Normalization of left ventricular nonuniformity late after valve replacement for aortic stenosis

The aim of the present study was to evaluate nonuniformity in pressure overload hypertrophy due to aortic stenosis. Twenty patients were included in the present analysis. Ten patients with severe aortic stenosis were studied preoperatively as well as early (21 ± 8 months) and late (89 ± 21 months) after aortic valve replacement (AVR) using left ventricular biplane angiograms, high-fidelity pressure measurements and endomyocardial biopsies. Ten normal subjects served as controls. LV systolic function was assessed from biplane ejection fraction, and diastolic function from the time constant of relaxation, the peak filling rate and the constant of myocardial stiffness. Nonuniformity was evaluated from the coefficient of variation of the time to end-systole (systolic asynchrony) and peak filling rate (diastolic asynchrony) of 12 regions in right anterior oblique and left anterior oblique projection. Ejection fraction was comparable in patients with aortic stenosis and in controls, whereas preoperatively diastolic dysfunction with prolonged relaxation and increased stiffness was present in patients with aortic stenosis and was normalized late after AVR. LV systolic asynchrony was present (>2SD of controls) in 7 and diastolic asynchrony in 10 of 10 patients with aortic stenosis. Early as well as late after AVR systolic asynchrony was normalized in 9 of 10 patients. Diastolic asynchrony was present early AVR in all but one patient, although there was a significant improvement with respect to the preoperative evaluation. Late after AVR there was a normalization of diastolic asynchrony in 9 of 10 patients with aortic stenosis. Thus, it is concluded that systolic asynchrony is normalized early after AVR probably due to its load-sensitivity, whereas diastolic asynchrony persists probably due to residual LV hypertrophy with increased interstitial fibrosis and myocardial stiffness. Late after AVR, diastolic asynchrony is normalized due to structural remodeling with regression of both myocardial hypertrophy and interstitial fibrosis.