Congratulations Dr. Blumenberg for correctly answering this month’s Rhythm Nation. Also, special thanks to Dr. Brian Tu for his help in creating my gif and adding it to my post! Now, for more on Takotsubos!!

 

Stress cardiomyopathy

Stress cardiomyopathy (AKA apical ballooning syndrome, takotsubo cardiomyopathy, broken heart syndrome) is a syndrome characterized by transient regional LV systolic dysfunction, mimicking an MI, but without CAD or acute plaque rupture.

“Takotsubo” is the Japanese name for an octopus trap, which has a shape that is similar to the systolic apical ballooning appearance of the LV, in the most common and typical form of this disorder.

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Epidemiology/Risk Factors

  • Found in 1-2 % of patients suspected for ACS
  • Found more in Women than Men
  • Found more in older adults (mean age was 66.4 years)
  • Over half (55.8%) have a history of a neurologic or psychiatric disorder, on medications
  • Physical triggers (acute medical illness or surgery) occurs in 35-36% of patients
  • Emotional triggers (death of relative, domestic abuse, financial debt ..etc) occurs in 27.7- 39%
    • Both physical and emotional triggers occur in 7.8%
    • Up to 28.5% have no evident trigger

Pathogenesis

  • Not well understood
  • Catecholamine excess theory
    • Physical or emotional triggers suggest a catecholamine-induced microvascular spasm or dysfunction, resulting in myocardial stunning
    • Studies show plasma catecholamines are significantly higher in the patients with stress cardiomyopathy as compared with those with an MI
    • Lastly, the reversible cardiomyopathy looks similar to patients with acute pheochromocytoma and acute brain injury, SAH, (which also has catecholamine release).
  • Coronary artery spasm theory
    • Coronary spasm, causing transient ischemia, which resolves, showing no obstruction
    • Occasional angiography has suggested findings that suggest multifocal coronary vasospasm, however this isn’t a widespread finding.
  • Microvascular dysfunction.
    • Transient occlusion in small vessels, with subsequent spontaneous thrombus lysis, could produce apical stunning and wall-motion abnormalities that would improve over follow-up.
  • Left Ventricular Outflow Tract obstruction
    • Unclear the role this plays.

Signs and Symptoms

  • The most common symptoms are chest pain (75.9%), dyspnea (46.9%), and syncope (7.7%)
  • Less common presentations:
    • Heart failure, tachycardias (V Tach/V Fib), bradycardias, or significant mitral regurg
    • Cardiogenic shock is presenting feature in 10%
    • Sx of a TIA or CVA may develop (likely from embolization of apical thrombus)

Diagnostics

  • EKG
    • ST elevation is frequent (43.7%), generally in anterior precordial leads
    • ST depression is a less common finding (7.7%)
    • Other findings include QT prolongation, T wave inversion and abnormal Q waves
  • Cardiac Markers
    • Troponin levels are inc (87%) (median initial troponin 7.7 times the upper limit of normal)
    • Creatine kinase levels are generally normal/ mildly elevated (median CK 0.85 times ULN)
    • BNP are elevated (82.9%) (median level 6.12 times the ULN)
  • Echocardiogram
    • Transient LV systolic dysfunction, which reveals regional wall motion abnormalities (hypokinesis, akinesis, or dyskinesis)
    • Apical ballooning- Most common type (81.7%). Reflecting depressed mid and apical segments, with hyperkinesis of the basal walls.
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    • Less common (atypical) variants:
      • Mid-ventricular type – Ventricular hypokinesis with relative sparing of the apex
      • Basal type – Hypokinesis of the base with sparing of the mid-ventricle and apex (reverse or inverted Takotsubo).
      • Focal type – A rare focal variant is characterized by dysfunction of an isolated segment (most commonly the anterolateral segment) of the LV
      • Global type – Rarely, patients have global hypokinesis

Approach to diagnosis

  • Mayo Clinic diagnostic criteria, (requires all 4):
    • Transient LV systolic dysfunction. The wall motion abnormalities are typically regional and extend beyond a single epicardial coronary distribution.
    • Absence of obstructive CAD or angiographic evidence of acute plaque rupture in the distribution of the wall motion abnormality found.
    • New EKG changes (either STEAnd/or T wave inversion) or modest elevation in troponin.
    • Exclusion:
      • Absence of pheochromocytoma or myocarditis.
      • Obstructive CAD with wall motion in single artery distribution
      • Death during acute phase before wall-motion recovery

Treatment

  • Stress cardiomyopathy is generally a transient disorder managed with supportive therapy.
  • In the ED, typically indistinguishable from ACS and/or CHF and should be treated and managed accordingly (activate cath lab, anticoagulate, heart failure management…etc).

Prognosis

  • In-hospital mortality is 4%. Death rate of any cause is 5.6% (more in men). Patients who survive the acute episode typically recover systolic LV function within 1-4 weeks.
  • Patients who survive face an approximately 2 % per year risk of recurrence. The efficacy of medical therapy in reducing the risk of recurrence is unknown

 

References

 

 

 

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