TextbookCardiologyTakotsubo Cardiomyopathy

Takotsubo Cardiomyopathy

Transient LV systolic dysfunction with apical ballooning, typically triggered by emotional or physical stress, mimicking acute MI but with unobstructed coronary arteries. Also known as stress cardiomyopathy.

Key Facts

Also known as: stress cardiomyopathy, broken heart syndrome, apical ballooning syndrome Predominantly affects postmenopausal women (~90% of cases; mean age 65-70) Triggered by intense emotional or physical stress: bereavement, surgery, critical illness, natural disasters Mimics ACS: chest pain, ST elevation (often anterior), troponin rise — but normal coronary arteries on angiography Apical ballooning on echo/ventriculography with hyperkinetic base — resembles a Japanese octopus trap (takotsubo) Usually reversible: LV function recovers within 4-8 weeks in most cases Complications: heart failure, cardiogenic shock (~10%), LVOT obstruction, arrhythmias, LV thrombus, cardiac rupture (rare) In-hospital mortality: ~4-5%; similar to NSTEMI

Overview

Key Facts

Takotsubo cardiomyopathy (TTC) is an acute, usually reversible cardiomyopathy characterised by transient regional LV wall motion abnormalities (typically apical ballooning), occurring in the setting of emotional or physical stress, in the absence of obstructive coronary artery disease.

Epidemiology

  • Accounts for ~1-3% of all patients presenting with suspected ACS
  • ~90% are postmenopausal women (age 60-75)
  • Rare in men; when it occurs, may have worse outcomes
  • Prevalence increasing (likely due to improved recognition)

Aetiology/Triggers

  • Emotional stress: bereavement, arguments, surprise, fear, financial crisis
  • Physical stress: surgery, critical illness, sepsis, stroke, seizures, asthma attack
  • No identifiable trigger: in ~30% of cases
  • Possible mechanisms: catecholamine surge, microvascular spasm, direct myocardial toxicity from catecholamines

Pathophysiology

  • Excessive catecholamine release (noradrenaline, adrenaline) causes direct myocardial stunning
  • Catecholamine-mediated coronary microvascular dysfunction
  • Apical segments have highest density of beta-adrenergic receptors → most vulnerable to catecholamine toxicity
  • Oestrogen may be protective → postmenopausal women are more susceptible
  • Transient myocardial oedema and dysfunction → recovery over weeks

Clinical Presentation

Typical Presentation

  • Acute chest pain (indistinguishable from ACS)
  • Dyspnoea
  • Syncope
  • Following identifiable emotional or physical stressor

Variants

  • Typical (apical): most common (~80%); apical and mid-ventricular akinesis with basal hyperkinesis
  • Mid-ventricular: mid-wall akinesis with apical and basal sparing
  • Basal (reverse/inverted): basal akinesis with apical sparing (more common in younger patients)
  • Focal: localised wall motion abnormality

Complications

  • Heart failure (~45%)
  • Cardiogenic shock (~10%)
  • LVOT obstruction from SAM of mitral valve (hyperkinetic base with apical ballooning)
  • Arrhythmias: AF, VT, QT prolongation, TdP
  • LV thrombus (~5%; due to apical akinesis)
  • Cardiac rupture (rare)
  • Recurrence: ~5-10% of cases

Red Flags

  • Cardiogenic shock or pulmonary oedema
  • Dynamic LVOT obstruction (avoid inotropes, volume deplete if needed)
  • QT prolongation (risk of TdP)
  • LV thrombus on echo

Differential Diagnosis

DiagnosisKey FeaturesInvestigation
ACS (STEMI/NSTEMI)Coronary occlusion/stenosis, regional wall motion abnormality matching coronary territoryAngiography
MyocarditisViral prodrome, non-coronary LGE pattern on MRICardiac MRI
Phaeochromocytoma crisisParoxysmal HTN, headache, sweatingUrinary metanephrines
Subarachnoid haemorrhageNeurogenic stunning, thunderclap headacheCT head
Acute PERV strain, hypotensionCTPA
Coronary artery spasm (Prinzmetal)Transient ST elevation, responds to nitratesProvocative testing

