Takotsubo syndrome

Circumferential wall-motion pattern beyond one coronary territory — and the complications that kill.

Numbers to remember

• In-hospital cardiogenic shock ≈10%, death ≈4% — comparable with ACS ^[135]
• LVOT obstruction in 10–25% — worsened by inotropes and vasodilators ^[134]
• RV involvement in about one-third, and a marker of worse outcome ^[133,134]
• Recovery of wall motion typically within days to weeks ^[133]

Questions echo must answer

Takotsubo syndrome is acute, usually reversible LV dysfunction whose wall-motion abnormality extends beyond a single coronary territory. It is often, but not always, triggered by emotional or physical stress ^[133]. In the International Takotsubo Registry the rate of serious in-hospital complications was similar to ACS ^[135]. Echo does not replace coronary angiography, but it defines the pattern and detects the complications that change treatment ^[134].

1. PatternApical ballooning (most common), mid-ventricular, basal ("inverted") or focal ^[133].
2. Circumferential?Does the abnormality wrap around the ventricle beyond one coronary territory?
3. LVOT obstruction and SAMThe basal hyperkinesis can create a gradient ^[134].
4. RV involvement, MR, thrombus, rupture, effusion.
5. OutputLVOT VTI, SVI, CI; shock staging ^[154].
6. RecoveryA repeat study confirms the diagnosis in retrospect ^[133].

Acquisition protocol

1. A4C / A2C / A3CSegmental wall motion (17 segments), biplane LVEF, WMSI. Look for the ballooning shape and the hyperkinetic base ^[1].
2. PSAX sweepIs the circumferential extent the same at mid and apical levels in all walls?
3. A5C / A3CCW through the LVOT for a late-peaking gradient. Look for SAM on 2D and M-mode. Record MR direction ^[134].
4. RV-focusedRV apical ballooning, TAPSE, S′.
5. ApexThrombus, with contrast if limited ^[140].
6. OutputLVOT VTI, SVI and CI; E/e′; IVC.
7. PericardiumEffusion. A new effusion with haemodynamic change suggests rupture.

• Pattern (apical / mid / basal / focal)
• Extends beyond one coronary territory?
• LVEF, WMSI
• LVOT gradient and SAM
• MR
• RV involvement
• Apical thrombus
• SVI, CI
• Follow-up echo planned

Diagnosis & severity

InterTAK diagnostic criteria (selected) ^[133]

• Transient LV dysfunction (hypokinesia, akinesia or dyskinesia) presenting as apical ballooning or mid-ventricular, basal or focal wall-motion abnormality. The regional abnormality usually extends beyond a single coronary vascular distribution.
• An emotional, physical or combined trigger may precede the event, but it is not obligatory.
• New ECG abnormalities, and modestly raised troponin with relatively marked natriuretic peptide rise.
• Significant coronary artery disease does not exclude takotsubo.
• No evidence of infectious myocarditis.

Thresholds that change management

• Shock with an LVOT gradient → stop inotropes and vasodilators. Give cautious fluids, a short-acting beta-blocker and phenylephrine if needed. Consider mechanical support rather than catecholamines ^[134].
• Shock without LVOTO → mechanical circulatory support is preferred over catecholamines, which may worsen the syndrome ^[134].
• Apical ballooning with akinesis → screen for thrombus. Anticoagulate if thrombus is present, and consider it with large akinetic regions ^[134,140].
• Repeat echo (days to weeks) to document recovery. Failure to recover should prompt reconsideration (MI, myocarditis, cardiomyopathy) ^[133].

Pitfalls & mimics

• Myocarditis: more patchy and often epicardial. CMR distinguishes it (LGE pattern, oedema) ^[125,134].
• Pheochromocytoma and subarachnoid haemorrhage produce takotsubo-like patterns. Consider them in the history.
• Inverted (basal) variants are missed if the base is not studied carefully.
• Foreshortening hides apical ballooning. Find the true apex.
• Hyperkinetic base plus hypovolaemia equals dynamic obstruction. Reassess after every haemodynamic change.