Inhibition of calcification of glutaraldehyde pretreated porcine aortic valve cusps with sodium dodecyl sulfate: Preincubation and controlled release studies

Abstract

Calcification of bioprosthetic heart valves fabricated from glutaraldehyde pretreated bovine pericardium or porcine aortic valves (PAV) is a frequent cause of the failure of these devices. Of all strategies considered thus far, only detergent preincubations using compounds such as sodium dodecyl sulfate (SDS) ingibited PAV bioprosthetic mineralization in circulatory sheep bioprosthetic valve replacements. The present study sought to characterize the mechanism of action of SDS preincubation. Results of transport and material characterization studies showed that SDS had a relatively high affinity for PAV, with a maximum uptake of 167.1 ± 6.8 μg SDS/mg tissue over 24 h at 37°C with a partition coefficient of 19.3. The PAV diffusion of SDS was 1.95 ± 0.35 10⁻⁶ cm²/sec. The principal effect of SDS on PAV was phospholipid extraction. The residual organic phospholipid extraction. The residual organic phosphate in the SDS pretreated tissue was 2.22 ± 0.72 nmol/mg tissue compared to the control untreated group with 18.52 ± 2.1 nmol/mg tissue. Incubations of PAV specimens in a 1% SDS solution for 24 h significantly inhibited calcification after 21 days in subdermal implants in 3-week-old male rats (PAV Ca²⁺ = 18.0 ± 11.8 μg/mg) compared to control (177.8 ± 6.0 μg/mg). In contrast, coimplants of 30% SDS silicone rubber polymers, for regional sustained SDS administration, did not impede PAV calcification in 21 day implants Ca²⁺ = 166.0 ± 14.0 μg/mg compared to the nondrug silicone matrix controls, (Ca²⁺ = 173.0 ± 6.6 μg/mg). Thus, we conclude that the mechanisms of SDS inhibition of PAV calcification is due to material effects which occur during preincubation, and is not facilitated by sustained SDS administration. © 1993 John Wiley & Sons, Inc.