Respective impacts of aortic stenosis and systemic hypertension on left ventricular hypertrophy.
It has been reported that 30-40% of patients with aortic stenosis are hypertensive. In such patients, the left ventricle faces a double (i.e. valvular and vascular) pressure overload, which results in subsequent wall volume hypertrophy. From a clinical standpoint, it is difficult to separate the respective contributions of aortic stenosis and systemic hypertension to left ventricular burden and patient's symptoms and thus to predict whether valve replacement would be beneficial. The objective of this theoretical study was therefore to investigate the relative effects of valvular and vascular afterloads on left ventricular hypertrophy. We used a ventricular-valvular-vascular mathematical model in combination with the Arts' model describing the myofiber stress. Left ventricular wall volume was computed for different aortic blood pressure levels and different degrees of aortic stenosis severity. Our simulations show that the presence of concomitant systemic hypertension has a major influence on the development of left ventricular hypertrophy in patients with aortic stenosis. These results also suggest that mild-to-moderate aortic stenosis has a minor impact on left ventricular wall volume when compared with hypertension. On the other hand, when aortic stenosis is severe, wall volume increases exponentially with increasing aortic stenosis severity and the impact of aortic stenosis on left ventricular hypertrophy becomes highly significant.
Garcia
Damien
D
Laboratory of Biomedical Engineering, Institut de Recherches Cliniques de Montréal, Université de Montréal, Canada. Damien.Garcia@ircm.qc.ca
Pibarot
Philippe
P
Kadem
Lyes
L
Durand
Louis-Gilles
LG
D001024:Aortic Valve Stenosis / Q000150:complications* / Q000503:physiopathology* / Q000601:surgery; D003198:Computer Simulation; D006801:Humans; D006973:Hypertension / Q000150:complications / Q000503:physiopathology*; D017379:Hypertrophy, Left Ventricular / Q000209:etiology / Q000503:physiopathology*; D008955:Models, Cardiovascular