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

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Abstract

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, as well as continued traction of the centrally displaced papillary muscles on the lateral leaflet margins. According to this mechanism, the malposition of the papillary-mitral apparatus plays a fundamental role in altering the balance of forces acting on the mitral leaflets and creating SAM of the mitral valve which has the morphology and time course observed echocardiographically.

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      The present study extends the understanding of MV pathology in patients with obstructive HCM, especially with regard to extended septal myectomy for relief of LVOT obstruction. Our findings support previous pathologic, echocardiographic, and cardiovascular magnetic resonance imaging studies that document increased leaflet length in patients with HCM compared with controls.2,10-15 Increased leaflet length, however, did not impact surgical outcome as measured by LVOT gradient relief and residual MV regurgitation.

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    Supported in part by grants HL-07535 and HL-34392 from the National Institutes of Health, Bethesda, MD; a Research Fellowship from The Medical Foundation, Inc, Boston, MA (Dr Levine); a Clinician-Scientist Award from the American Heart Association, Dallas, TX (Dr Levine); and grants from the American Heart Association, Dallas, TX, and the American Heart Association, Massachusetts Affiliate, Inc.

    Presently at the Shanghai Institute of Cardiovascular Diseases, Shanghai, PRC.

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