Diastolic Function During Development and Correction of Chronic LV Volume Overload Produced by Mitral Regurgitation

Background. Mitral regurgitation (MR) causes an augmentation in left ventricular (LV) diastolic function, increasing early diastolic filling rate and decreasing LV stiffness. Whether these changes in diastolic function persist, return to normal, or become abnormal after mitral valve replacement (MVR) is unknown. Methods and Results. Simultaneous LV echocardiography and catheterization studies were performed in six dogs in the baseline state (baseline), 3 months after creation ofMR (chronic MR), and 3 months after MVR. Chronic MR caused LV dilation (end-diastolic dimension increased from 4.5±0.1 cm in baseline to 5.8+0.1 cm in chronic MR,p<0.05) and eccentric LV hypertrophy (LV-to-body weight ratio increased from 3.6±0.2 g/kg in baseline to 4.9±0.4 g/kg in chronic MR, p<0.05). Chronic MR caused an increase in LV early diastolic filling rate (peak rate of increase in minor-axis dimension increased from 11±1 cm/sec in baseline to 18+1 cm/sec in chronic MR,p<0.05), did not change the time constant of myocardial relaxation (T was 31±4 msec in baseline and 30±2 msec in chronic MR), and caused a decrease in the modulus of regional chamber stiffness from 7.7± 1.2 in baseline to 2.4±0.03 in chronic MR,p<0.05. MVR caused the resolution ofLV dilation (end-diastolic dimension returned to normal [4.8±0.2 cm]), but three months after MVR, regression of LV hypertrophy was incomplete (LV-to-body weight ratio remained elevated [4.4±0.5 g/kg]). After MVR, LV early diastolic filling rate (8±1 cm/sec), the relaxation time constant (31±2 msec), chamber stiffness (7.1± 1.8), myocardial stiffness (11.2 ±3.1), and LV end-diastolic