Aortic valve stenosis (AVS), including a range of disorder severities, from mild leaflet thickening without valve obstruction, ‘aortic sclerosis’, to severe calcific aortic stenosis, is a progressive, active process of valve modification, mediating by chronic inflammation (similar to atherosclerosis for cardiovascular risk factors) and biological features. AVS is the expression of early tissue damage due to endothelial damage and oxidative, inflammatory processes, and appears as a surrogate marker for cardiovascular events associated with coronary artery disease (CAD). AVS progression correlates with coronary artery risk factors, such as hypertension, age and cholesterol, and a quantitative evaluation of valve and coronary calcium score comprises a useful marker for cardiovascular prognosis. The low concordance of AVS with CAD appears to be due to other genetic or metabolic factors more specific for calcification processes. Moreover, both pathologies appear to be included within atherosclerotic disease and may be the object of the same clinical therapy and prevention.
aCNR Institute of Clinical Physiology, Ospedale G. Pasquinucci, Massa, Italy
bCNR Institute of Clinical Physiology, Pisa, Italy
Received 25 September, 2006
Revised 28 November, 2006
Accepted 5 December, 2006
Correspondence and requests for reprints to Annamaria Mazzone, Department of Cardiology and Cardiac Surgery, CNR Institute of Clinical Physiology, Ospedale Pasquinucci, Massa 54100, Italy Tel: +39 5854 93634; fax: +39 5854 93601; e-mail: firstname.lastname@example.org