BACKGROUND: The aim of the present study was to evaluate the mechanism of diastolic dysfunction (DD) after aortic valve replacement (AVR) in patients with aortic stenosis (AS). METHODS AND RESULTS: Supine bicycle exercise Doppler echocardiography (EDE) with measurement of early diastolic peak velocities of transmitral flow (E) and mitral septal annular movement (E') was performed in 38 patients with AS at least 24 months after AVR and in 19 sex- and age-matched normal controls. AS patients had a 27.4±32.7% decrease in the ratio of left ventricular (LV) mass index to LV end-diastolic volume index (LVMI/LVEDVI) after AVR. Pre-AVR E' was significantly lower in AS patients (4.3±1.6 cm/s vs. 7.7±1.6 cm/s, P<0.005), resulting in a higher E/E' (16.7±5.4 vs. 9.3±1.8, P<0.001). E/E' at rest did not change significantly after AVR. Both E and E' increased progressively with exercise, and the increase in E' (P<0.001) but not E (P=0.675) was greater in normal controls than in AS patients (P<0.001). Peak E/E' >13 during EDE was more common in AS patients than in controls (89.5%, 34/39 vs. 0%, 0/19, P<0.001). On multivariate analysis, LVMI/LVEDVI (Y=8.703+4.199X, r=0.433, P=0.001) was the only factor associated with peak E/E' during EDE. CONCLUSIONS: Persistent DD is present after AVR, due primarily to failure in normal physiologic augmentation of LV relaxation during exercise, associated with incomplete or inadequate regression of LV hypertrophy.
BACKGROUND: The aim of the present study was to evaluate the mechanism of diastolic dysfunction (DD) after aortic valve replacement (AVR) in patients with aortic stenosis (AS). METHODS AND RESULTS: Supine bicycle exercise Doppler echocardiography (EDE) with measurement of early diastolic peak velocities of transmitral flow (E) and mitral septal annular movement (E') was performed in 38 patients with AS at least 24 months after AVR and in 19 sex- and age-matched normal controls. AS patients had a 27.4±32.7% decrease in the ratio of left ventricular (LV) mass index to LV end-diastolic volume index (LVMI/LVEDVI) after AVR. Pre-AVR E' was significantly lower in AS patients (4.3±1.6 cm/s vs. 7.7±1.6 cm/s, P<0.005), resulting in a higher E/E' (16.7±5.4 vs. 9.3±1.8, P<0.001). E/E' at rest did not change significantly after AVR. Both E and E' increased progressively with exercise, and the increase in E' (P<0.001) but not E (P=0.675) was greater in normal controls than in AS patients (P<0.001). Peak E/E' >13 during EDE was more common in AS patients than in controls (89.5%, 34/39 vs. 0%, 0/19, P<0.001). On multivariate analysis, LVMI/LVEDVI (Y=8.703+4.199X, r=0.433, P=0.001) was the only factor associated with peak E/E' during EDE. CONCLUSIONS: Persistent DD is present after AVR, due primarily to failure in normal physiologic augmentation of LV relaxation during exercise, associated with incomplete or inadequate regression of LV hypertrophy.