Reversed takotsubos cardiomyopathy
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reverse takotsubo cardiomyopathy
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"reverse takotsubo" OR "inverted takotsubo"
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reverse takotsubo cardiomyopathy basal ballooning apical hyperkinesis
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reverse takotsubo cardiomyopathy basal ballooning definition pathophysiology clinical features
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Reverse Takotsubo Cardiomyopathy (rTTC)
Definition & Classification
Reverse (or "inverted") Takotsubo cardiomyopathy is a morphological variant of Takotsubo syndrome (TTS) in which the basal segments of the left ventricle are hypokinetic/akinetic while the apex contracts normally or is hyperkinetic — the exact mirror image of classic TTS.
Shimizu et al. classified TTS into four wall-motion subtypes:
| Type | Pattern |
|---|---|
| Classic (apical) | Apical akinesia + basal hyperkinesia (~80% of cases) |
| Reverse (basal) | Basal akinesia/hypokinesis + apical hyperkinesia (~2–5%) |
| Mid-ventricular | Mid-wall hypokinesis + basal and apical hyperkinesia |
| Focal | Any other segmental ballooning pattern |
The InterTAK diagnostic criteria formally recognise all four subtypes, stating: "regional wall motion abnormality usually extends beyond a single epicardial vascular distribution" and that "transitions between all types can exist." — Fuster & Hurst's The Heart, 15th Ed.
Pathophysiology
The prevailing mechanism is catecholamine-mediated myocardial stunning, but the regional distribution in rTTC differs from classic TTS due to heterogeneous adrenergic receptor density:
- Classic TTS — The apex is rich in β₂-adrenoceptors (higher density than the base). During catecholamine surges, the apical β₂ receptors switch their signalling from Gs (stimulatory) to Gi (inhibitory), causing apical stunning while the base continues contracting.
- Reverse TTS — The basal segments are predominantly affected, suggesting either:
- A different sympathetic innervation pattern (higher basal adrenergic sensitivity in some individuals)
- A physical/pharmacological trigger (rather than emotional) — adrenergic agonists such as dobutamine, epinephrine, or exogenous catecholamines (as in pheochromocytoma or inotrope infusion) tend to preferentially stun the base
- Notably, rTTC is more commonly associated with physical triggers and pharmacological stress (e.g., dobutamine stress testing, liver transplantation, pheochromocytoma crisis) rather than emotional stress
Clinical Profile
Demographics: rTTC affects a younger population on average compared to classic TTS, and has a less pronounced female preponderance. Men and younger women are relatively more represented.
Common triggers:
- Pheochromocytoma / catecholamine-secreting tumours
- Exogenous catecholamines (dobutamine, epinephrine infusion)
- Dobutamine stress echocardiography
- Liver transplantation (reperfusion catecholamine surge)
- Subarachnoid haemorrhage / neurological events
- Emotional stress (less common than in classic TTS)
Symptoms: Indistinguishable from classic TTS and ACS:
- Chest pain, dyspnea, palpitations
- Pulmonary oedema, hypotension
- Syncope
ECG Findings
The ECG pattern mirrors the wall-motion distribution:
Panel A: Widespread T-wave inversions in lateral (I, aVL), inferior (II), and precordial leads (V1–V6). Panels B–C: Left ventriculography showing basal hypokinesis (dotted lines) with apical hyperkinesis (arrowheads) — the "reverse" pattern.
- ST elevation or T-wave inversions (may be less prominent in leads V4–V6 compared to classic TTS)
- QT prolongation (risk of torsades de pointes)
- ST elevation in inferior or lateral leads may be more prominent (reflecting basal ischaemia)
Echocardiography
Apical 4-chamber view: yellow arrows = hyperkinetic apex; blue arrows = hypokinetic mid-to-basal LV segments. LVEF severely reduced at ~25%.
- Basal and mid-ventricular hypokinesis/akinesis
- Preserved or hyperdynamic apical contraction
- LV outflow tract obstruction is not a feature (it occurs in classic TTS due to basal hyperkinesis + septal bulge causing SAM of the mitral valve)
- Right ventricular involvement can co-occur
Diagnosis
Requires exclusion of:
- Obstructive CAD — coronary angiography (no culprit stenosis)
- Pheochromocytoma — especially in rTTC, given the strong association; 24-hr urine/plasma metanephrines should be obtained
Cardiac MRI confirms:
- Diffuse myocardial oedema without late gadolinium enhancement (distinguishes from MI and myocarditis)
- Basal distribution of wall motion abnormality
Acute Complications
Generally similar to classic TTS but note:
- No LVOT obstruction (a key difference from classic)
- Cardiogenic shock (from severe basal dysfunction)
- Arrhythmias: QTc prolongation → torsades de pointes
- LV thrombus (rare, but possible in akinetic basal segments)
Management
No randomised trials exist specific to rTTC; management follows general TTS principles:
| Situation | Approach |
|---|---|
| Pulmonary oedema | IV nitrates, diuretics |
| Haemodynamic instability | Cautious inotropes (avoid if pheochromocytoma suspected); IABP if no LVOT obstruction |
| Catecholamine surge (e.g. phaeo) | Alpha-blockade first, then beta-blockade |
| Arrhythmia / QT prolongation | Magnesium sulphate; avoid QT-prolonging drugs |
| Pharmacological trigger (dobutamine) | Cease the offending agent |
| Long-term | ACEi/ARB, beta-blocker during recovery (expert consensus); reassess for pheochromocytoma |
⚠️ If pheochromocytoma is the underlying trigger (which should always be excluded in rTTC), selective beta-blockade alone is contraindicated — it can precipitate hypertensive crisis by leaving alpha-receptors unopposed. Alpha-blockade must come first.
Prognosis
- The condition is transient and reversible in the vast majority — LV function normalises within days to weeks
- Primary rTTC (emotional trigger) has a benign prognosis
- Secondary rTTC (associated with severe physical illness or pharmacological triggers) carries a higher event rate, similar to secondary classic TTS — Fuster & Hurst's The Heart, 15th Ed.
- Recurrence risk: ~10% at follow-up (similar to classic TTS), estimated at ~2%/year — Harrison's Principles of Internal Medicine, 22nd Ed.
Key distinction summary:
| Feature | Classic TTS | Reverse TTS |
|---|---|---|
| Wall motion | Apical ballooning, basal hyperkinesis | Basal ballooning, apical hyperkinesis |
| Trigger | Emotional > physical | Physical/pharmacological > emotional |
| Demographics | Older postmenopausal women | Younger; less female-predominant |
| LVOT obstruction | Common | Absent |
| Pheochromocytoma | Occasional | Strongly associated |
| Prognosis | Benign; transient | Transient; secondary forms higher risk |
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