01OverviewDefinition, clinical context and the essential points that orientate the chapter.
Takotsubo syndrome is an acute myocardial-injury syndrome that closely mimics MI. The correct early stance is diagnostic humility: manage suspected ACS, image urgently and define coronary anatomy.
The key inpatient task is not merely naming the wall-motion pattern but finding complications—shock mechanism, LVOTO, MR, arrhythmia and thrombus—because standard heart-failure drugs can be harmful in obstructive physiology.
Recovery is typical but the episode is not benign; recurrence and early complications justify cardiology follow-up and repeat imaging.
Key points
- Takotsubo is transient LV and/or RV dysfunction, often beyond one coronary territory, after emotional, physical or neurological stress—but a trigger is not required.
- It commonly affects postmenopausal women but can occur in any adult; do not use demographics to dismiss ACS.
- ECG changes and troponin rise are common; coronary angiography is often needed because MI remains the immediate competing diagnosis.
- Echo must look for the wall-motion pattern, LV outflow obstruction, MR, RV involvement and apical thrombus.
- CMR helps exclude infarction and myocarditis and usually shows oedema without infarct-pattern late enhancement.
- Shock management depends on mechanism: pump failure, dynamic LVOTO, acute MR, RV failure and arrhythmia require different treatment.
- Apical ballooning with severe akinesis can form LV thrombus and embolise; use contrast imaging when the apex is unclear.
- Repeat imaging should demonstrate recovery; persistent dysfunction or scar requires diagnostic reconsideration.
02AetiologyUnderlying causes, associations and risk factors, with why each one matters.
Emotional stress
Bereavement, conflict, fear or other intense emotional events may provoke marked sympathetic activation. A recognisable trigger supports the history but is not required for the diagnosis.
Physical or neurological stress
Surgery, sepsis, respiratory crisis and acute neurological illness can produce a strong catecholamine response. Physically triggered presentations often have substantial competing illness and a complicated course.
Postmenopausal susceptibility
Takotsubo disproportionately affects postmenopausal women, suggesting altered autonomic, endothelial and hormonal protection may increase myocardial vulnerability, although demographic pattern alone cannot establish or exclude it.
Catecholamine excess
Exogenous adrenergic exposure or endogenous catecholamine excess can precipitate the syndrome. The history should therefore include medicines, acute physiological stress and features suggesting an endocrine source.
03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.
- 1Sympathetic surge
A stressor activates central and peripheral sympathetic pathways, exposing the myocardium and coronary microcirculation to an abrupt rise in catecholamine signalling.
- 2Reversible myocardial injury
Catecholamine-mediated cellular stress, altered calcium handling and microvascular dysfunction predominantly cause myocardial stunning in a pattern not confined to one obstructed epicardial artery.
- 3Regional dysfunction
Transient akinesis or dyskinesis typically extends beyond one coronary territory. Apical ballooning is typical, but mid-ventricular, basal and focal distributions also occur.
- 4Dynamic obstruction
In some patients, hypercontractile basal segments narrow the left ventricular outflow tract and draw the mitral valve anteriorly, worsening mitral regurgitation and hypotension.
- 5Recovery phase
Myocardial oedema and repolarisation abnormalities gradually resolve as contractility returns. Persistent regional dysfunction or infarct-pattern scar should prompt reconsideration of the original diagnosis.
04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.
Acute chest pain, dyspnoea, ST elevation/depression, T-wave inversion or QT prolongation with a troponin rise.
Emotional distress, surgery, sepsis, respiratory crisis, neurological injury or catecholamine exposure may precede symptoms; absence of a trigger does not exclude it.
Apical ballooning is classic, but mid-ventricular, basal and focal patterns occur; dysfunction generally extends beyond one epicardial vascular territory.
A new systolic murmur, basal hyperkinesis, SAM/MR or hypotension worsening with vasodilation suggests dynamic obstruction.
Pulmonary oedema, shock, ventricular arrhythmia, high-grade block, RV failure or embolic signs require critical-care cardiology.
05InvestigationsWhat to request, why it matters and how to interpret it.
Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.
- 01
Serial ECG and high-sensitivity troponinFirst step - Why
- Run the ACS pathway and identify evolving repolarisation/QT risk.
