(Circulation. 1995;91:1189-1195.)
© 1995 American Heart Association, Inc.
Articles |
Papillary Muscle Displacement Causes Systolic Anterior Motion of the Mitral Valve
Experimental Validation and Insights Into the Mechanism of Subaortic Obstruction
From the Non-Invasive Cardiology Laboratory (R.A.L., J.L.G., A.E.W.), Department of Medicine, and the Surgical Cardiovascular Unit (G.J.V.), Department of Surgery, Massachusetts General Hospital, Harvard Medical School, Boston, Mass; the Cardiovascular Fluid Mechanics Laboratory (X.L., A.P.Y.), School of Chemical Engineering, Georgia Institute of Technology, Atlanta, Ga; and the Division of Pediatric Cardiology (E.G.C.), Children's Hospital of Pittsburgh, University of Pittsburgh School of Medicine, Pittsburgh, Pa.
Correspondence to Robert A. Levine, MD, Cardiac Ultrasound Laboratory, Vincent-Burnham 5, Massachusetts General Hospital, Boston, MA 02114.
Background Systolic anterior motion (SAM) of the mitral valve in hypertrophic cardiomyopathy (HCM) has generally been explained by a Venturi effect related to septal hypertrophy, causing outflow tract narrowing and high velocities. Patients with HCM, however, also have primary abnormalities of the mitral apparatus, including anterior and inward or central displacement of the papillary muscles, and leaflet elongation. These findings have led to the hypothesis that changes in the mitral apparatus can be a primary cause of SAM by altering the forces acting on the mitral valve and its ability to move in response to them. Despite suggestive observations, however, it has never been prospectively demonstrated that such changes can actually cause SAM.
Methods and Results To test this hypothesis in vivo, anterior papillary muscle displacement was created in 7 dogs studied by echocardiography, with controlled cardiac output and heart rate. In all 7 dogs, papillary muscle displacement caused SAM, with an outflow tract gradient (33±19 mm Hg) and mitral regurgitation in 6. As in patients with HCM, the mitral valve was displaced anteriorly and the coaptation point shifted toward the insertion of the leaflets, creating longer distal residual leaflets that moved anteriorly.
Conclusions Primary changes in the mitral apparatus can cause SAM without septal hypertrophy. In this model, SAM appears to be determined by the ability of the leaflets to move anteriorly (papillary muscle displacement causing slack and increased residual leaflet length) and their interposition into the outflow stream by anterior displacement, determining the direction of this motion. Geometric factors observed in HCM and in patients with SAM without HCM can therefore play a primary role in causing SAM.
Key Words: cardiomyopathy • echocardiography • hypertrophy
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