The term “Systolic Anterior Motion” (SAM) defines a systolic displacement of the distal portion of the anterior leaflet of the mitral valve towards the outflow tract of the left ventricle (LV). This abnormal motion, first described in “muscular subvalvular aortic stenosis,” has two possible consequences: left ventricular outflow tract (LVOT) obstruction and mitral valve regurgitation ( Fig. 15-1 ).
SAM is seen most commonly in hypertrophic obstructive cardiomyopathy (HOCM) or in Barlow’s disease after mitral valve repair. The mutual finding between these two conditions is a discrepancy between the amount of valvular tissue and the mitral valve orifice area. In HOCM, there is a small orifice area with a normal amount of valvular tissue. In Barlow’s disease, the contributing cause is excess valvular tissue with an orifice area restored to normal or overcorrected by annuloplasty.
SAM results from a discrepancy between the amount of valvular tissue and the mitral valve orifice area.
PATHOPHYSIOLOGY
Systolic anterior motion of the mitral valve after valve repair was first reported by Gallerstein et al and Kronzon et al. Early in our experience, Mihaileanu observed SAM in 4.5% of all of our valve reconstruction procedures. Since all cases of SAM at that time were associated with the use of the Classic ring, SAM was thought to be linked to the rigidity of the ring itself.
Our understanding of the true mechanism of SAM evolved from two observations: (1) SAM was never seen in patients with rheumatic or ischemic mitral valve disease despite the use of the Classic ring ; (2) SAM was also observed in degenerative valvular disease after reduction annuloplasties using circular or semicircular flexible bands. Thus it became apparent that it was not the rigidity of the ring but a mismatch between the amount of leaflet tissue and the size of the reconstructed mitral annulus , which was the “sine qua non” *
* See Glossary .
condition to trigger SAM.The two major risk factors for producing SAM after mitral valve repair ( Fig. 15-2 ) are excess leaflet tissue (a) and an undersized ring (b) . Additional potential contributing factors are a narrow aorto-mitral angle (c) , a small hyperkinetic ventricle (d) , and an abnormal configuration of the anterior leaflet (e) . A narrow aorto-mitral angle facilitates SAM by positioning the anterior leaflet close to the outflow tract and by displacing the filling chamber of the left ventricle, which becomes part of the subaortic region. A hyperkinetic small ventricle contributes to a discrepancy between the amount of leaflet tissue and the mitral valve orifice area. A severe left atrial dilatation may play a role in SAM by displacing the mitral valve orifice towards the left ventricular outflow tract. Finally, an abnormal configuration of the anterior leaflet with an increased height of this leaflet, as seen in HOCM, is also a risk factor. SAM usually occurs when either two major or one major and two minor risk factors are present ( Table 15-1 ).
| Major: | Excess valvular tissue |
| Undersized annuloplasty | |
| Minor: | Narrow aorto-mitral angle |
| Hyperkinetic small ventricle | |
| Septum bulging | |
| Abnormal configuration of anterior leaflet |
SAM after valve reconstruction is due to excess posterior leaflet tissue and/or to an inappropriately undersized ring.
Echocardiography allows identification of the different phases of anterior leaflet motion in SAM ( Fig. 15-3 ). Early in diastole, the blood flow, which is normally directed towards the apex (inset) , is now directed towards the septum (a) . During isovolumic ventricular contraction, the forward flow, which is normally oriented towards the left outflow tract, is directed towards the inflow chamber and the posterior leaflet, which closes first (b) . As the ventricular volume diminishes, the anterior leaflet closes but the excess tissue of the posterior leaflet occupies approximately two thirds of the mitral valve orifice and pushes the belly of the anterior leaflet towards the left ventricular outflow tract (c) . Then, the systolic flow displaces the distal portion of the anterior leaflet towards the aorta, resulting in varying degrees of turbulence and ventriculo-aortic obstruction. In the last step, the systolic flow further displaces the anterior leaflet, separating the coapting surface of the leaflets, which results in mitral regurgitation (d) .
CLINICAL PRESENTATION
Intraoperatively , the typical presentation of SAM is a patient with Barlow’s disease who, following mitral valve reconstruction, displays the following characteristics from transesophageal echocardiography ( Fig. 15-4 ): excess tissue of the posterior leaflet; anterior displacement of the distal portion of the anterior leaflet associated with left outflow tract obstruction (a); and late systolic mitral valve regurgitation with a posteriorly oriented jet (b) . In this setting, the three factors that are known to contribute to SAM must first be corrected: (1) suboptimal ventricular filling is addressed by increasing the preload of the left ventricle and raising the afterload with a pure alpha-agonist agent such as Neo-Synephrine; (2) atrioventricular asynchrony is corrected by atrioventricular pacing to further improve the ventricular filling; (3) hypercontractility of the ventricle is reversed by discontinuing the administration of inotropes, if present, and by occasionally adding beta-blockers. Once all these measures have been implemented, monitoring of both the left ventricular pressure and the aortic pressure followed by repeat echocardiography shows in most instances the resolution of SAM.
Correction of risk factors for SAM resolves this functional anomaly in most instances.
Figure 15-5 shows the same case of post repair SAM with left ventricular outflow tract obstruction (a) and severe mitral regurgitation displaying a posteriorly oriented jet (b) . Complete resolution of SAM and mitral regurgitation was obtained by the discontinuation of inotropic agents and optimization of left ventricular filling pressures (c-f) . Despite the previously described measures, if SAM persists, the patient should be reexamined to diagnose and correct the underlying anomaly, usually excess posterior leaflet tissue.