- Interpretation and limitations
- Neither modest troponin nor widespread ECG change distinguishes Takotsubo reliably from MI.
- 02
Urgent TTE with contrast if needed - Why
- Define wall motion, LVEF, LVOTO, SAM/MR, RV involvement, effusion and thrombus.
- Interpretation and limitations
- Measure LVOT gradient in hypotension; adequate apical visualisation is essential before declaring no thrombus.
- 03
Coronary angiography with ventriculography when appropriate - Why
- Exclude culprit coronary occlusion and demonstrate non-territorial dysfunction.
- Interpretation and limitations
- Incidental coronary disease can coexist; decide whether it explains the wall-motion pattern rather than requiring pristine arteries.
- 04
CT coronary angiography in selected stable patients - Why
- Non-invasively exclude important coronary disease when invasive angiography risk/benefit favours CT.
- Interpretation and limitations
- Not a substitute for urgent invasive treatment when STEMI or unstable ACS is suspected.
- 05
CMR - Why
- Characterise oedema, function and scar; exclude myocarditis or infarction.
- Interpretation and limitations
- Oedema with absent infarct-pattern LGE supports Takotsubo; persistent or territorial enhancement redirects diagnosis.
- 06
FBC, U&E/Mg, glucose, CRP, NT-proBNP and targeted trigger tests - Why
- Assess complications and physical triggers.
- Interpretation and limitations
- Correct electrolyte disturbance and investigate infection, endocrine or neurological causes when clinically indicated.
06Differential diagnosisRealistic alternatives and the features that help distinguish them.
Acute myocardial infarction
Both conditions cause chest pain, ECG change and troponin release. An acute culprit lesion matching the wall-motion territory favours infarction; Takotsubo usually extends beyond one artery.
Spontaneous coronary dissection
This can produce an acute coronary syndrome in a similar demographic. Careful coronary imaging demonstrates a dissected vessel rather than solely the non-territorial dysfunction of Takotsubo.
Myocarditis
Viral symptoms, inflammatory features and a non-ischaemic pattern of myocardial injury on cardiac magnetic resonance favour myocarditis, particularly when dysfunction does not recover as expected.
Pulmonary embolism
Acute dyspnoea, pleuritic pain, hypoxaemia and predominant right-heart strain suggest pulmonary embolism. Dedicated pulmonary vascular imaging identifies embolic disease, which can occasionally coexist with or trigger Takotsubo syndrome.
Acute aortic syndrome
Abrupt maximal-at-onset chest or back pain, pulse asymmetry, neurological deficit or new aortic regurgitation should redirect assessment towards urgent aortic imaging.
Additional chapter-specific clues
Dissection, pulmonary embolism, myocarditis, pheochromocytoma crisis and spontaneous coronary dissection remain important alternatives.
07ManagementImmediate care, first-line treatment, alternatives and escalation.
01Front doorPossible TakotsuboFirst stepAcute chest pain/dyspnoea with ECG change or troponin rise.+
- 1Activate the ACS pathway: ABCDE, ECG within 10 minutes, troponin, monitoring, aspirin if not contraindicated and immediate reperfusion assessment when indicated.
- 2Obtain urgent echo but do not use a ballooning pattern to delay coronary angiography in an unstable or STEMI-pattern presentation.
- 3Define coronary anatomy and exclude dissection, PE and myocarditis according to presentation; use CMR after stabilisation when diagnostic uncertainty remains.
- 4Once Takotsubo is established, review whether ongoing antiplatelet or statin therapy has another indication rather than continuing automatically.
02ShockMechanism-directed instabilityHypotension, hypoperfusion or pulmonary oedema.+
- 1Perform immediate echo to distinguish severe pump failure, LVOTO/SAM-MR, RV failure and mechanical complication; correct arrhythmia and reversible triggers.
- 2If significant LVOTO is present, avoid nitrates and other preload/afterload reduction and avoid catecholamine inotropes where possible; cautious fluid and short-acting beta-blockade may be considered only with specialist haemodynamic supervision.
- 3If pump failure occurs without LVOTO, involve shock specialists early; choose vasoactive or mechanical support by haemodynamics and minimise catecholamine exposure when feasible.
