Aortic stenosis

The most common etiology of aortic stenosis (AS) in adults is calcific degeneration of the normal trileaflet valve or bicuspid valve. This degeneration begins at the base of the leaflets and progresses onto the cusps, ultimately leading to decreased leaflet motion. Characteristically this degeneration is without commissural fusion, as opposed to the next leading cause of AS in the adult, rheumatic fever. Rheumatic AS begins with fusion of the commissures and fibrotic changes leading to decreased movement of the cusps. This condition is usually accompanied by similar pathology on the mitral valve as well. Congenital malformations of the aortic valve can accelerate calcific degeneration of the valve, which presents in early adulthood.

Patients with rheumatic disease usually develop symptoms in the fifth or sixth decades of life, while patients with calcific degeneration develop symptoms in the seventh through ninth decades. The classic triad of symptoms in AS includes angina, syncope, and congestive heart failure (CHF). The natural history of each of these symptoms may independently predict a limited life expectancy: 5 years, 3 years, and 2 years respectively. This adverse prognosis is related to the rapid progression of aortic stenosis: a predicted decrease in valve area of 0.1 cm per year and an increase in mean pressure gradient of 7 mmHg per year. There is significant variability among individuals in the progression of disease; therefore, close follow-up is mandatory for all patients with asymptomatic mild and moderate AS. Sudden death may occur in 15–20% of cases; the onset of symptoms, particularly near the age of 60, usually heralds precipitous decline leading to death. Twenty percent of patients with severe AS will develop an acquired von Willebrand syndrome. These patients will demonstrate clinically evident bleeding, which resolves after valve replacement.