Abstract 2654: Persistent Diastolic Dysfunction Late After Valve Replacement In Severe Aortic Regurgitation
Introduction: Regression of left ventricular (LV) hypertrophy with normalization of diastolic function has been reported in patients with aortic stenosis. The purpose of the present study was to evaluate the effect of aortic valve replacement (AVR) on LV systolic and diastolic function an LV structure in chronic aortic regurgitation (AR) early and late after AVR.
Methods: 25 patients were included in the present analysis. Ten patients with severe AR were studied before, early (21 months) and late (89 months) after AVR using LV biplane angiograms, high-fidelity pressure measurements, and endomyocardial biopsies. Fifteen healthy subjects were used as controls. LV systolic function was determined from biplane ejection fraction (EF) and midwall fractional shortening, LV diastolic function from the time constant of LV relaxation, peak filling rates, and myocardial stiffness constant. LV structure was assessed from muscle fiber diameter, interstitial fibrosis and volume fraction of myofibrils.
Results: LV muscle mass was significantly increased preoperatively but decreased by 38% early and 55% late after surgery, but remained (ns) elevated compared to controls. LV EF and midwall fractional shortening did not change after AVR. LV relaxation was significantly prolonged before (89±28 ms vs. controls 47±11 ms, p<0.001) and early (67±19 ms) but normal late after AVR (42±14 ms). Early and late peak filling rates were increased preoperatively and were normalized early after surgery. Myocardial stiffness constant was increased in AR patients before surgery (22±6 vs. controls 9±3, p<0.001) but decreased significantly after AVR. However, it remained increased at late follow-up (15±4, p<0.05). Muscle fiber diameter decreased significantly early and late after AVR, but remained hypertrophied at late follow-up. Interstitial fibrosis was increased preoperatively and increased even further early but decreased only late after AVR.
Conclusions: Patients with AR show normalization of macroscopic LV hypertrophy late after AVR, altough fiber hypertrophy persists. These changes in LV myocardial structure late after AVR are accompanied by a change in passive elastic properties with persistent diastolic dysfunction due to the increased interstitial fibrosis.