Systolic Anterior Motion (SAM) Of The Mitral Valve – Left Ventricular Outflow Tract (LVOT) Obstruction

Left ventricular outflow tract (LVOT) obstruction is a potentially catastrophic etiology for hypotension due to several etiologies: idiopathic hypertrophic subaortic stenosis (IHSS), hypertrophic obstructive cardiomyopathy (HOCM), systolic anterior motion (SAM) of the mitral valve, and even mid-cavity obstructive hypertrophic cardiomyopathy. These obstructions can be dynamic in nature and consequently vary based on cardiac parameters like preload, afterload, contractility, heart rate, etc.

For a specific example, let’s look at systolic anterior motion (SAM) of the mitral valve causing a dynamic LVOT obstruction. Risk factors for this process include a narrowed LVOT diameter from a thick intraventricular septum (IVS), an elongated anterior mitral valve leaflet which gets “sucked” into the LVOT with high blood velocities during systole (Venturi effect), and papillary muscles positioned more apically moving the mitral plane towards the IVS. In LVOT obstructions from any of the aforementioned etiologies, we have several hemodynamic goals to reduce the obstruction and improve forward flow.

In general, we aim to increase ventricular volume (“preload“) and reduce contractility. We can accomplish this by administering fluids, elevating the legs to increase venous return, and using agents like beta blockers for the dual benefit of negative inotropy and negative chronotropy. By keeping the heart rate on the low-normal side, we prolong diastole and allow the heart to fill more to alleviate the LVOT obstruction.

Here are some transesophageal echo (TEE) clips I acquired of SAM. You can see how the anterior leaflet of the mitral valve (ALMV) moves into the LVOT causing a dynamic obstruction. Furthermore, the classic finding of aortic valve (AoV) leaflet fluttering is also present.

Now consider this example around the time of inducing general anesthesia. We routinely administer medications like succinylcholine, nondepolarizing neuromuscular blockers, and antibiotics which can cause anaphylaxis at the beginning of surgery. How does anaphylaxis present in a patient under general anesthesia? Typically hypotension and tachycardia. How does a dynamic LVOT obstruction present? Typically hypotension and tachycardia.

Okay, but why does that matter?

Epinephrine is the mainstay treatment for true anaphylactic reactions to stabilize mast cell degranulation and support hemodynamics. However, epinephrine will drastically increase a patient’s contractility and heart rate… a bad idea in dynamic LVOT obstruction. The presentations are the same. The treatments are different. This is the benefit of bedside echocardiography to differentiate between the two! 🙂

Drop me a comment below with questions! 🙂

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14 responses to “Systolic Anterior Motion (SAM) Of The Mitral Valve – Left Ventricular Outflow Tract (LVOT) Obstruction”

  1. Karen D Avatar

    Could you explain this for me:
    Findings
    Mitral Valve
    Significant systolic anterior motion of the mitral valve is present.
    Mild mitral regurgitation is present.
    Aortic Valve
    The aortic valve is trileaflet with normal leaflet excursion.

  2. Jim Avatar

    Dr Rishi;

    I’m a retired 66 yoa pathologist who has had recent problems with atrial fibrillation & flutter which has been treated with Watchman, b/l atrial rf ablation since Nov 2023. I developed a postop pericardial effusion with tamponade in. They drained ~2,000 cc bloody fluid that was neg for infection. My most recent 2d echocardiogram reveals the following:

    • The left ventricular systolic function is hyperdynamic. The visually estimated ejection fraction is 65%
    • Severe predominantly basal septal hypertrophy. Rest PG = 5 mmHg, with Valsalva PG = 15 mmHg.
    • Chordal SAM, mild anterior mitral leaflet SAM, mild dynamic LVOT gradient, rest LVOT PG = 5 mmHg, Valsalva LVOT PG = 15 mmHg
    • The pulmonary artery pressure could not be estimated due to inadequate tricuspid regurgitation signal.
    • No pericardial effusion.

    My question is the septal hypertrophy and LVOT going to seriously impact my quality of life? What are your thoughts? I used to deal with pieces and parts, not echocardiograms. The numbers and what I have read doesn’t look that bad, but I am not a cardiologist.

    Thank you for your input, Doctor

    1. Rishi Avatar

      Hey Jim! Please call me Rishi – we’re colleagues! Without getting into too much “giving medical advice over the Internet”, therapies are usually based on symptoms and can range from medical management (beta blockers, staying hydrated) to alcohol septal ablation in the cath lab and even surgical myectomies in the OR. I’ve seen plenty of patients in the OR and ICU with gradients worse than that who are completely asymptomatic, so I agree, your numbers are reassuring. Needless to say, it’ll be important to follow-up periodically with your specialist and log any symptoms you have.

