September 14, 2010Open Access
View Full PaperIn Vivo Measurement of Mitral Leaflet Surface Area and Subvalvular Geometry in Patients With Asymmetrical Septal Hypertrophy
Key Result
Indexed total mitral leaflet area (adjusted OR 5.651; 95% CI 1.573-20.304; P=0.008) and inter-papillary muscle distance were independent determinants of LVOT obstruction in septal hypertrophy.
Study Design
Type
Observational (n=79)
Structured PICO
Does abnormal mitral valve and papillary muscle geometry contribute to LVOT obstruction in patients with asymmetrical septal hypertrophy?
P
Population
79 individuals, comprising 47 patients with asymmetrical septal hypertrophy (20 with resting LVOT obstruction and 27 without) and 32 normal controls, evaluated using real-time 3-dimensional echocardiography.
E
Exposure
Real-time 3-dimensional echocardiography with customized software (Omni 4D) analysis of mitral leaflet area and subvalvular geometry
C
Comparator
Normal controls (n=32) and comparison between hypertrophy patients with vs without LVOT obstruction
O
Outcome
Determinants of LVOT obstruction and minimal LVOT area during systolesurrogate
Primary changes of the mitral apparatus, including increased mitral leaflet area and papillary muscle displacement, are independent determinants of LVOT obstruction in asymmetrical septal hypertrophy.
Main Result
Odds Ratio: 5.651 (95% CI 1.573–20.304)
p-value: p=0.008
Abstract
BACKGROUND: Analyzing the determinants of systolic anterior motion of the mitral valve and consequent left ventricular outflow tract (LVOT) obstruction in patients with asymmetrical septal hypertrophy requires a comprehensive 3-dimensional analysis of mitral leaflet (ML) area, papillary muscle (PM) geometry, and the distribution of left ventricular hypertrophy. METHODS AND RESULTS: Real-time 3-dimensional echocardiography was performed in 47 patients with asymmetrical septal hypertrophy and 32 normal controls. Patients included 20 with resting LVOT obstruction (group I) and 27 without (group II). Customized software (Omni 4D) provided a validated measure of ML surface area, LVOT area, mitral annular area and nonplanarity, LVOT hypertrophy index by topography (percent area with wall thickness >16 mm), and 3-dimensional PM positions relative to annulus. ML area was more than twice as large in group I than normal and 1.4 times normal in group II (P<0.001). Group I patients were also characterized by higher LVOT hypertrophy index and medial and anterior displacements of both PMs, resulting in a shorter inter-PM distance. Independent determinants of LVOT obstruction were indexed total ML area (adjusted odds ratio, 5.651; 95% confidence interval, 1.573 to 20.304; P=0.008) and inter-PM distance (adjusted odds ratio, 0.416; 95% confidence interval, 0.203 to 0.854; P=0.0169). Minimal LVOT area during systole correlated well with peak LVOT pressure gradient (R(2)=0.83, P<0.001); its independent determinants were left ventricular end-systolic volume (P=0.0183), indexed total ML area (P=0.0108), inter-PM distance (P=0.0378), annular height (P=0.0047), and LVOT hypertrophy index (P=0.0098). CONCLUSIONS: Myocardium is not the only tissue affected in patients with asymmetrical septal hypertrophy, and primary changes of the mitral apparatus, including ML area increase and PM displacement, are independent determinants of LVOT obstruction and provide a comprehensive mechanism that determines leaflet slack and anteriorly directed motion. Abnormal PM-mitral valve geometry assessed by real-time 3-dimensional echocardiography can provide reasonable new targets for individualized intervention.