Reversible left ventricular dysfunction "takotsubo" cardiomyopathy related to catecholamine cardiotoxicity
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Updated: Sep 10, 2026

Permanent Ligation of the Left Anterior Descending Coronary Artery in Mice: A Model of Post-myocardial Infarction Remodelling and Heart Failure
Published on: December 2, 2014
Yoshihiro J Akashi1, Kiyoshi Nakazawa, Masayoshi Sakakibara
1Division of Cardiology, Department of Internal Medicine, St Marianna University School of Medicine, Kawasaki-city, Kanagawa-pref, Japan. johnny@marianna-u.ac.jp
Insights
This study details a case of reversible left ventricular dysfunction in an elderly woman, likely caused by high catecholamine levels. The condition mimicked myocardial infarction but resolved spontaneously.
Area of Science:
- Cardiology
- Endocrinology
- Internal Medicine
Background:
- Persistent consciousness disturbance warrants thorough investigation.
- Electrocardiography is crucial for diagnosing cardiac events.
Observation:
- An 80-year-old female presented with altered consciousness and ST-segment elevation mimicking myocardial infarction.
- Coronary angiography showed normal arteries, but left ventriculography revealed left ventricular dysfunction.
- Elevated plasma catecholamines and cardiac autonomic dysfunction were noted.
Findings:
- Transient left ventricular dysfunction and ST-segment elevation resolved spontaneously without specific treatment.
- Cardiac catecholamine dynamics showed transient dysfunction on (123)I-metaiodobenzyl guanidine scintigraphy.
- The patient experienced significant ST-segment elevation and subsequent deep inverted T waves on ECG.
Implications:
- High catecholamine levels can induce reversible left ventricular dysfunction, mimicking acute coronary syndromes.
- This case highlights the importance of considering endocrine causes in cardiac emergencies.
- Understanding catecholamine effects on the heart is vital for accurate diagnosis and management.
Abstract:
An 80-year-old female was admitted for a persistent consciousness disturbance. Electrocardiography revealed ST-segment elevation in leads II, III, aVf, and V3-V6. Coronary angiography demonstrated normal arteries, while left ventriculography revealed asynergy of apical akinesis and basal hyperkinesis. The creatinine kinase and creatinine kinase MB levels were not elevated after the initial measurement on admission. The diffuse ST-segment elevation reached a maximum level 24 hours after admission. In leads V3-V6, ST-segment elevation continued for 48 hours, and was followed-up by deep inverted T waves. Within 24 days, the asynergy improved without any specific treatment, but the giant negative T waves were present on the electrocardiogram. The plasma norepinephrine and brain natriuretic peptide levels on the first hospital day were 2.9ng/mL and 906pg/mL, respectively. The left ventricular dysfunction appeared to be induced by the exposure to high-level plasma catecholamines. (123)I-metaiodobenzyl guanidine scintigraphy also revealed transient dysfunction of the cardiac catecholamine dynamics.
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