Until recently I didn´t really know what SAM was. I do now. Boy am I happy. SAM stands for Systolic Anterior Motion of the Mitral valve and is a not too uncommon complication of hypertrophic cardiomyopathies (HCM), myocardial infarction and mitral valve repair or dysfunction.

Normal anatomy
In SAM, instead of the mitral valve closing in systole it flips over and obstructs the left ventricular aortic outflow tract (LVOT).

When looking at the normal parasternal 4-chamber view on the right one can see how this can happen.

The mitral valve inlet and the aortic outflow tract share the same space except for them being separated by the anterior leaflet of the mitral valve.

Now, in order for SAM to occur there has to be some anatomical variation that predisposes the mitral valve to flip over.

Anatomy in SAM
It is easy to see how an hypertrophic cardiomyopathy of the heart and the septum could predispose by reducing the distance the wayward anterior leaflet has travel.

One can also grasp how variations of valve and papillary muscle anatomy, like after an AMI or valve surgery, could have the same effect.

However, 25% of all patients with hypertrophic cardiomyopathies have SAM to some extent without necessarily having any valve defects. Reduction in cross-sectional area of the LVOT alone does not explain how this happens.

Most articles I found emphasise how there also has to be an Venturi effect at play in the LVOT.  The venturi effect describes how pressure in a fluid is reduced, and how flow is increased, as it passes a section with reduced cross-sectional area.

In humans, the normal LVOT in itself is causing some resistance to blood flow from the left ventricle. The resistance is normally minimal and the resulting pressure drop and flow speed increase in the LVOT is marginal.

However, in patients with hypertrophic cardiomyopathies and perhaps a hypertrophic, bulging septum the reduction in cross sectional area can be significant and the venturi effect so strong that it sucks the anterior leaflet into the LVOT.

The result is sometimes severe aortic outflow obstruction and severe mitral regurgitation.

SAM and the pressure drop over the constriction gets worse in states where blood flow through the LVOT is increased. In fact, in some cases it is only evident if the heart is hypercontractile. Some patients have their SAMs de-masked when they have inotrope stress tests with dobutamine.

Why is this important?
SAM is common finding in patients with hypertrophic cardiomyopathies. As many as 25% of these patients have SAM to some extent. In a worst case scenario your are dealing with a crashing patient with critically low cardiac output and severe mitral regurgitation. Their sympathetic system working in overdrive hardly helps as it boosts the venturi effect that sucks the mitral valve into the LVOT.

What these patients don´t need is more inotropes. Increased flow is only going to make things worse.  The correct treatment is to increase preload and decreasing the hyperdynamic state.

Increasing preload will result in increased ventricular dimensions and a reduced Venturi effect. Preload is increased with fluids and vasopressors.

Betablockers will reduce hypercontractility.

Some references:

Interesting case report where SAM was improved by treating the patient with fluid boluses and  esmolol (a beta blocker)

An  study demonstrating how SAM can exist in the absence of hypertrophic disease. In this series of patients it was triggered by exercise.

The best video I could find on youtube. It´s not great.

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3 Responses to SAM

  1. Taylor says:

    Great article. You can also treat SAM by increasing afterload, which will decrease LVEF, and increase LVEDV.

  2. this web site is very much helpful for learners or any doubts
    today i learnt lot about HOCM WITH SAM
    very good information and videos seen about HOCM and SAM

  3. Pingback: The LITFL Review 102 - LITFL

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