Mechanism of mitral regurgitation in hypertrophic cardiomyopathy: mismatch of posterior to anterior leaflet length and mobility.
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.


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
E
E
Massachusetts General Hospital, Department of Medicine, Harvard Medical School, Boston 02114, USA.
Nakatani
S
S
He
S
S
Hopmeyer
J
J
Sagie
A
A
Weyman
A E
AE
Lever
H M
HM
Yoganathan
A P
AP
Thomas
J D
JD
Levine
R A
RA
D000328:Adult; D000368:Aged; D000818:Animals; D002312:Cardiomyopathy, Hypertrophic / Q000150:complications / Q000503:physiopathology*; D004195:Disease Models, Animal; D004452:Echocardiography; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D008943:Mitral Valve / Q000033:anatomy & histology* / Q000503:physiopathology*; D008944:Mitral Valve Insufficiency / Q000150:complications / Q000000981:diagnostic imaging / Q000503:physiopathology*; D008945:Mitral Valve Prolapse / Q000150:complications / Q000000981:diagnostic imaging / Q000503:physiopathology; D010210:Papillary Muscles / Q000033:anatomy & histology / Q000503:physiopathology; D013552:Swine; D018615:Ultrasonography, Doppler, Color