An integrated mechanism for systolic anterior motion of the mitral valve in hypertrophic cardiomyopathy based on echocardiographic observations

Although many mechanisms have been proposed to explain systolic anterior motion (SAM) of the mitral valve in hypertrophic cardiomyopathy, the precise mechanism of its onset and cessation remain undefined. The Venturi theory, based on increased flow velocity in a narrowed outflow tract, is widely accepted but falls to explain several important characteristics of SAM. It also neglects the potential role of drag forces generated by interposition of the leaflets into the path of ejection and of factors that would decrease the effectiveness of papillary muscle restraint. In order to obtain further insight into the mechanism of SAM, a detailed geometric study of the left ventricle and mitral apparatus was performed with cross-sectional echocardiography in three equal-sized groups of patients with hypertrophic cardiomyopathy and SAM, patients with hypertrophy and no anterior motion, and normal control subjects. A salient finding was that SAM began prior to ejection in patients with hypertrophic cardiomyopathy, which cannot be explained by the Venturi theory. Further, SAM began and was most prominent in the central portion of the leaflet as opposed to its lateral edges; this finding is not predicted by the Venturi mechanism. In addition to outflow tract narrowing, other structural changes unique to patients with SAM included anterior and inward displacement of the papillary muscles, anterior displacement of the mitral leaflets, and elongation of the mitral leaflets, which were, on the average, 1.5 to 1.7 cm longer than in the other subjects ( p < 0.0001). On the basis of these observations, an integrated mechanism for the initiation and resolution of SAM is proposed that would explain observed features such as onset before ejection and central prominence. This mechanism combines the effects of outflow tract narrowing with those of papillary muscle displacement. In particular, anterior and inward displacement of the papillary muscles can be predicted to alter the effectiveness of chordal support so that the central leaflet portions become relatively slack and are more readily displaced anteriorly. The altered distribution of chordal tension can also be predicted to orient the distal leaflets upward into the outflow tract at the onset of systole, prior to aortic valve opening, so that ventricular ejection will actually drag the interposed leaflets anteriorly. The resolution of SAM can be understood in terms of a reverse Venturi effect created by mitral regurgitation