title: [Anterolateral papillary muscle motion before and after septal myotomy in hypertrophic obstructive cardiomyopathy].
abstract: The left ventricular outflow pressure gradient in hypertrophic cardiomyopathy results from systolic anterior motion of the mitral valve (SAM). This abnormal orientation of the valve was previously proposed to be caused by inappropriately hypertrophied papillary muscles which protrude to the interventricular septum (IVS). Septal myotomy can alter the orientation of the papillary muscles and resolve the pressure gradient, without myectomy. Recently, we have experienced two instructive cases to prove our previously advocated hypothesis. Case 1: This 54-year-old man complained of effort dyspnea, and his echocardiogram disclosed marked SAM, and a thickened IVS (28 mm) and left ventricular posterior wall (16 mm). The intraventricular pressure gradient was 134 mmHg, and there was mitral regurgitation of grade 2/4. A longitudinal incision via the aorta on the anterior portion of the IVS, toward the base of the anterolateral papillary muscle, resolved the pressure gradient and mitral regurgitation, and two-dimensional echocardiography demonstrated that the SAM resolved at the lateral aspect of the valve, but it remained on the medial side. Case 2: This 57-year-old man complained of dyspnea during effort. He had marked SAM. The intraventricular pressure gradient was 65 mmHg, and there was grade 3/4 mitral regurgitation. Longitudinal incisions on the anterior, medial and posterior parts of the IVS abolished the SAM and reduced mitral regurgitation to grade 1/4. In both cases, during systole, the anterolateral papillary muscle protruded into the left ventricular ontflow tract, causing SAM. After surgery, the direction of the muscle axis moved toward the mitral orifice during systole, resulting in alleviation of SAM on the same side of the location of septotomy. This further confirmed our concept that disoriented papillary muscles play essential roles in causing SAM. If the Venturi forces previously stressed by other investigators cause SAM, the latter should resolve on both the medial and lateral aspects, even by septotomy. Thus, the Venturi theory seems untenable.
authors.affiliation: Department of Medicine, National Cardiovascular Center, Suita.
authors.forename: S
authors.initials: S
authors.lastname: Nagata
authors.forename: Y D
authors.initials: YD
authors.lastname: Park
authors.forename: F
authors.initials: F
authors.lastname: Ohmori
authors.forename: S
authors.initials: S
authors.lastname: Beppu
authors.forename: K
authors.initials: K
authors.lastname: Kawazoe
authors.forename: T
authors.initials: T
authors.lastname: Fujita
authors.forename: H
authors.initials: H
authors.lastname: Sakakibara
authors.forename: Y
authors.initials: Y
authors.lastname: Nimura
mesh_terms: D002312:Cardiomyopathy, Hypertrophic / Q000503:physiopathology* / Q000601:surgery; D004452:Echocardiography; D004562:Electrocardiography; D006346:Heart Septum / Q000601:surgery*; D006801:Humans; D008297:Male; D008875:Middle Aged; D008943:Mitral Valve / Q000503:physiopathology; D009200:Myocardial Contraction; D010210:Papillary Muscles / Q000503:physiopathology*; D013599:Systole