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ETIOLOGY AND PATHOLOGY

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Degenerative disease of the aortic valve occurs with age. Areas of cusp flexion over time develop fibrosis and calcification, impeding valve excursion and creating obstruction to left ventricular outflow.1 The most common cause of aortic stenosis (AS) is calcification of a normal trileaflet or congenital bicuspid valve.2 Calcific AS is an active disease process characterized by lipid accumulation, inflammation, and calcification, with many similarities to atherosclerosis.3-5 The degenerative process usually occurs in the sixth decade of life and beyond, but patients with additional valve pathology (bicuspid aortic valves, rheumatic heart valvular disease, radiation valvulopathy) can present much earlier in life with deterioration of valve function and consequent symptoms.6,7

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The 2 most common etiologies of AS amenable to percutaneous treatment are: (1) congenitally bicuspid aortic valves and (2) calcified tricuspid valves. Unicuspid or quadricuspid valves are not normally candidates for a percutaneous approach, with unicuspid disease typically associated with stenosis and quadricuspid valves with regurgitation. Isolated rheumatic AS, rare even in countries with a high prevalence of rheumatic heart disease, is highly amenable to percutaneous intervention because the mechanism of improvement is splitting of the fused commissures.

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Bicuspid aortic valves occur in approximately 1.5% of the population, and associated stenosis presents much earlier in life than tricuspid aortic valve disease.7 AS in adolescents and young adults is usually noncalcific, is the result of fused bileaflet valves, and is highly amenable to percutaneous balloon intervention. In contrast, AS in bicuspid and tricuspid valves of adults is associated with calcification of the valve that results in thickening, rigidity, and immobility of leaflets, often without commissural fusion.

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Balloon aortic valvuloplasty (BAV) has been shown to relieve obstruction of the stenotic valve by 3 mechanisms: (1) fracture of calcium deposits in the leaflets, (2) splitting of fused commissures, and (3) stretching of the aortic annulus.8,9 Calcium deposits are broken into separate fragments with balloon inflation, facilitating leaflet flexion and allowing better excursion during systole. Splitting of commissures is quite effective by BAV. Stretching of the valve may explain the early gains by BAV, but valve recoil can occur within hours to days, and in this case, results of BAV may be fleeting. Late restenosis (after several months) probably results from progression of the original lesions that produced stenosis.

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CLINICAL FEATURES AND INDICATIONS FOR TREATMENT

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The development of symptoms can trail the onset of degeneration of the aortic valve by several decades.10 When present, initial symptoms tend to be dyspnea on exertion and effort angina, although some patients may present with syncope or heart failure.11 Exertional fatigue may be the first manifestation of severe AS in the elderly. Once symptoms are detected, the prognosis is poor without intervention: patients often have mortality within 5 years of angina, 3 years of syncope, and 2 years of heart failure.12...

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