Importance of leaflet elongation in causing systolic anterior motion of the mitral valve.

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.

Systolic anterior motion of the mitral valve in hypertrophic cardiomyopathy: an in vitro pulsatile flow study.

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.

Insights from in-vitro flow visualization into the mechanism of systolic anterior motion of the mitral valve in hypertrophic cardiomyopathy under steady flow conditions.

Hypertrophic obstructive cardiomyopathy is a heart disease characterized by a thickened interventricular septum which narrows the left ventricular outflow tract, and by systolic anterior motion (SAM) of the mitral valve which can contact the septum and create dynamic subaortic obstruction. The most common explanation for SAM has been the Venturi mechanism which postulates that septal hypertrophy, by narrowing the outflow tract, produces high velocities and thus low pressure between the mitral valve and the septum, causing the valve leaflets to move anteriorly. This hypothesis, however, fails to explain why SAM often begins early in systole, when outflow tract velocities are low or negligible or why it may occur in the absence of septal hypertrophy. The goal of this study was therefore to investigate an alternative hypothesis in which structural abnormalities of the papillary muscles act as a primary cause of SAM by altering valve restraint and thereby changing the geometry of the closed mitral apparatus and its relationship to the surrounding flow field. In order to test this hypothesis, an in vitro model of the left ventricle which included an explanted human mitral valve with intact chords and papillary muscle apparatus was constructed. Flow visualization was used to observe the ventricular flow field and the mitral valve geometry. Displacing the papillary muscles anteriorly and closer to each other, as observed clinically in patients with cardiomyopathy and obstruction produced SAM in the absence of septal hypertrophy. Flow could be seen impacting on the upstream (posterior) surface of the leaflets; such flow is capable of producing form drag forces which can initiate and maintain SAM.(ABSTRACT TRUNCATED AT 250 WORDS)

Pulsatile flow visualization in a model of the human abdominal aorta and aortic bifurcation.

The infrarenal abdominal aorta and aortic bifurcation are frequent sites of atherosclerosis. The local hemodynamics are considered to be atherogenetic factors; a detailed description of these flow fields is, therefore, essential to understand their relationship to atherosclerosis. The aim of this study was, therefore, to provide such detailed information using a flow visualization technique in an anatomically realistic flow model of the abdominal aorta and its main branches in which the complex pulsatile flow waveforms and flow rates were simulated for two physiologic flow conditions (rest and exercise). At rest, the particle path lines in the suprarenal abdominal aorta were straight with no visible signs of flow reversal. Vortices were initiated opposite to the main branches. In the infrarenal aorta, large flow separation zones formed at the posterior aortic wall and at the lateral walls in the aortic bifurcation during systolic deceleration, and flow reversal was present during diastole. Under exercise conditions, the particle path lines were straight, and only slight flow reversal was seen. This study emphasizes, that rather than being a straight tube with forward-moving fluid, the abdominal aorta has to be considered as a complex part of the arterial tree. Distinct local hemodynamic qualities of importance for explaining atherogenesis were pointed out. At rest, the suprarenal abdominal aorta had much less complicated flow characteristics than the infrarenal abdominal aorta where the distal, posterior vessel wall and the lateral walls of the bifurcation were sites of flow patterns thought to be associated with atherosclerosis. During exercise, the infrarenal flow patterns changed dramatically away from the flow patterns associated with the induction of atherosclerosis.