Aortic stenosis is the most common type of valvular heart disease and its recent increase is related to aging.
The decreased aortic valve area imposes a chronic systolic pressure overload to the left ventricle. In response, the ventricle
hypertrophies in an attempt to normalize the increased wall stress, but this response is not uniform in patients with similar
degrees of stenosis and its regression after surgical correction is variable, suggesting that several factors, other than load,
can explain these differences. These findings are particularly important since the presence of left ventricular hypertrophy
after aortic valve replacement is an independent predictor of worse outcome, probably because it indicates irreversible
remodeling. Age, gender, hypertension, patient-prosthesis mismatch and interstitial remodeling also play an important role
in this setting, raising the possibility of intervention beyond valve replacement. The possibility of combining estrogen
treatment, antihypertensive agents, antioxidants and modulators of the renin-angiotensin-aldosterone system with surgical
treatment to promote reverse remodeling is very appealing. On the other hand, a preventive strategy to intervene earlier in
patients with significant left ventricular mass and avoid patient-prosthesis mismatch, especially in the younger and those
with systolic dysfunction, can have a significant impact on prognosis. Further evidence, with well designed clinical trials,
is needed but the spotlight must be in the ventricle, not the valve.