Takotsubo cardiomyopathy (TTS), also known as stress cardiomyopathy or broken heart syndrome, is a type of non-ischemic cardiomyopathy characterized by a sudden, temporary weakening of the heart muscle, usually affecting the left ventricle's apex ^{1, 2, 3, 4, 5}. It often occurs after significant physical or emotional stress ^{1, 2, 3, 4, 5}. The condition is also referred to as apical ballooning syndrome due to the characteristic shape the left ventricle takes during systole ^{1, 2, 3, 4, 5}.

Epidemiology

Takotsubo cardiomyopathy occurs worldwide and is estimated to account for about 2% of cases presenting as acute coronary syndrome ¹. It is more common in postmenopausal women ^{1, 4}. The incidence increased during the COVID-19 pandemic ⁴.

Aetiology

TTS is often triggered by a stressful event, either physical (e.g., sepsis, hemorrhage, surgery, asthma attack) or emotional (e.g., bereavement, divorce, job loss) ^{1, 2, 3, 4, 5}. However, a significant proportion of cases (around one-third) occur without an identifiable trigger ^{1, 3, 4}. Certain endocrine disorders like pheochromocytoma and thyrotoxicosis have also been associated with TTS ^{1, 4}.

Pathophysiology

The exact pathophysiology is not fully understood, but a surge of catecholamines (like adrenaline and noradrenaline) is thought to play a central role ^{1, 2, 3, 4}. This catecholamine surge can cause direct myocardial toxicity ("stunning"), coronary artery spasm, and microvascular dysfunction ^{2, 3, 4}. The resulting dysfunction typically involves apical ballooning with hyperkinesis of the base ^{1, 2, 3, 4, 5}.

Clinical presentation

The typical presentation mimics an acute myocardial infarction, with symptoms like chest pain and shortness of breath ^{1, 2, 3, 4, 5}. Electrocardiogram (ECG) changes, such as ST-segment elevation or T-wave inversion, are common ^{1, 2, 3, 4, 5}. Echocardiography often reveals characteristic apical ballooning and reduced left ventricular ejection fraction ^{1, 2, 3, 4, 5}.

Investigations

Diagnosis involves excluding obstructive coronary artery disease (usually via coronary angiography) and identifying characteristic left ventricular wall motion abnormalities (e.g., apical ballooning) ^{1, 2, 3, 4, 5}. Other investigations include ECG, cardiac biomarkers (troponin may be elevated), echocardiography, left ventriculogram, cardiac MRI, and potentially coronary angiography ^{2, 3, 4}.

Management

Management is primarily supportive, focusing on treating heart failure symptoms and complications ^{1, 2, 3, 4, 5}. Conventional heart failure therapies are often used. While beta-blockers and ACE inhibitors/ARBs are commonly employed, evidence for their specific efficacy in TTS is limited, although ACE inhibitors/ARBs may reduce recurrence ^{3, 4, 5}. There are currently no specific guidelines for TTS management ⁴.

Differential diagnosis

The main differential diagnosis is acute myocardial infarction (STEMI, NSTEMI) ^{1, 2, 3, 4, 5}. Other conditions to consider include myocarditis, pericarditis, and other forms of cardiomyopathy ^{1, 2, 3, 4, 5}.

Prognosis & complications

TTS is generally considered reversible, with left ventricular function typically recovering within days to weeks ^{1, 2, 3, 4, 5}. However, it can be associated with complications such as heart failure, pulmonary oedema, cardiogenic shock, arrhythmias, and even death, particularly when triggered by severe physical stressors ^{1, 2, 3, 4, 5}. While generally benign, it has significant morbidity and mortality ³.

See also

Acute myocardial infarction, Heart failure, Cardiomyopathy

Sources & licence

This article was drafted with AI assistance and is subject to clinical review. Portions are adapted from the Wikipedia article “Takotsubo cardiomyopathy” by Wikipedia contributors, licensed under CC BY-SA 4.0; this adapted text is likewise available under CC BY-SA 4.0. Clinical facts are cross-checked against the PubMed references below.