MECHANISM OF MITRAL REGURGITATION IN HYPERTROPHIC CARDIOMYOPATHY - MISMATCH OF POSTERIOR TO ANTERIOR LEAFLET LENGTH AND MOBILITY

Citation
E. Schwammenthal et al., MECHANISM OF MITRAL REGURGITATION IN HYPERTROPHIC CARDIOMYOPATHY - MISMATCH OF POSTERIOR TO ANTERIOR LEAFLET LENGTH AND MOBILITY, Circulation, 98(9), 1998, pp. 856-865
Citations number
36
Categorie Soggetti
Peripheal Vascular Diseas",Hematology,"Cardiac & Cardiovascular System
Journal title
ISSN journal
00097322
Volume
98
Issue
9
Year of publication
1998
Pages
856 - 865
Database
ISI
SICI code
0009-7322(1998)98:9<856:MOMRIH>2.0.ZU;2-D
Abstract
Background-In hypertrophic cardiomyopathy: a spectrum of mitral leafle t abnormalities has been related to the mechanism of mitral systolic a nterior motion (SAM), which causes both subaortic obstruction and mitr al regurgitation. In the individual patient, SAM and regurgitation var y in parallel; clinically, however, great interindividual differences in mitral regurgitation can occur fur comparable degrees of SAM. We hy pothesized that these differences relate to variations in posterior le aflet length and mobility, restricting its ability to follow the anter ior leaflet (participate in SAM) and coapt effectively. Methods and Re sults-Different mitral geometries produced surgically in porcine valve s were studied in vitro. Comparable degrees of SAM resulted in more se vere mitral regurgitation for geometries characterized by limited post erior leaflet excursion. Mitral geometry was also analyzed in 23 patie nts with hypertrophic cardiomyopathy by intraoperative transesophageal echocardiography. All had typical anterior leaflet SAM with significa nt outflow tract gradients but considerably more variable mitral regur gitation; therefore, regurgitation did not correlate with obstruction, Ln contrast, mitral regurgitation correlated inversely with the lengt h over which the leaflets coapted (r= -0.89), the most severe regurgit ation occurring with a visible gap. Regurgitation increased with incre asing mismatch of anterior to posterior leaflet length (r=0.77) and de creasing posterior leaflet mobility (r= -0.79). Conclusions-SAM produc es greater mitral regurgitation if the posterior leaflet is limited in its ability to move anteriorly, participate in SAM, and coapt effecti vely. This can explain interindividual differences in regurgitation fo r comparable degrees of SAM. Thus, the spectrum of leaflet length and mobility that affects subaortic obstruction also influences mitral reg urgitation in patients with SAM.