title: Systolic anterior motion of the mitral valve in hypertrophic cardiomyopathy: an in vitro pulsatile flow study.
abstract: Hypertrophic cardiomyopathy, or HCM, is a relatively common disease which results in the hospitalization of more than 13,000 patients every year. It is characterized by a thickening of the interventricular septum and by systolic anterior motion, or SAM, of the mitral valve, which occurs when the distal tip of the mitral leaflets contacts the hypertrophied septum during systole and obstructs the left ventricular outflow tract. Using an in vitro pulsatile flow model of the left ventricle, the objective of the study was to investigate the relationship between the ventricular flow field and the mechanism of SAM and to specifically address the hypothesis that papillary muscle displacement can alter left ventricular flow patterns and create drag forces that can initiate SAM. Flow visualization revealed the presence in the ventricle of a large organized recirculation region throughout diastole. Besides maintaining the mitral leaflets close to the posterior wall, normally positioned papillary muscles also caused the diastolic vortex to help the mitral valve close near the posterior wall while simultaneously prepositioning the upcoming systolic outflow stream close to the septum, thereby minimizing the flow forces acting on the mitral valve. In contrast, the anterior displacement of the papillary muscles moves the entire mitral apparatus into the outflow tract. It also reverses the direction of the recirculating diastolic flows: The diastolic vortex now promotes the initiation of SAM by displacing the closing mitral leaflets anteriorly and by positioning the systolic outflow stream close to the posterior wall. These events lead to the creation of form drag forces as the systolic flow impacts the posterior side of the mitral leaflets, initiating SAM.
authors.affiliation: Cardiovascular Fluid Mechanics Laboratory School of Chemical Engineering Georgia Institute of Technology, Atlanta 30332-0100, USA.
authors.forename: X P
authors.initials: XP
authors.lastname: Lefebvre
authors.forename: S
authors.initials: S
authors.lastname: He
authors.forename: R A
authors.initials: RA
authors.lastname: Levine
authors.forename: A P
authors.initials: AP
authors.lastname: Yoganathan
mesh_terms: D002302:Cardiac Output; D002312:Cardiomyopathy, Hypertrophic / Q000473:pathology / Q000503:physiopathology*; D003971:Diastole; D006339:Heart Rate; D006346:Heart Septum / Q000473:pathology / Q000503:physiopathology; D018056:Hemorheology; D006801:Humans; D007834:Lasers; D020366:Methylmethacrylate; D008768:Methylmethacrylates; D008863:Microspheres; D008943:Mitral Valve / Q000473:pathology / Q000503:physiopathology*; D008953:Models, Anatomic; D008955:Models, Cardiovascular; D010210:Papillary Muscles / Q000473:pathology / Q000503:physiopathology; D011673:Pulsatile Flow; D012117:Resins, Synthetic; D013599:Systole; D016277:Ventricular Function, Left; D014694:Ventricular Outflow Obstruction / Q000473:pathology / Q000503:physiopathology
chemical_list: D008768:Methylmethacrylates; D012117:Resins, Synthetic; D020366:Methylmethacrylate; C046797:amberlite