Stress-Induced Cardiomyopathy

What is it

Stress-induced cardiomyopathy is a type of non-ischemic cardiomyopathy caused by a sudden temporary dysnfuction of the myocardium. The etiology is unclear, but thought to be related to the autonomic nervous system and an excessive release of adrenalin. The effect is possible HF, lethal ventricular dysrhythmias, and possible ventricular rupture. This condition is also known as Takotsubo, apical ballooning syndrome, or broken heart syndrome.

It is most commonly seen in postmenopasual women with a history of a recent and severe emotional or physical stress. The average age at onset is between 58-75 years. This condition is usually sudden, and acute with the heart returning to normal in about two months.

Diagnostics
  • Coronary Angiogram
    • Angiography will show no acute blockages to the coronaries and no significant coronary disease.
  • ECHO
    • Will show bulging of the left ventricular apex with hypercontractile base of the LV.
  • ECG
    • ECG findings may be similar to those found with an acute anterior wall MI
  • Chest X-ray
    • May show an enlarged cardiac silhouette.
Treatment
  • Optimize Fluid
    • Ensure adequate fluids to promote preload without over stressing the heart.
    • Mild fluid resuscitation may be needed if there is a right ventricular involvement.
    • ACE-I or ARBs to limit the effect of RAAS (both medications help avoid excessive preload and decrease afterload to improve emptying of the LV).
  • Minimize Myocardial Oxygen Demand
    • Beta blockers (minimize oxygen demand)
    • Calcium Channel blockers (minimize oxygen demand)
    • ACE-I or ARBs (reduce afterload)
  • Decrease Afterload
    • ACE-I or ARBs
    • IABP (intra-aortic balloon pump)
  • Prevent Embolism
    • ASA, or other anticoagulants as indicated (impaired blood flow through LV increases risk of mural thrombus formation)
  • Continuous Cardiac Monitoring
    • Monitor for lethal dysrhtyhmias
Contraindications

Hypotensive patients require careful titration of treatments that affect preload, contractility, and afterload. However, the use of inotropes is contraindicated.

Inotropes increase the myocardial oxygen demand, increase the myocardial workload, and exacerpabe patient symptoms. Avoid:

  • Dopamine
  • Dobutamine
  • Digoxin
  • Epinephrine
  • Norepinephrine
  • Milrinone