The significance of systolic anterior motion (SAM) on the mitral valve echo pattern in hypertrophic cardiomyopathy

Abstract The systolic anterior motion (SAM) of valve structures in the mitral echogram in hypertrophic cardiomyopathy (HCM) has previously been considered to be anterior motion and re‐opening of mitral valve leaflets, causing left ventricular outflow tract (LVOT) obstruction and mitral regurgitation. Fifteen patients with HCM underwent cardiac catheterisation and were also examined by M‐scan and mechanical real‐time B‐scan techniques. In all patients SAM was seen during M‐scan echocardiography. The mitral valve leaflets were visualised during the entire cardiac cycle during real‐time B‐scanning without showing any re‐opening in systole. Thickened papillary muscles have been observed in 12 patients and prominent chordae tendineae moving in the opposite direction to the anterior mitral valve leaflet in 10 patients. Four patients with SAM did not show mitral regurgitation during left ventricular angiography. In two patients without fixed haemodynamic obstruction, a complete SAM touching the interventricular septum was observed with prolonged apposition in one case. These findings suggest that SAM is due to the motion of chordae tendineae and/or papillary muscles traversing the single dimensional ultrasonic beam in systole, thus producing single linear or multiple spotty echoes within SAM. The mechanism of the upward motion of the subvalvular mitral valve apparatus in systole appears to be due to forceful contraction of the apical left ventricular posterior wall. The observation of SAM in patients without HCM also indicates that its presence during single dimensional echocardiography is neither diagnostic nor specific for HCM, LVOT obstruction or mitral regurgitation, and contradicts the assumption that the anterior mitral valve leaflet plays a significant role in the mechanism of LVOT obstruction. The salient feature of all conditions associated with abnormal mitral subvalvular motion is hyperkinetic contraction of the apical left ventricular posterior wall. Hyperkinetic left ventricular ejection appears to be the main factor in the complex development of an LVOT gradient in hypertrophic cardiomyopathy.