PROGRESSION OF AORTIC-STENOSIS IN 394 PATIENTS - RELATION TO CHANGES IN MYOCARDIAL-VALVE AND MITRAL-VALVE DYSFUNCTION

Citation
Sj. Brener et al., PROGRESSION OF AORTIC-STENOSIS IN 394 PATIENTS - RELATION TO CHANGES IN MYOCARDIAL-VALVE AND MITRAL-VALVE DYSFUNCTION, Journal of the American College of Cardiology, 25(2), 1995, pp. 305-310
Citations number
19
Categorie Soggetti
Cardiac & Cardiovascular System
ISSN journal
07351097
Volume
25
Issue
2
Year of publication
1995
Pages
305 - 310
Database
ISI
SICI code
0735-1097(1995)25:2<305:POAI3P>2.0.ZU;2-A
Abstract
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 mitra l regurgitation and left ventricular hypertrophy and systolic dysfunct ion. Background. Progressive aortic stenosis often causes left ventric ular dysfunction and mitral regurgitation. Doppler echocardiography ha s greatly assisted in the noninvasive evaluation and follow up of aort ic stenosis. Nevertheless, the longitudinal follow-up of patients with Doppler echocardiography for the progression of aortic stenosis and t he significance of progressive ventricular hypertrophy and mitral regu rgitation have not been reported. Methods. Serial Doppler echocardiogr aphy was performed in 394 consecutive patients with valvular aortic st enosis at baseline and after a mean follow-up period of 37 +/- 16 mont hs. Mean and peak aortic gradients, aortic valve area, left ventricula r systolic and diastolic diameters and percent area change (shortening fraction) were expressed as continuous variables, and systolic dysfun ction, mitral regurgitation, ventricular hypertrophy and filling prope rties were tabulated as categoric variables using a semiquantitative g rading system. Results. Peak and mean gradients increased by an averag e of 8.3 and 6.3 mm Hg/year, respectively; end-systolic and end-diasto lic diameters increased by 1.9 and 1.6 mm/year, respectively; and aort ic valve area decreased by 0.14 cm(2)/year during the follow-up interv al (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 ch ange compared with those in the highest quartile of aortic valve area and lowest quartile of mean and peak gradients (p < 0.01 for all). Pat ients with more mitral regurgitation at follow-up than at baseline had higher mean percent increase in mean and peak gradients as well as mo re 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 h ypertrophy had larger mean percent increase in mean and peak gradients than those with stable left ventricular hypertrophy (p < 0.01) but ma intained stable ventricular volumes and systolic function. There was n o correlation between the amount of change in mean or peak gradients a nd degree of deterioration in systolic function. Conclusions. Aortic s tenosis progresses predictably over time; however, systolic dysfunctio n is an inconsistent marker of the hemodynamic consequences of severe aortic stenosis. As an adaptive response to pressure overload, progres sive hypertrophy appears to prevent ventricular dilation and developme nt or worsening of mitral regurgitation. Conversely, progressive mitra l regurgitation may be seen as a maladaptive consequence of increasing aortic stenosis.