What is Takotsubo (stress cardiomyopathy)?

Takotsubo Cardiomyopathy (Stress Cardiomyopathy)

Takotsubo cardiomyopathy is a reversible heart condition characterized by temporary weakening of the heart muscle triggered by emotional or physical stress, typically presenting with chest pain and ECG changes that mimic a heart attack, but without blocked coronary arteries.

Fifth Grade Level Explanation

• Takotsubo cardiomyopathy is also called "broken heart syndrome" because it often happens after something very sad or stressful 1
• Your heart is a muscle that pumps blood. During takotsubo, part of your heart (usually the tip) gets weak and bulges out like a balloon 2
• It happens most often to older women after something very upsetting or stressful 3
• The good news is that your heart usually gets better completely in a few weeks 2
• Doctors can tell it's not a regular heart attack because your heart arteries aren't blocked 2

College Level Explanation

• Takotsubo cardiomyopathy was first described in Japan and named after a traditional octopus trap ("tako-tsubo") because the affected heart resembles this shape 4
• It accounts for approximately 2% of all suspected acute coronary syndrome cases 2
• Key characteristics include:
  • Acute onset of chest pain or shortness of breath 5
  • ECG changes similar to heart attack (ST elevation or T-wave inversion) 6
  • Mild elevation of cardiac enzymes (troponin) 2
  • Temporary wall motion abnormalities, typically affecting the apex of the left ventricle 2
  • Absence of significant coronary artery blockage 2
• The condition is triggered by:
  • Emotional stressors (grief, fear, anger) 3
  • Physical stressors (illness, surgery, extreme exertion) 3
• About 90% of cases occur in women, typically postmenopausal 2
• Recovery is usually complete within weeks, with excellent prognosis 1

Doctor Level Explanation

• Takotsubo cardiomyopathy (TCM) is characterized by transient regional systolic dysfunction of the left ventricle in the absence of obstructive coronary artery disease 2

• Pathophysiology:

  • Catecholamine surge is the primary proposed mechanism with documented supraphysiological elevations during acute episodes 3
  • β2-adrenergic receptor signaling switch from Gs to Gi protein occurs with high epinephrine levels, causing negative inotropy but protecting against apoptosis 3
  • Regional differences in adrenergic receptor density explain the characteristic apical involvement, as the apex has increased β2-adrenergic receptor density 3
  • Microvascular dysfunction and coronary vasospasm may contribute 3
  • Transient left ventricular outflow tract obstruction can occur 3

• Clinical presentation variants:

  • Classic apical ballooning (most common) 2
  • Mid-ventricular variant with sparing of apex and base 3
  • Basal variant (inverse takotsubo) with hyperkinesis of the apex 3
  • Biventricular involvement occurs in approximately 25% of cases 2
  • Mid-ventricular involvement reported in 40% of cases 2

• Diagnostic approach:

  • Consider in patients with apparent ACS and non-obstructive CAD at angiography (Class I recommendation) 2
  • Imaging with ventriculography, echocardiography, or cardiac MRI to confirm diagnosis (Class I recommendation) 2
  • Echocardiography shows characteristic wall motion abnormalities not corresponding to single coronary territory 2
  • Complete recovery of LV function is required to confirm diagnosis 2

• Management (Class I recommendations):

  • Conventional heart failure therapy (ACE inhibitors, beta blockers, aspirin, diuretics) if hemodynamically stable 2
  • Anticoagulation for patients who develop LV thrombi 2
  • For hemodynamic compromise: catecholamines if no outflow tract obstruction (Class IIa) 2
  • IABP for refractory shock (Class IIa) 2
  • Beta blockers and alpha-adrenergic agents in patients with outflow tract obstruction (Class IIa) 2
  • Consider prophylactic anticoagulation to prevent LV thrombi (Class IIb) 2

• Recovery time ranges from several days to many weeks, with excellent long-term prognosis in most cases 2, 1