Circulation · 1991
Mitral regurgitation following mitral balloon valvotomy. Differing mechanisms for severe versus mild-to-moderate lesions.
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Essop M R, Wisenbaugh T, Skoularigis J, Middlemost S, Sareli P
Аннотация
BACKGROUND: This study was designed to evaluate the incidence and mechanisms of mitral regurgitation following mitral balloon valvotomy (MBV) in 40 consecutive patients with symptomatic tight pliable mitral stenosis.
METHODS AND RESULTS: Transthoracic echocardiography with color flow mapping was performed before and 24 hours after the procedure. Patients who developed significant mitral regurgitation following MBV also underwent transesophageal echocardiography. The relation between increased mitral regurgitation and both valvular morphology and procedure-related factors was examined. Gorlin mitral valve area increased from 0.81 +/- 0.3 to 1.95 +/- 0.7 cm2 (p less than 0.001). No patient had more than 2+ mitral regurgitation by angiography and color Doppler prior to MBV. There was a moderate correlation between Doppler and angiographic increase in mitral regurgitation (r = 0.73, p less than 0.0001). By Doppler criteria 33 patients had no (n = 6) or mild (n = 27) increase in mitral regurgitation (group 1), and seven developed significant new mitral regurgitation (group 2). Baseline clinical, echocardiographic, and procedure-related data for the two groups were similar. Multiple regression analysis did not select any individual valve characteristic (valvular thickening, mobility, calcification, and subvalvular disease), total echocardiographic score, balloon diameter, or ratio of balloon to mitral annular diameter as disruption with a torn anterior or posterior mitral leaflet in six and a ruptured papillary muscle in one. Two of these patients have required mitral valve replacement (6 and 9 months following the procedure), whereas the remainder are significantly symptomatic. By contrast, mitral regurgitation in group 1 either occurred at the site of commissural split (n = 20) or was associated with prolapse of the anterior mitral leaflet (n = 6).
CONCLUSIONS: Thus, severe new mitral regurgitation following MBV is due to noncommissural tearing of the mitral leaflet and confers an adverse long-term prognosis. A mild increase in mitral regurgitation following MBV is frequent and occurs at the site of commissural split or is associated with prolapse of the anterior leaflet. Furthermore, in this study, an increase in mitral regurgitation could not be predicted from any valvular or procedure-related factor.
METHODS AND RESULTS: Transthoracic echocardiography with color flow mapping was performed before and 24 hours after the procedure. Patients who developed significant mitral regurgitation following MBV also underwent transesophageal echocardiography. The relation between increased mitral regurgitation and both valvular morphology and procedure-related factors was examined. Gorlin mitral valve area increased from 0.81 +/- 0.3 to 1.95 +/- 0.7 cm2 (p less than 0.001). No patient had more than 2+ mitral regurgitation by angiography and color Doppler prior to MBV. There was a moderate correlation between Doppler and angiographic increase in mitral regurgitation (r = 0.73, p less than 0.0001). By Doppler criteria 33 patients had no (n = 6) or mild (n = 27) increase in mitral regurgitation (group 1), and seven developed significant new mitral regurgitation (group 2). Baseline clinical, echocardiographic, and procedure-related data for the two groups were similar. Multiple regression analysis did not select any individual valve characteristic (valvular thickening, mobility, calcification, and subvalvular disease), total echocardiographic score, balloon diameter, or ratio of balloon to mitral annular diameter as disruption with a torn anterior or posterior mitral leaflet in six and a ruptured papillary muscle in one. Two of these patients have required mitral valve replacement (6 and 9 months following the procedure), whereas the remainder are significantly symptomatic. By contrast, mitral regurgitation in group 1 either occurred at the site of commissural split (n = 20) or was associated with prolapse of the anterior mitral leaflet (n = 6).
CONCLUSIONS: Thus, severe new mitral regurgitation following MBV is due to noncommissural tearing of the mitral leaflet and confers an adverse long-term prognosis. A mild increase in mitral regurgitation following MBV is frequent and occurs at the site of commissural split or is associated with prolapse of the anterior leaflet. Furthermore, in this study, an increase in mitral regurgitation could not be predicted from any valvular or procedure-related factor.