-elevations on electrocardiography (ECG), and elevated cardiac biomarkers. She was an ex-smoker and had a family history of heart disease, but did not report other significant cardiovascular risk factors such as hypertension, diabetes, or hyperlipidemia. Notably, she also described experiencing a recent period of emotional stress due to her friend being diagnosed with cancer. The case was initially considered a routine presentation of STEMI. However, on the day of admission (day 0), a coronary angiogram was performed, which revealed unobstructed coronary arteries. The left ventricular angiogram demonstrated mid-ventricular ballooning with a normal apex. Subsequent imaging included an echocardiogram on day 1, which showed a normal left ventricular size but impaired systolic function with ejection fraction (EF) of approximately 45% and regional wall motion abnormalities. A cardiac magnetic resonance imaging (MRI) scan performed on day 5 showed normal cardiac size and function with hypokinesia in the mid- to apical anteroseptal and anterior wall regions and a normal apex, along with mild edema, patchy diffuse late gadolinium enhancement, and elevated T1 values. These imaging features were consistent with atypical Takotsubo cardiomyopathy (TTC) or regional myocarditis. The improvement in EF from 45% to 63% over a few days, along with the absence of viral prodrome and pericardial effusion, indicates reversible ventricular dysfunction, further supporting the diagnosis of TTC. She showed significant improvement during her hospital stay, with left ventricular function returning to normal. She was started on a beta-blocker, and we advised her general practitioner (GP) to prescribe ramipril once her blood pressure improves. She was followed up at her local hospital and has returned to her usual daily activities. This case underscores the importance of considering stress-induced cardiomyopathy in differential diagnosis when patients present as acute coronary syndrome but have normal coronary arteries. While typical TTC is characterized by apical ballooning, atypical variants such as basal hypokinesia, mid-ventricular hypokinesia, and isolated right ventricular involvement can occur, often presenting with variable echocardiographic findings. In this patient, regional wall motion abnormalities were seen without typical apical involvement. Although B-type natriuretic peptide (BNP) was not measured in this case, a relatively high BNP-to-troponin ratio is seen in TTC due to marked ventricular wall stress. If this had been measured in our patient, it might have facilitated a quicker diagnosis and steered the management strategy away from ischemic etiologies. This will be considered in future similar cases to support earlier diagnosis and management.
Publisher
Cureus Inc
Subject