BACKGROUND AND AIMS OF THE STUDY: There is growing evidence for mitral leaflet elongation in patients with hypertrophic cardiomyopathy. Such elongation could predispose to systolic anterior motion (SAM) of the mitral valve by increasing leaflet mobility and providing a geometry that promotes this condition. METHODS: To test this postulate, five porcine mitral valves were studied in a physiologic left heart pulsatile flow duplicator. They were elongated with patches sutured to the basal posterior leaflet (three sizes per valve) or anterior leaflet (basal, middle, or distal). Each geometry was studied with normal papillary muscle position and with anterior and inward displacement, as seen in hypertrophic cardiomyopathy, to shift the leaflets into the outflow stream. RESULTS: Four points became clear. 1) Leaflet elongation promoted the development of SAM in response to papillary muscle displacement by creating long overlapping residual leaflets capable of moving anteriorly. 2) Posterior leaflet elongation also promoted SAM by shifting leaflet coaptation anteriorly, with progressive increases in SAM. 3) Basal and mid-anterior leaflet elongation caused SAM with prolapse; distal anterior leaflet elongation created SAM with a mobile flap (leaflet elongation without papillary muscle displacement created prolapse). 4) Residual leaflet length correlated well with total leaflet length (r = 0.87-0.98 for each valve), and the degree of SAM in turn correlated well with residual leaflet length (r = 0.62-0.98 for individual valves). CONCLUSIONS: Mitral leaflet elongation, by increasing the residual leaflet length and leaflet mobility, can play an important role in promoting SAM in response to outflow forces, as demonstrated by prospectively altering leaflet length. These findings are consistent with recent observations that reducing leaflet redundancy and posterior leaflet height can reduce obstructive SAM following mitral valve repair in patients with mitral valve prolapse and help relieve obstruction in patients with hypertrophic cardiomyopathy and enlarged leaflets.
BACKGROUND AND AIMS OF THE STUDY: There is growing evidence for mitral leaflet elongation in patients with hypertrophic cardiomyopathy. Such elongation could predispose to systolic anterior motion (SAM) of the mitral valve by increasing leaflet mobility and providing a geometry that promotes this condition. METHODS: To test this postulate, five porcine mitral valves were studied in a physiologic left heart pulsatile flow duplicator. They were elongated with patches sutured to the basal posterior leaflet (three sizes per valve) or anterior leaflet (basal, middle, or distal). Each geometry was studied with normal papillary muscle position and with anterior and inward displacement, as seen in hypertrophic cardiomyopathy, to shift the leaflets into the outflow stream. RESULTS: Four points became clear. 1) Leaflet elongation promoted the development of SAM in response to papillary muscle displacement by creating long overlapping residual leaflets capable of moving anteriorly. 2) Posterior leaflet elongation also promoted SAM by shifting leaflet coaptation anteriorly, with progressive increases in SAM. 3) Basal and mid-anterior leaflet elongation caused SAM with prolapse; distal anterior leaflet elongation created SAM with a mobile flap (leaflet elongation without papillary muscle displacement created prolapse). 4) Residual leaflet length correlated well with total leaflet length (r = 0.87-0.98 for each valve), and the degree of SAM in turn correlated well with residual leaflet length (r = 0.62-0.98 for individual valves). CONCLUSIONS:Mitral leaflet elongation, by increasing the residual leaflet length and leaflet mobility, can play an important role in promoting SAM in response to outflow forces, as demonstrated by prospectively altering leaflet length. These findings are consistent with recent observations that reducing leaflet redundancy and posterior leaflet height can reduce obstructive SAM following mitral valve repair in patients with mitral valve prolapse and help relieve obstruction in patients with hypertrophic cardiomyopathy and enlarged leaflets.
Authors: Robert A Levine; Albert A Hagége; Daniel P Judge; Muralidhar Padala; Jacob P Dal-Bianco; Elena Aikawa; Jonathan Beaudoin; Joyce Bischoff; Nabila Bouatia-Naji; Patrick Bruneval; Jonathan T Butcher; Alain Carpentier; Miguel Chaput; Adrian H Chester; Catherine Clusel; Francesca N Delling; Harry C Dietz; Christian Dina; Ronen Durst; Leticia Fernandez-Friera; Mark D Handschumacher; Morten O Jensen; Xavier P Jeunemaitre; Hervé Le Marec; Thierry Le Tourneau; Roger R Markwald; Jean Mérot; Emmanuel Messas; David P Milan; Tui Neri; Russell A Norris; David Peal; Maelle Perrocheau; Vincent Probst; Michael Pucéat; Nadia Rosenthal; Jorge Solis; Jean-Jacques Schott; Ehud Schwammenthal; Susan A Slaugenhaupt; Jae-Kwan Song; Magdi H Yacoub Journal: Nat Rev Cardiol Date: 2015-10-20 Impact factor: 32.419
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