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Stress Cardiomyopathy: In the perspective of critical care management


Stress cardiomyopathy is a condition in which intense emotional or physical stress can cause rapid and severe heart muscle weakness.1 It mimics myocardial infarction with changes in the electrocardiogram and echocardiogram, but without any obstructive coronary artery disease.3 Stress CMP and Tako-tsubo CMP are used synonymously but Takutsubo is the most common and typical form of this disorder.  A midventricular type, basal type, focal type and global type have also been described.2


The pattern of left ventricular dysfunction was first described in Japan in 1991and has been referred to as “tako‐tsubo cardiomyopathy,”named after the fishing pot with a narrow neck and wide base that is used to trap octopus. “Tako‐tsubo cardiomyopathy”, also known as “apical ballooning syndrome”, “ampulla cardiomyopathy”, “stress cardiomyopathy” or “broken‐heart syndrome” is now increasingly recognised in other countries as well.3 “Transient left ventricular apical ballooning” has also been used to describe similar cardiac contractile function in patients after physical or emotional stress.

Stress Cardiomyopathy occurs in approximately 1-2% of patients presenting with troponin-positive suspected ACS or Suspected STEMI. A prevalence of 1.2% was reported from a registry of 3265 patients with troponin-positive ACS. Similarly, Stress CMP accounted for 1.7-2.2% of cases presenting with suspected ACS or STEMI in a systematic review.2

Etiology: The exact cause of this condition is unclear. But it is often preceded by an intense physical or emotional event in 85% of cases. Some potential triggers are- unexpected death of a loved one, a frightening medical diagnosis, sudden financial loss, strong arguments, job loss anddivorce. Physical stressors include acute asthma, surgery, chemotherapy and stroke.4

It’s also possible that some drugs, rarely, may cause broken heart syndrome by causing a surge of stress hormones. Drugs that may contribute to broken heart syndrome include:Epinephrine, Duloxetine,Venlafaxine,Levothyroxine.4

Pathophysiology: The exact pathogenesis of Stress Cardiomyopathy is unclear but there are few theories that have been suggested:

  1. Catecholamine Induced-In some studies it was found that serum catecholamine concentration was 2-3 times higher in SCMP than in MI. It was also seen that exogenously administered catecholamines and pheochromocytoma produce similar picture. Catecholamine triggers α1-mediated coronary vasospasm and β1-mediated hyperdynamic basal contraction, as basal contraction has higher density of sympathetic nerve endings and higher content of norepinephrine.
  2. Microvascular Dysfunction- the characteristic findings of microvascular dysfunction found were endothelium-dependent vasodilatation, excessive vasoconstriction and impairment of myocardial perfusion. Afonso et al demonstrated that circulatory disturbance, indicating coronary microvascular dysfunction was found on a myocardial contrast echocardiography and epicardial coronary arteries were normal.
  3. Cytokine Induced-Frencesco et al.5 found higher levels of circulating cytokines, viz.IL-2, IL-4,IL-10, TNFα, IFNγ and EGF on admission whereas IL-2 and EGF were higher even at 120hrs. Ahmad Abdin presented a case of Takotsubo Cardiomyopathy in a patient of Hemophagocytic Lymphohistiocytosis.6
  4. Dynamic mid-cavity or LV outflow tract obstruction due to any cause

Clinical Features: Stress CMP occurs most commonly in females(90%).Patients typically present with chest pain, shortness of breath, sweating, dizziness, nausea, vomiting, palpitation, etc.

Investigations and findings:

  1. ECG: ST-segment elevation seen in half of all cases. St segment depression, QT prolongation, T-wave inversion, abnormal Q-waves are also seen but rarely.
  2. Troponin- Serum troponin are raised in most of the cases(median initial troponin 7.7 times the upper limit of normal).
  3. BNP and NT proBNP- are elevated in most patients. BNP levels were elevated in 82.9% of patients with StressCMP in the International Takotsubo Registry study.
  4. ECHO: RWMA with moderate to severe LV systolic dysfunction.
  5. Coronary Angiograpthy: Normal coronaries in angiography documentation of which is must for diagnosis of this condition.


  • First line
    • Sedation/anxiolytics/analgesics is therapeutic
    • If possible, treat with combined α/β-blockers to reverse “catecholamine toxicity”; avoid unopposed β-blockade
  • If hypotensive / cardiogenic shock
    • No LVOT obstruction:
      • standard therapy- ↓ preload/afterload; judicious inotropes
    • LVOT obstruction: (due to compensatory hyperdynamic contractions of basal segment of LV)
      • Peripheral vasoconstrictors; potential worsening of obstruction with catecholamines
      • Gentle volume resuscitation to decrease LVOT gradient
      • Early consideration of MCS- IABP or preferably pVAD to decompress LV and bypass LVOT
  • If in pulmonary edema
    • Diuretics and fluid management
    • PA catheter helpful to optimize filling pressures


  1. Retrieved from https://www.hopkinsmedicine.org/heart_vascular_institute/conditions_treatments/conditions/stress_cardiomyopathy/symptoms_diagnosis.html
  2. Retrieved from https://www.uptodate.com/contents/clinical-manifestations-and-diagnosis-of-stress-takotsubo-cardiomyopathy
  3. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2600114/
  4. Retrieved from https://www.mayoclinic.org/diseases-conditions/broken-heart-syndrome/symptoms-causes/syc-20354617
  5. https:// doi.org/10.1016/j.atherosclerosis.2018.05.017
  6. https://doi.org/10.1016/j.chest.2016.08.448


Dr.RitankurBarkotoky MD DM FACC FSCAI FCSI
Senior Consultant Cardiologist, Narayana Hrudayalay Guwahati

Dr.KallolBasak, MBBS, MD Masters in non invasive cardiology
Associate Consultant, Narayana Hrudayalay, Guwahati

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