Cardiology > Takotsubo cardiomyopathy 

Background

Takotsubo cardiomyopathy (TTC), also known as stress cardiomyopathy or broken heart syndrome, is a transient cardiac syndrome characterized by acute left ventricular (LV) systolic dysfunction in the absence of obstructive coronary artery disease. It mimics acute myocardial infarction, often presenting with chest pain and ECG changes, but without significant coronary blockage. The term “Takotsubo” comes from a Japanese octopus trap, reflecting the classic apical ballooning of the LV observed on imaging. 

II) Classification/Types

By Anatomic Variant (Wall Motion Pattern): 

• • Apical type (classic): Apical ballooning with basal hyperkinesis 

• • Midventricular type: Mid-LV hypokinesis, sparing apex and base 

• • Basal (inverse) type: Basal hypokinesis with apical hyperkinesis 

• • Focal type: Localized wall motion abnormality 

• • Global type: Diffuse LV hypokinesis (rare) 

By Trigger Type: 

• • Emotional stress-induced (e.g., grief, fear) 

• • Physical stress-induced (e.g., stroke, sepsis, surgery) 

• • No identifiable trigger 

III) Pathophysiology 

Takotsubo cardiomyopathy is thought to result from catecholamine surge-induced myocardial stunning due to acute emotional or physical stress. The exact mechanism is not fully understood, but potential contributors include: 

• • Microvascular dysfunction 

• • Myocardial energy metabolism impairment 

• • Direct catecholamine-mediated myocardial toxicity 

• • Coronary artery spasm 

This leads to transient systolic dysfunction typically involving the apical and mid-ventricular segments. 

IV) Epidemiology

• • Sex: ~90% of cases occur in postmenopausal women 

• • Age: Most common in women >50 years 

• • Geography: Reported worldwide; increasing recognition with more use of angiography 

• • Comorbidities: May coexist with anxiety, depression, neurological disorders, and malignancy 

Etiology

I) Causes

• • Emotional stress (e.g., death of a loved one, panic attack) 

• • Physical stress (e.g., acute illness, surgery, stroke, trauma) 

• • Acute neurologic conditions (e.g., subarachnoid hemorrhage, seizure) 

• • Use of catecholamines (e.g., epinephrine, dobutamine) 

• • Idiopathic (no identifiable stressor in some patients) 

II) Risk Factors

• • Female sex 

• • Postmenopausal status 

• • Recent intense emotional or physical stress 

• • Pre-existing psychiatric or neurologic disorders 

• • Use of catecholaminergic medications 

Clinical Presentation

I) History (Symptoms)

• • Acute-onset chest pain (similar to MI) 

• • Dyspnea 

• • Palpitations 

• • Syncope 

• • May occur after a stressful event (emotional or physical) 

• • In severe cases: cardiogenic shock, heart failure, arrhythmias 

II) Physical Exam (Signs)

Vital Signs: 

• • May be normal or show hypotension, tachycardia 

• • Rarely: signs of shock 

Cardiac Exam: 

• • Often normal 

• • S4 gallop or systolic murmur if LV outflow obstruction present 

Pulmonary: 

• • Rales if pulmonary edema 

• • Hypoxia in severe LV dysfunction 

Peripheral: 

• • May have signs of low perfusion (cold extremities, weak pulses) 

Differential Diagnosis (DDx)

• • Acute coronary syndrome (STEMI/NSTEMI) 

• • Myocarditis 

• • Pulmonary embolism 

• • Aortic dissection 

• • Pheochromocytoma 

• • Sepsis-induced cardiomyopathy 

• • Hypertrophic obstructive cardiomyopathy (HOCM) 

• • Pericarditis 

Diagnostic Tests

Initial Tests: 

Electrocardiogram (ECG): 

• • ST-segment elevation (often precordial leads) 

• • T-wave inversion 

• • QT prolongation 

• • LBBB or new Q waves occasionally 

Cardiac Biomarkers: 

• • Elevated troponins (usually modest vs MI) 

• • Elevated BNP or NT-proBNP 

Chest X-ray: 

• • Pulmonary edema 

• • Normal or cardiomegaly 

Transthoracic Echocardiogram (TTE): 

• • Regional wall motion abnormalities not confined to a single coronary artery 

• • Apical ballooning or other variant wall motion pattern 

• • May show LV outflow tract obstruction or mitral regurgitation 

Coronary Angiography: 

• • No significant coronary artery obstruction (required to rule out MI) 

Cardiac MRI: 

• • Helps differentiate TTC from myocarditis or infarction 

• • Absence of late gadolinium enhancement 

Treatment

I) Medical Management:

Supportive Care: 

• • Often self-limiting with complete recovery within weeks 

• • Admit and monitor (initial management similar to ACS) 

Heart Failure Management (if present): 

• • Diuretics 

• • ACE inhibitors or ARBs 

• • Beta-blockers (used cautiously if LVOT obstruction is present) 

Anticoagulation: 

• • Consider if apical akinesis or LV thrombus risk 

Avoid: 

• • Inotropes if possible (may worsen catecholamine toxicity) 

• • Nitrates in LVOT obstruction 

II) Interventional/Surgical:

• • Rarely needed 

• • Intra-aortic balloon pump (IABP) or mechanical support in cardiogenic shock 

Patient Education, Screening, Vaccines

• • Educate about the transient nature and favorable prognosis 

• • Avoid emotional and physical stressors when possible 

• • Monitor for recurrence (about 5-10% risk) 

• • Smoking cessation, stress-reduction strategies (e.g., therapy, meditation) 

Vaccinations: 

• • Influenza annually 

• • Pneumococcal vaccine 

• • COVID-19 vaccination 

Consults

• • Cardiology: Required for diagnosis and management 

• • Psychiatry/Psychology: If emotional trigger or underlying mood disorder 

• • Primary Care/Internal Medicine: For long-term monitoring and prevention 

• • Neurology: If associated neurologic condition (e.g., seizure, stroke) 

 Follow-Up

• • Repeat Echocardiogram: 4–8 weeks to confirm recovery 

• • Cardiac MRI: In unclear cases or atypical course 

• • Monitor for recurrence 

• • Beta-blockers: Consider long-term in selected patients, though benefit is uncertain 

• • Address mental health: Evaluate for depression/anxiety and provide support