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Systolic Anterior Motion in Takotsubo’s Cardiomyopathy

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The Pre-brief

Systolic anterior motion (SAM) is defined as the displacement of the anterior mitral leaflet towards the left ventricular outflow tract, which results in left ventricular outflow tract obstruction (LVOTO). We need to discuss this, because in severely ill patients without prior cardiac disease, SAM has been thought to be the culprit for death. It is a frequently missed diagnosis in critically ill patients. SAM can also result from lethal hypovolemia, ultimately causing higher mortality.  This article highlights some of the physiology behind transient LVOTO by SAM and it’s role in determining care in stress-induced cardiomyopathy.

What are the predisposing conditions

    There are certain features of a patient’s physiology that predispose them to Transient LVOTO. These include, reduced LV cavity size during systole, LV hypertrophy, and . Physiologically tachycardia which contributes to reduced diastolic filling volume and hypovolemia both cause decreased end diastolic volume. For this reason, they are considered features that may lead to displacement of the anterior mitral leaflet.

Considerations for treatment in SAM

  Because there is a physiological basis for SAM, the treatment should be tailored to address the patient’s hemodynamic state. For hypovolemia, consider fluid bolus. You may see resolution of the transient LVOTO with this.

   When starting a hemodynamically unstable patient on pressors in this setting, consider the major mechanisms of SAM. Specifically, we are concerned about increased cardiac contractility, increased LVOT velocity and increased heart rate. Pressors that have mixed alpha and beta-adrenergic effects such as norepinephrine, epinephrine, dopamine contribute in some degree to worsening state in patients with SAM. This is opposed to phenylephrine, which reduces cardiac contractility, heart rate and LVOT velocity thereby actually improving cardiac function. 

Considerations for observed SAM in Takotsubo’s Syndrome

    Takotsubo’s cardiomyopathy, or stress induced cardiomyopathy is a syndrome of transient cardiac dysfunction with still perplexing pathophysiologically. Many studies propose a catecholamine surge as a main culprit for the observed features in patients with Takotsubo’s.
   There are a few different phenotypes of Takotsubo’s, the most common one being apical ballooning with basal sparing. In this state it is possible that SAM contributes to transient LVOTO. Even for patients with stress induced cardiomyopathy, the treatment will require consideration for volume status. If hypovolemic, IV hydration may improve the state. Overall consideration should be given to prevent those factors thought to exacerbate SAM including tachycardia. Given its clinical significance, SAM should be taken into consideration even in the treatment for Takotsubo.

The Debrief

  • Systolic Anterior Motion causes transient LVOTO in critically ill patients.
  • Consider optimizing volume status and use of phenylephrine as a preferred pressor choice in these patients
  • In Takotsubo’s, dynamic LVOTO requires early identification and prompt treatment.

References

  1. Dugar S, Latifi M, Moghekar A, Duggal A. All Shock States Are Not the Same. Systolic Anterior Motion of Mitral Valve Causing Left Ventricular Outflow Tract Obstruction in Septic Shock. Ann Am Thorac Soc. 2016 Oct;13(10):1851-1855. doi: 10.1513/AnnalsATS.201604-288CC. PMID: 27726435.

  2. Mingo S, Benedicto A, Jimenez MC, Pérez MA, Montero M. Dynamic left ventricular outflow tract obstruction secondary to catecholamine excess in a normal ventricle. Int J Cardiol. 2006;112:393–6.

  3. Meuwese CL, Boulaksil M, van Dijk J, Polad J, Meijburg HW. Transient left ventricular outflow tract obstruction with systolic anterior motion of the mitral valve: a stunning cause. Echocardiography. 2017 34 : 1089 – 1091.

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