Diagnosis / Investigation

Bedside

  • ECG: ST elevation (often anterior leads), T-wave inversion (evolving), QT prolongation, pathological Q waves possible
  • Observations: tachycardia, hypotension in severe cases

Bloods

  • Troponin: elevated but often disproportionately low relative to extent of wall motion abnormality
  • BNP/NT-proBNP: often markedly elevated (can be very high)
  • Catecholamine levels: may be elevated (not routinely measured)
  • FBC, U&Es, glucose: baseline

Imaging

  • Echocardiography: characteristic apical ballooning with basal hyperkinesis; reduced LVEF (20-40%); may show LVOT obstruction, MR, LV thrombus
  • Coronary angiography: normal or non-obstructive coronary arteries (essential to exclude ACS)
  • LV ventriculography: classical apical ballooning pattern
  • Cardiac MRI: oedema without significant fibrosis; absence of LGE (differentiates from MI and myocarditis); wall motion abnormality extending beyond single coronary territory

InterTAK Diagnostic Criteria

  1. Transient LV wall motion abnormality beyond single coronary territory
  2. Emotional or physical trigger often (but not always) present
  3. New ECG abnormalities, modest troponin rise
  4. No obstructive coronary disease
  5. No myocarditis (confirmed by MRI)
  6. Postmenopausal women predominantly affected

Management

Non-pharmacological

  • Supportive care, cardiac monitoring
  • Psychological support and stress management
  • Avoid catecholamine-augmenting agents if possible

Pharmacological

  • Heart failure management: ACEi/ARB, beta-blockers, diuretics as needed
  • Anticoagulation: if LV thrombus present or LVEF severely reduced (warfarin or DOAC)
  • If LVOT obstruction: avoid inotropes and vasodilators
    • Phenylephrine (alpha-agonist) for hypotension with LVOTO
    • IV fluids
    • Short-acting beta-blocker (esmolol)
  • If no LVOTO with cardiogenic shock: cautious use of inotropes and IABP
  • Beta-blockers: may reduce recurrence (evidence limited)
  • Avoid dobutamine, adrenaline in LVOTO variant

Surgical/Interventional

  • Mechanical circulatory support (IABP, Impella, ECMO): for refractory cardiogenic shock without LVOTO
  • IABP contraindicated if significant LVOTO
  • Rarely needed; most recover with supportive care

Referral Criteria

  • All suspected Takotsubo: admission and coronary angiography to exclude ACS
  • Cardiogenic shock: CCU/ICU with advanced HF team involvement
  • Follow-up echocardiography at 4-8 weeks to confirm recovery

Prognosis

  • LV function recovers in ~95% of cases within 4-8 weeks
  • In-hospital mortality: ~4-5% (comparable to NSTEMI)
  • Cardiogenic shock: occurs in ~10%; mortality in this subgroup ~15-20%
  • Recurrence: ~5-10% over 5 years
  • Male patients: worse in-hospital outcomes
  • Long-term mortality after Takotsubo may be slightly higher than age-matched controls (ongoing research)
  • Most patients: excellent long-term prognosis after recovery

Other Relevant Information

Takotsubo vs ACS

FeatureTakotsuboACS
TriggerEmotional/physical stressPlaque rupture
CoronariesNormal/non-obstructiveObstructive disease
Wall motionBeyond single territoryMatches coronary territory
TroponinModest riseProportional to infarct
BNPOften very highVariable
MRI LGEAbsent/minimalSubendocardial
RecoveryWeeksPermanent damage

Takotsubo Variants

VariantWMA PatternFrequency
Typical (apical)Apical ballooning~80%
Mid-ventricularMid-wall akinesis~15%
Basal (inverted)Basal akinesis~3%
FocalLocalised~2%