- 4EscalationEscalate refractory shock to a tertiary mechanical-circulatory-support service; reassess frequently because the physiology can change.
03ThrombusApical akinesis or LV thrombusSevere apical ballooning, spontaneous echo contrast, visible thrombus or embolism.+
- 1Use contrast TTE or CMR if the apex is not fully seen; screen for embolic neurological or limb symptoms.
- 2For confirmed LV thrombus, start therapeutic anticoagulation after bleeding and coronary-treatment review; select agent and duration with cardiology because evidence is limited and use may be off-label.
- 3Repeat imaging to document thrombus resolution and ventricular recovery before stopping anticoagulation; extend treatment if thrombus or severe akinesis persists.
04RecoveryDischarge and confirmationStable after acute complications are controlled.+
- 1Reconcile medicines to confirmed indications; there is no single proven recurrence-prevention regimen for every patient.
- 2Arrange repeat echo, usually within weeks to a few months, to demonstrate LVEF and wall-motion recovery and exclude late thrombus.
- 3Address the physical or emotional trigger without implying the illness was imagined; safety-net recurrent chest pain, syncope, breathlessness or focal neurology.
Key medicines and prescribing safety1 treatment · regimens, roles and cautions+
Aspirin
300 mg orally once as soon as possible for suspected ACS, unless contraindicated; maintenance depends on the final coronary diagnosis.Active bleeding, true severe hypersensitivity and anticoagulant/bleeding context; do not let administration delay emergency reperfusion assessment.
08ComplicationsImportant consequences, why they occur and why they matter clinically.
Cardiogenic shock
Extensive ventricular stunning, right-ventricular involvement, dynamic outflow obstruction or acute mitral regurgitation can each reduce forward flow. Identifying the mechanism is crucial because their haemodynamic responses differ.
Acute heart failure
Abrupt systolic dysfunction rapidly raises ventricular and pulmonary venous pressures, causing breathlessness or pulmonary oedema despite previously normal cardiac function.
Ventricular arrhythmia
Myocardial injury and QT prolongation create electrical instability, allowing ventricular tachycardia, torsades or fibrillation during the acute phase. High-grade conduction block may also occur.
Left-ventricular thrombus
Severe apical akinesis causes blood stasis, permitting mural thrombus formation. Embolisation can then produce ischaemic stroke or infarction in another systemic organ.
Recurrence
A later emotional or physical stressor may trigger another episode, sometimes with a different wall-motion pattern, so recovery from the index event does not remove future risk.
09Monitoring and follow-upTreatment response, safety checks and longer-term review.
- Continuous telemetry during the acute phase; track QTc, ventricular arrhythmia and conduction block.
- Serial BP, perfusion, oxygenation, urine output and congestion, with repeat echo if haemodynamics change.
- Review potassium and magnesium and avoid additional QT-prolonging medicines when QTc is prolonged.
- Repeat TTE to document recovery and reassess MR, LVOTO and thrombus.
- If anticoagulated for thrombus, monitor bleeding, renal function and interval imaging.
- Reconsider the diagnosis if function fails to recover or CMR shows persistent scar.
10Special situationsVariants, exceptions and circumstances that change the usual approach.
Coronary disease can coexist
A stenosis does not exclude Takotsubo; ask whether it explains the distribution and acute physiology.
Trigger is optional
No identifiable emotional stress is required, and physical triggers often predict a complicated course.
Shock is not one mechanism
Echo-defined LVOTO reverses the usual instinct to vasodilate or give inotrope.
Troponin cannot settle it
Biomarker magnitude may seem disproportionate to dysfunction but is not sufficiently specific to avoid coronary assessment.
Recovery confirms the story
Transient dysfunction supports the diagnosis; persistent abnormalities reopen myocarditis, infarction and cardiomyopathy differentials.
11Common pitfallsFrequent interpretation and management errors.
- 01
Calling Takotsubo from a stress history before excluding coronary occlusion.
- 02
Giving nitrates or inotropes reflexively in shock without checking for LVOTO.
- 03
Accepting a technically limited apical echo as proof that no thrombus exists.
- 04
Continuing dual antiplatelet therapy indefinitely with no coronary indication after the diagnosis is revised.
- 05
Failing to arrange imaging that documents recovery.