Key points are not available for this paper at this time.
Design
Review
May guide antimineralization strategy development; leaves open prospective validation before clinical adoption.
Clinical and experimental studies indicate that calcification of bioprosthetic valves depends on host, implant, and biomechanical factors. The earliest mineral deposits in both clinical and experimental bioprosthetic tissue are localize to transplanted connective tissue cells; collagen involvement occurs later. Passive calcium entry occurs unimpeded in cells modified by aldehyde cross-linking, but the mechanisms for calcium removal are dysfunctional; calcium influx contributes to apatite formation by reacting with compartmentalized, bound phosphorus. Specific strategies for prevention of bioprosthetic tissue mineralization involve modification of either valve preparation details or the local implant environment. Efficacy, mechanisms and safety must be demonstrated for any antimineralization strategy.
No takes yet. Share an insight, caveat, or question.
Schoen et al. (1992) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: