Objectives: This study reports the results of echocardiographic follow-up in a large cohort of patients with aortic stenosis and correlates the progression of aortic stenosis with changes in the degree of mitral regurgitation and left ventricular hypertrophy and systolic dysfunction.
Background: Progressive aortic stenosis often causes left ventricular dysfunction and mitral regurgitation. Doppler echocardiography has greatly assisted in the noninvasive evaluation and follow-up of aortic stenosis. Nevertheless, the longitudinal follow-up of patients with Doppler echocardiography for the progression of aortic stenosis and the significance of progressive ventricular hypertrophy and mitral regurgitation have not been reported.
Methods: Serial Doppler echocardiography was performed in 394 consecutive patients with valvular aortic stenosis at baseline and after a mean follow-up period of 37 +/- 16 months. Mean and peak aortic gradients, aortic valve area, left ventricular systolic and diastolic diameters and percent area change (shortening fraction) were expressed as continuous variables, and systolic dysfunction, mitral regurgitation, ventricular hypertrophy and filling properties were tabulated as categoric variables using a semiquantitative grading system.
Results: Peak and mean gradients increased by an average of 8.3 and 6.3 mm Hg/year, respectively; end-systolic and end-diastolic diameters increased by 1.9 and 1.6 mm/year, respectively; and aortic valve area decreased by 0.14 cm2/year during the follow-up interval (p < 0.001 for all), indicating progression of aortic stenosis and ventricular dilation. Patients in the lowest quartile of aortic valve area and highest quartiles of mean and peak gradients had the least change compared with those in the highest quartile of aortic valve area and lowest quartile of mean and peak gradients (p < 0.01 for all). Patients with more mitral regurgitation at follow-up than at baseline had higher mean percent increase in mean and peak gradients as well as more progression of ventricular dilation and worsening systolic function compared with those with stable or improving mitral regurgitation (p < 0.05 for all). Similarly, subjects with worsening left ventricular hypertrophy had larger mean percent increase in mean and peak gradients than those with stable left ventricular hypertrophy (p < 0.01) but maintained stable ventricular volumes and systolic function. There was no correlation between the amount of change in mean or peak gradients and degree of deterioration in systolic function.
Conclusions: Aortic stenosis progresses predictably over time; however, systolic dysfunction is an inconsistent marker of the hemodynamic consequences of severe aortic stenosis. As an adaptive response to pressure overload, progressive hypertrophy appears to prevent ventricular dilation and development or worsening of mitral regurgitation. Conversely, progressive mitral regurgitation may be seen as a maladaptive consequence of increasing aortic stenosis.