Decalcification of the aortic valve does not prevent early recalcification

The excellent results with atrioventricular valve reconstruction have stimulated surgeons to attempt reconstruction of calcified aortic valves using decalcifying techniques, but long-term results have been disappointing. The aim of this in vitro study was to evaluate the surface structure of decalcified aortic valve tissue and its potential for recalcification.

Aortic leaflets were removed from 26 patients with aortic stenosis during elective valve replacement and decalcified by meticulous dissection. Representative specimens were prepared for scanning electron microscopy (SEM) and calcium content in the heavily calcified part of the leaflet in both macroscopically non-calcified and decalcified tissue was determined by atomic absorption spectroscopy (AAS). Additional probes of 'non-calcified' and decalcified tissue were incubated for two and four weeks with medium containing a physiological concentration of calcium to determine their potential for recalcification. As a control, 13 specimens from non-calcified valves were incubated according to the same protocol.

All calcified specimens contained high calcium levels (142.70+/-53.76 mg/g). Surgical dissection reduced tissue calcium content significantly (10.04+/-13.43 mg/g). Following two weeks' incubation with calcium, these specimens retained significantly higher levels of calcium (2.88+/-5.17 mg/g) than the 'non-calcified' specimens (19.17+/-7.61 versus 13.49+/-6.27 mg/g; p<0.05); after four weeks similar calcium levels were reached (32.00+/-10.27 versus 28.35+/-9.84 mg/g; p = NS). Non-calcified tissue showed the lowest calcium uptake (4.75+/-4.55 mg/g and 12.29+/-9.43 mg/g at two and four weeks; p<0.05). SEM revealed a loss of endothelial coverage in the calcified areas; decalcification led to an irregular fibrillar surface. Only parts of the macroscopically normal tissue contained endothelial cells, whereas the control tissue showed intact cellular coverage.

Aortic valve decalcification can effectively remove calcifications, but leaves a fibrillar structure that tends rapidly to accumulate calcium. Even normal-appearing tissue from diseased valves has a higher potential for calcification than normal valvular tissue. These data support the observation of only limited clinical benefits being derived after aortic valve decalcification for aortic stenosis.