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Br Heart J. May 1991; 65(5): 277–279.
PMCID: PMC1024630
In vitro balloon dilatation of mitral valve stenosis: the importance of subvalvar involvement as a cause of mitral valve insufficiency.
A S Sadee and A E Becker
Department of Cardiology, University of Amsterdam, Academic Medical Center, The Netherlands.
Abstract
To investigate the mechanism that increases the orifice area of the mitral valve during balloon dilatation 43 surgically excised intact rheumatic mitral valves were studied. The main pathological features were (a) fibrosis of mitral valve leaflets and commissures (10 valves); (b) fibrosis with calcification of one commissure (eight anterolateral, seven posteromedial); (c) fibrosis with calcification of both commissures (seven valves); and (d) predominant involvement of the subvalvar apparatus (11 valves). The valves were assessed by photography and radiography before and after balloon dilatation (balloons up to 38 mm (bifoil 2 x 19 mm) and pressures up to 4 atmospheres). The valve was dilated in stages under direct visual control by balloons of increasing diameter. Splitting of the fused commissures was the most common mode of widening the orifice. However, the mitral valve leaflets were torn in two fibrotic valves and in six valves with extensive involvement of the subvalvar apparatus. In the fibrotic valves (group (a] the tear originated near the valve perimeter, at the thinnest part of the remaining valve leaflet. In the valves with subvalvar involvement splitting started at the apex of spaces between the fused chordal columns and proceeded upward. Where there is extensive involvement of the subvalvar apparatus in rheumatic mitral valve disease the risk of tearing of the valve leaflets by balloon dilatation is increased and this is likely to predispose to the development of acute valvar insufficiency.
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