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Presently, conventional wisdom is that an asymptomatic patient, even with severe aortic stenosis (AS), can be followed medically. The basis for this recommendation is that sudden death as the first "symptom" in an asymptomatic patient is rare. Unfortunately, symptoms are subjective and can be ignored or explained away by both patient and physician, and once symptoms are recognized, sudden death accounts for at least one third of the deaths from AS in unoperated patients. There is evidence that once AS becomes severe, ischemia and fibrosis occur rapidly, setting up the possibility of heart failure and sudden death even after successful valve replacement. Aortic valve replacement should be performed before extensive fibrosis occurs. Multiple studies have shown that in severe AS, symptoms will occur rapidly when there is heavy valve calcification, an aortic valve area <0.8 cm, an annual rate of progression of aortic valve velocity of >/=0.3 m/sec, or a positive exercise stress test. These findings are excellent evidence that asymptomatic patients with severe AS and any of the above findings should be considered for aortic valve replacement.

Deciding when to operate on a patient with chronic aortic regurgitation may be extremely difficult. The timing of surgery requires consideration of the etiology and pathophysiology of the aortic regurgitation, because aortic valve replacement carries morbidity and mortality that must be weighed against the potential problems of continued medical management. Guidelines for the use of surgery in patients with valvular disease have been developed by a joint task force of the American College of Cardiology and the American Heart Association. Practical recommendations based on these guidelines are presented.

A valve-spreading catheter capable of producing graded reversible acute aortic regurgitation has been described. We modified this device to improve its safety and steerability. The modified valve-spreading catheter was composed of a removable core flexible guidewire and a caged catheter. The guidewire could easily and safely be steered into the left ventricle. The caged catheter could then be advanced over the guidewire to the aortic valve area with greater safety and ease. Opening of the caged catheter resulted in graded reversible acute aortic regurgitation. The modified valve-spreading catheter was used in 5 anesthetized mongrel dogs to create reversible graded acute aortic regurgitation, demonstrating its safety, and thus its utility. This device qualifies as an ideal instrument for creating variable and transient acute aortic regurgitation in intact animals.

Serial echocardiograms of a patient with enterococcal endocarditis and aortic insufficiency suggested the presence of vegetations on the aortic valve with progression of the lesion to frank prolapse of an aortic valve cusp. At surgery, the patient was found to have a flail noncoronary cusp to which an 8 mm vegetation was adherent. Anatomic correlations are presented, and a possible mechanism for the unusual echographic findings is discussed.

The hearts of nine children with clinical evidence of congenital valve stenosis and a congenital bicuspid aortic valve were reviewed. Aortic stenosis was diagnosed on the basis of cardiac catheterization data in four patients, operative findings in two and auscultatory findings in three. The patients were 1 month to 9 years old; six were male and three female. In each patient the two commissures of the valve were free to the aortic wall. The cusps were thickened, rolled and redundant; microscopic studies revealed that they consisted of immature loose connective tissue consistent with a dysplastic or incompletely differentiated valve. The valve orifice was obstructed by the dysplastic cusps, and dysplastic changes rather than the commissural fusion were responsible for the observed aortic stenosis. These valves do not appear amenable to valvotomy because obstruction is due to the abnormal valve tissue. These findings may explain the occasional poor results of valvotomy in infants and children with congenital aortic valve stenosis.

Forty-seven cases of quadricuspid semilunar valves which were autopsied were reviewed. The ratio of quadricuspid pulmonic valve to quadricuspid aortic valve was 5:1. Among the 35 patients with quadricuspid pulmonic valves, there were ten patients with clinical and pathologic evidence of coexisting congenital cardiac defects, eight of which resulted in severe cyanotic heart disease in infancy. In the remaining 25 patients the quadricuspid pulmonic valve was an incidental finding at autopsy. Three of the seven patients with quadricuspid aortic valves had aortic insufficiency, while the remaining four had no other clinical or pathologic evidence of congenital heart disease.

The bicuspid aortic valve is recognized as a frequent cause of aortic stenosis in adults. Aortic stenosis has been reported to occur in as many as 72 percent of adults with a congenital bicuspid aortic valve, with peak incidence occurring in the 5th and 6th decades of life. Review of the clinical records of 152 patients aged 20 years and older found to have a bicuspid aortic valve at autopsy revealed aortic stenosis in only 28 percent. The incidence of aortic stenosis increased progressively with age; 46 percent of patients over age 50 years and 73 percent over age 70 years had some degree of stenosis. The stenotic valves were obstructed by nodular, calcareous masses but commissural fusion was present in only eight cases. The largest group of patients in the series (40 percent) died of infective endocarditis; 77 percent of these were under age 50 years. Primary aortic regurgitation without infective endocarditis was uncommon. Thirty-two percent of the patients in this series had an apparently normally functioning aortic valve, and this rate remained relatively constant with increasing age; 37 percent of patients over age 50 years and 27 percent over age 70 years had an apparently normal valve. The bicuspid aortic valve in patients over age 20 does not invariably become stenotic or insufficient.