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Systolic anterior motion (SAM) of the mitral valve was first reported as a feature of hypertrophic cardiomyopathy (HCM) in the late 1960s. In association with asymmetrical hypertrophy of the inter-ventricular septum, and characteristic histological appearances of the cardiac muscle, it was noted to be a finding quite specific to HCM.1 Initial findings suggested that when SAM was present in HCM, left ventricular outflow tract (LVOT) obstruction was almost always present. However, it is now clear that SAM may be present in the absence of LVOT obstruction, and may even be seen without other echocardiographic features of HCM. Estimates of the prevalence of SAM in HCM are based on small numbers of patients, and range from 31–61%.2–4 Of the HCM patients with SAM, between 25–50% have evidence of resting LVOT obstruction—these patients generally have pronounced SAM, usually with contact between the mitral valve leaflets and the septum. The haemodynamic consequences of outflow obstruction due to SAM include prolongation of systolic ejection and reduction in stroke volume. Mitral coaptation may also be disrupted resulting in mitral regurgitation, further impairing cardiac output.
The mechanism of SAM in HCM remains unclear. The mitral valve is a complex structure consisting of a D-shaped annulus, anterior and posterior leaflets and subvalvar apparatus made up of chordae tendinae and the anterolateral and posteromedial papillary muscles. Although subvalvar structures may be involved, SAM typically involves the anterior leaflet and, less often, the posterior leaflet. Many investigators hypothesise that raised flow velocities in an outflow tract anatomically distorted by septal hypertrophy create a Venturi effect, pulling the mitral valve leaflets towards the septum and obstructing ventricular outflow.5 The precise mechanism is almost certainly more complex. Cross-sectional echocardiography of HCM patients demonstrated that SAM began before ventricular ejection commenced,6 a finding that the Venturi …
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