Systolic Anterior Motion of MV

Case:

  • 82 yo
  • TF regional centre post I/O pacing wire
  • PMH – HTN, smoker, hypercholesterolaemia.
  • Admitted on 4/6 with STEMI, cath lab PCI to LAD
  • Third degree HB
    • Failed pericardiocentesis at parent hospital.
    • Repair of RV lac, CABG x 2, Insertion of IABP.
    • Paced 92 bpm, NA 18, Dobutamine 10, IABP 1:1

 

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What does this TOE MO AV LAX show?[showhide]The anterior mitral valve leaflet is getting dragged into the left ventricular outflow tract in systole

Now look at the CFD on the MV.

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What can you see?[showhide]There is flow acceleration across the LVOT as evidenced by the mosaic appearance. There is also an eccentric posteriorly directed mitral regurgitant jet. To the right, the AMVL is dragged into the LVOT in systole.

What is SAM ( Systolic Anterior Motion) ?

  • dynamic movement of the mitral valve (MV) during systole anteriorly towards the left ventricular outflow tract (LVOT).
  • first documented by Termini et al three-decades ago, and was initially considered to be specific to hypertrophic cardiomyopathy (HCM), but is now recognized to arise in any setting that alters the complex dynamic anatomy of the left ventricle
  • Associated with severe LVOT obstruction and MR.
  • typically observed in patients with HCM or following MV repair

Why do I need to know about SAM?

  • An important cause of obstructive shock
  • Treatment pathway may be significantly different to other causes of shock – “SLOW, SQUEEZE, FILL”
  • Echocardiography is vital in making the diagnosis. Listen out for a loud systolic murmur!

How to manage

  • Management of SAM includes early recognition and treatment.
  • Initial medical management include: Volume expansion, Cease inotropes and rate control, vasoconstrictor. More often, volume replacement is usually adequate. Remember, an IABP reduces afterload- not very useful in a patient with SAM.
  • Surgical management is required when medical therapy has failed.
  • TOE is the imaging of choice. MRI can be used in a stable patient.
  • Screen Shot 2014-12-26 at 7.29.14 pm

Echo imaging in SAM

2D + CFD
  • Visualization of LVOT obstruction by the mitral valve apparatus (leaflet, chordae or papillary muscles)
  • Flow acceleration across the the LVOT
  • Mitral regurgitation (or pansystolic murmur on auscultation)
M-Mode
  • Movement of mitral valve in systole
  • MMode also allows assessment of severity by determining the onset of SAM, the closeness of AMVL to IVS and the duration of MV to septal contact
Spectral Doppler
  • Gradient across the LVOT can be determined (NB patient behaves like they have severe aortic stenosis)

SAM not due to HCM

  • Since the MV is partly responsible for non HCM related SAM, the reasons for this lies in the MV unit – leaflets (anterior, posterior), annulus and subvalvular apparatus ( chordae, papillary muscles); other factors such as a bulging or S-shaped septum (see below) and a hyperdynamic left ventricle.
S shaped septum with movement of AMVL in systole

S shaped septum with movement of AMVL in systole

  • The position of the anterior relative to posterior leaflet, the difference in length of the leaflets (AL to PL ratio <1), the distance between MV coaptation point to the septum (C-Sept of <2.5cm) , mitral-aortic angle, the size of the mitral annulus, (more likely for SAM if small ring inserted) are important considerations for our anaesthetic colleagues during MV repair to reduce the risk of SAM post bypass.
  • Pre CPB predictors of SAM:-
  1. Anteriorly displaced coaptation point
  2. Redundant AMVL (>30mm)
  3. Hypertrophied hyperdynamic LV
  • post-operative incidence to range between 1 and 16% of mitral surgery patients.
  • The disruption of the MV unit causes SAM by means of Venturi effect (fluid pressure reduction at a stenosed area, results in the need to increase the flow velocity) and drag forces (resulting from the high flow of blood through the LVOT- look for flow acceleration on Colour Flow Doppler), drawing the MV anteriorly and towards the LV.
  • A elongated, floppy chordae also predisposes to SAM.
  • SAM peaks at the end of systole in non-HCM hypertrophied ventricles
  • Other conditions associated with risk of developing SAM: diabetes, post myocardial infarction, general anaesthesia in a hypovolaemic patient, dobutamine stress echo.

SAM due to HCM

  • Due to anterior displacement of papillary muscles, septal hypertrophy causing drag forces and Venturi effect, and or smaller LVOT diameter.

Following the TOE for the above patient, fluid bolus was given, the IABP weaned to 1:2, Dobutamine ceased.

References:

  • Michael Ibrahim el al. Modern management of systolic anterior motion of the mitral valve. Eur J Cardiothorac Surg  January 18, 2012
  • Maslow, A. D., Regan, M. M. et al. Echocardiographic predictors of left ventricular outflow tract obstruction and systolic anterior motion of the mitral valve after mitral valve reconstruction for myxomatous valve disease. Journal of the American College of Cardiology, 34(7), 2096 LP-2104. 
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