      1. Jim Avatar

        Thank you, Rishi. After reviewing your website, I have pondered how you have all of the time to devote to your many interests. After all, there’s only 24 hours in a day,but I digress.

        I am meeting with my general cardiologist in August to go over my treatment plan. I’m feeling better now than I have over a number of years. I’m trying to improve my strength and stamina via T’ai Chi, Qigong, meditation, walking, biking, and strength training. My diet is based on my modified Mediterranean version. I will f/u with you Rishi late summer to early fall.

  3. Brittany Avatar

    When evaluating the anterior mitral valve and SAM, not every instance results in LVOT obstruction. How do we know for sure that there is an LVOT obstruction? Is the only way to observe the dagger sign? What else can we look for to diagnose obstruction? Is valve replacement an option if the SAM is severe enough?

    1. Rishi Avatar

      Yes, the “dagger” shape on spectral doppler interrogation of the LVOT does suggest a dynamic outflow obstruction. A lot of SAM we see isn’t clinically significant (ie, chordal SAM), and there are various levels of severity. 3D TEE of the aortic valve apparatus (LVOT – valve – ascending aorta) cropped down to the level of outflow can sometimes show the anterior mitral leaflet obstructing the outflow too.

      We initially treat SAM with medical therapy. Beta-1 receptor blockade (reducing contractility and increasing ventricular filling) coupled with volume loading is typically attempted first. Surgery is usually a last resort, and many techniques are summarized in Table 1 of this article. Essentially, the surgical goal would be to move the mitral leaflet coaptation point more posteriorly and/or increase the distance between the coaptation point and the interventricular septum (Csept).

  4. Mary Avatar

    My reading for SAM was 1.8 m/ sec and now 4.6 m/sec what does that mean

    1. Rishi Avatar

      They’re velocities, but I’m not sure of what. Ask the physician who ordered/interpreted the study.

  5. Sharon Avatar

    Ok. So I looked at this last night but I wasn’t sure what you were asking. When I first looked, I thought Cardiomyopathy, and Mitral Valve Prolapse seemed to obvious to me. But, bc of the extent of the disease process, bad things can happen. So, I believe that Pulmonary Hypertension is already an issue. I see what you wrote about treating the Mitral Valve. So, my question is, How do you treat the patients who have progressed to pulmonary htpertension along with the other symptoms in the short term? What can we offer them for a comfortable, quality of life after the crisis? I also wanted to say that I’ve experienced Anaphylaxis response 3 times. SO very scary. Once to PCN, once to a Cephalosporin, and once to Peanuts. All allergies developed as an adult. Always carry an Epi-Pen, an inhaler, and Benadryl. Have chewed Benadryl many times to slow down the effects. Another question totally out there, but interesting. Have you ever had a patient with Malignant Hyperthermia yet? My nephew had it, really scary stuff! Was scared when my kids were put to sleep the first time. Thank you Rishi for this lesson. Look forward to ypur response?

    1. Rishi Avatar

      So remember this isn’t a true mitral valve prolapse. This is systolic anterior motion (SAM) of the leaflet intermittently causing obstruction of the left ventricular outflow tract (LVOT). In general, for any degree of chronic mitral regurgitation leading to pulmonary hypertension, one must focus on the pulmonary vascular resistance (PVR), volume status, and right heart metrics. Maneuvers to decrease PVR (avoiding hypoxia and hypercarbia, using meds like epinephrine and milrinone, considering inhaled Flolan), optimizing volume status (usually keeping the patient a little on the dry side with diuresis), and supporting the right heart (optimizing volume, epinephrine and milrinone) can all help. There are better long term options for pulmonary hypertension like home oxygen, sildenafil, Bosentan, etc. Sometimes a mitral valve replacement is the best option, but we try to optimize patients the best we can before surgery.

      That’s scary about anaphylaxis, but I’m glad you’re taking the necessary precautions!

      I’ve never had a patient with malignant hyperthermia (MH), but it’s definitely a high-yield topic in the world of anesthesiology. Please make sure that this history is relayed for all future anesthetics, and if your nephew has any siblings, perhaps they should be aware of the potential for MH too.

      1. Sharon Avatar

        I get what you’re saying now. I’m alwsys thinking treat with a surgically first. That’s not always best, or posible. Patient’s not always healthy enough to have surgery first. When treating with the right meds, and O2, and then if needed, surgery. Thank you Rishi?

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