Takotsubo Cardiomyopathy (Stress-Induced Cardiomyopathy)

 Definition

Takotsubo cardiomyopathy (TTC), also called stress-induced cardiomyopathy or “broken heart syndrome”, is a transient left ventricular (LV) systolic dysfunction that mimics acute myocardial infarction but occurs in the absence of significant coronary artery obstruction.

The name “Takotsubo” is derived from the Japanese word for an octopus trap, which has a narrow neck and round bottom, resembling the LV shape during systole in this condition.


Pathophysiology

1. Catecholamine Excess

  • Sudden emotional or physical stress leads to surge of catecholamines (epinephrine, norepinephrine).
  • This causes:
    • Myocardial stunning (especially in the LV apex)
    • Coronary microvascular dysfunction
    • Direct catecholamine-induced myocyte injury (toxic effect)

2. Neurogenic Mechanisms

  • Stress activates sympathetic nervous system, leading to excessive β-adrenergic stimulation.
  • High circulating epinephrine causes switch of β2-receptor coupling from Gs to Gi protein — producing negative inotropy at the apex (where β2 receptors are denser).

3. Microvascular Spasm

  • Coronary microcirculation constricts transiently → regional ischemia without epicardial occlusion.

4. Estrogen Deficiency

  • Explains the high prevalence in postmenopausal women — estrogen normally has a cardioprotective, anti-sympathetic effect.


 Epidemiology

  • >90% of patients are postmenopausal women (50–75 years).
  • Represents 1–2% of all cases initially diagnosed as acute coronary syndrome (ACS).
  • Common triggers:
    • Emotional stress: bereavement, argument, fear, shock
    • Physical stress: surgery, critical illness, sepsis, stroke, trauma, asthma exacerbation, subarachnoid hemorrhage
    • Occasionally no identifiable trigger.


Clinical Features

Symptoms

  • Sudden onset chest pain, dyspnea, palpitations — similar to ACS.
  • May present with syncope, cardiogenic shock, or sudden cardiac arrest.

Signs

  • Hypotension or heart failure signs in severe cases.
  • May develop pulmonary edema, arrhythmias (AF, VT, torsades), or LV outflow tract obstruction (LVOTO).


 Investigations

1. Electrocardiogram (ECG)

  • Mimics acute MI:
    • ST-segment elevation (especially in precordial leads)
    • T-wave inversion
    • QT prolongation
    • No reciprocal ST depression typical of MI

2. Cardiac Biomarkers

  • Troponin mildly elevated, but disproportionate to wall motion abnormalities.
  • BNP/NT-proBNP markedly elevated due to wall stress.

3. Echocardiography

  • Typical finding: Apical ballooning with basal hyperkinesis.
  • Variants:
    • Apical type (most common, ~75%)
    • Mid-ventricular type
    • Basal (reverse) type
    • Focal type
  • LV ejection fraction usually 20–45%.
  • May show LVOTO and mitral regurgitation.

4. Coronary Angiography

  • Normal or non-obstructive coronaries (<50% stenosis).
  • Used to exclude acute coronary occlusion.

5. Cardiac MRI

  • Demonstrates myocardial edema without late gadolinium enhancement, helping to differentiate from infarction or myocarditis.


🩺 Diagnostic Criteria

 Revised Mayo Clinic Criteria (2008)

All four should be present:

  1. Transient LV systolic dysfunction (apical, mid, or basal segments) extending beyond a single coronary distribution.
  2. Absence of obstructive coronary artery disease or acute plaque rupture.
  3. New ECG abnormalities (ST elevation/T-wave inversion) or modest troponin rise.
  4. Absence of myocarditis or pheochromocytoma.


 Pathological Findings

  • Myocyte injury with contraction band necrosis, interstitial infiltrates, and fibrosis — consistent with catecholamine toxicity.


Management

1. Initial Management (like ACS)

  • Oxygen, aspirin, nitrates, and morphine — until MI is ruled out.
  • Avoid fibrinolysis until coronary anatomy known.

2. Supportive Therapy

  • Usually self-limiting, with recovery in 1–4 weeks.

If LV dysfunction present:

  • β-blockers (reduce catecholamine effect)
  • ACE inhibitors/ARBs (LV remodeling, afterload reduction)
  • Diuretics (for pulmonary congestion)

If LVOTO present:

  • Avoid inotropes (can worsen obstruction)
  • Use β-blockers and gentle IV fluids to increase preload.

If cardiogenic shock:

  • Prefer vasopressors (phenylephrine) or mechanical support (IABP, ECMO) instead of inotropes.

3. Anticoagulation

  • If severe LV dysfunction/apical thrombus → anticoagulate until recovery.

4. Treat Underlying Stressor

  • Emotional or physical trigger should be addressed.


Prognosis

  • Excellent in most; LV function recovers completely in 4–8 weeks.
  • In-hospital mortality: ~1–2%.
  • Recurrence in 2–5% of patients.
  • Complications:
    • LV failure and shock
    • Arrhythmias (AF, VT)
    • LV thrombus and embolism
    • LV rupture (rare)


📚 References

  • Lyon AR et al. Eur Heart J. 2022;43(13):1275–1291. (ESC Consensus)
  • Prasad A et al. Mayo Clin Proc. 2008;83(3):275–279.
  • Harrison’s Principles of Internal Medicine, 21st ed.
  • StatPearls: Takotsubo Cardiomyopathy.