In hypertrophic cardiomyopathy, mitral regurgitation severity correlated inversely with leaflet coaptation length (r=-0.89) and posterior leaflet mobility (r=-0.79).
Observational (n=23)
Does mitral geometry (posterior leaflet length and mobility) explain interindividual differences in mitral regurgitation severity in patients with hypertrophic cardiomyopathy and SAM?
In hypertrophic cardiomyopathy with SAM, the severity of mitral regurgitation is largely determined by the posterior leaflet's length and mobility, which restricts its ability to coapt with the anterior leaflet.
Effect estimate: r= -0.89
BACKGROUND: In hypertrophic cardiomyopathy, a spectrum of mitral leaflet abnormalities has been related to the mechanism of mitral systolic anterior motion (SAM), which causes both subaortic obstruction and mitral regurgitation. In the individual patient, SAM and regurgitation vary in parallel; clinically, however, great interindividual differences in mitral regurgitation can occur for comparable degrees of SAM. We hypothesized that these differences relate to variations in posterior leaflet length and mobility, restricting its ability to follow the anterior leaflet (participate in SAM) and coapt effectively. METHODS AND RESULTS: Different mitral geometries produced surgically in porcine valves were studied in vitro. Comparable degrees of SAM resulted in more severe mitral regurgitation for geometries characterized by limited posterior leaflet excursion. Mitral geometry was also analyzed in 23 patients with hypertrophic cardiomyopathy by intraoperative transesophageal echocardiography. All had typical anterior leaflet SAM with significant outflow tract gradients but considerably more variable mitral regurgitation; therefore, regurgitation did not correlate with obstruction. In contrast, mitral regurgitation correlated inversely with the length over which the leaflets coapted (r= -0.89), the most severe regurgitation occurring with a visible gap. Regurgitation increased with increasing mismatch of anterior to posterior leaflet length (r=0.77) and decreasing posterior leaflet mobility (r= -0.79). CONCLUSIONS: SAM produces greater mitral regurgitation if the posterior leaflet is limited in its ability to move anteriorly, participate in SAM, and coapt effectively. This can explain interindividual differences in regurgitation for comparable degrees of SAM. Thus, the spectrum of leaflet length and mobility that affects subaortic obstruction also influences mitral regurgitation in patients with SAM.
Schwammenthal et al. (Tue,) conducted a observational in Hypertrophic cardiomyopathy (n=23). Echocardiographic assessment of mitral geometry was evaluated on Correlation of mitral regurgitation with leaflet coaptation length (r= -0.89). In hypertrophic cardiomyopathy, mitral regurgitation severity correlated inversely with leaflet coaptation length (r=-0.89) and posterior leaflet mobility (r=-0.79).
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