ABSTRACT
INTRODUCTION AND HISTORICAL PERSPECTIVE Valvular aortic stenosis represents an important cardiac disease affecting up to 5% of the elderly population (1). A severe, symptomatic stenosis signifies a class I indication for valve replacement (2), as patients with medical treatment face a high morbidity and mortality (3). Similar to the pathogenesis of arteriosclerosis, shear stress, inflammation, and lipid accumulation play an important role in the development of aortic stenosis (4). Attempts to reduce the progression of aortic valve disease with different drugs have failed since the use of lipid-lowering drugs (5), or angiotensin-converting enzyme (6) inhibitors have demonstrated no beneficial effect so far. Until 2002, the only therapeutic treatment for severe aortic valve stenosis consisted of surgical open-heart valve replacement. Perioperative and clinical short-term data show a low operation-related morbidity and mortality (7,8), but the incidence of perioperative, major adverse cardiovascular events increase with age (9) and with the number of comorbidities or cardiac factors such as depressed systolic left ventricular function or concomitant coronary artery disease.
