Reversal of increased diastolic stiffness in mitral stenosis after successful balloon valvuloplasty.
OBJECTIVE
Abnormal passive elastic properties have been reported in patients with severe mitral stenosis and have been attributed to either: (i) chamber atrophy due to unloading; (ii) myocardial fibrosis; (iii) right and left ventricular (LV) interaction; or (iv) internal restrictions due to the rigid mitral valve apparatus. The study aim was to evaluate the effect of percutaneous mitral balloon valvuloplasty (PMV) on passive elastic properties in 19 patients with severe mitral stenosis. Ten patients with normal coronary arteries and LV function served as controls.


METHODS
LV high-fidelity pressure measurements and simultaneous biplane LV angiograms were obtained before and after PMV (n = 11). The constant of chamber stiffness (b; ml(-1)) was calculated from the diastolic pressure-volume relationship and the constant of myocardial stiffness (beta) from the diastolic stress-strain relationship. The time constant of relaxation (T; ms) was calculated from the LV pressure decay during isovolumic relaxation. Regional ejection fraction (radial axis system) was determined in six regions of the right anterior oblique (RAO) and left anterior oblique (LAO) angiographic projections.


RESULTS
Mitral valve area was increased from 1.0 to 2.2 cm2 after PMV, whereas diastolic pressure gradient was reduced from 14 to 4 mmHg. Global LV ejection fraction (EF) was slightly reduced (57% versus 63%; p<0.05) before valvuloplasty and normalized thereafter. Regional EF increased significantly (p<0.05) in the posterolateral region of the LAO projection after intervention. Myocardial stiffness was increased before, and decreased significantly after balloon valvuloplasty (from 16 to 11; p<0.05). The rate of relaxation and chamber stiffness remained unchanged.


CONCLUSIONS
Myocardial stiffness is increased in patients with mitral stenosis, but normalized after successful PMV. The improvement in passive elastic properties after valvuloplasty can be explained by the mobilization of the subvalvular apparatus with an improvement in regional LV function.
Mayer
I V
IV
Division of Cardiology, University Hospital, Zurich, Switzerland.
Fischer
A
A
Jakob
M
M
Mandinov
L
L
Hug
R
R
Vassalli
G
G
Hess
O M
OM
D000328:Adult; D000368:Aged; D001794:Blood Pressure / Q000502:physiology; D006328:Cardiac Catheterization; D002306:Cardiac Volume / Q000502:physiology; D002404:Catheterization; D003971:Diastole / Q000502:physiology; D004548:Elasticity; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D008944:Mitral Valve Insufficiency / Q000503:physiopathology* / Q000628:therapy*; D016277:Ventricular Function, Left / Q000502:physiology*