J Thorac Cardiovasc Surg 1998;115:259-260
© 1998 Mosby, Inc.
Role of lipid in calcification of porcine pulmonary and aortic valves
Jyotirmay Chanda MD, ,
Ryosei Kuribayashi, MD,
Tadaaki Abe, MD
To the Editor:
We read with great interest the article by Dunmore-Buyze and colleagues,
1 in which the authors presume that lipids might act as nucleation site for calcification in leaflets of bioprosthetic valves. We attempted to prove this hypothesis using cusps of porcine pulmonary valves partly containing pulmonary artery and right ventricular wall (with intact fatty tissue firmly adherent to the outer surface mainly at the infundibular region). The cusps were cross-linked in 0.625% glutaraldehyde in phosphate buffer solution and implanted subcutaneously in 3-week-old male Wistar rats for 3 and 12 weeks. Histologic study of the explanted tissue demonstrated that the fatty layer on the outer surface of the infundibular wall virtually disappeared after implantation. Although most of the lipids are located in the basal region of the cusp within the spongiosal layer, 1 and no lipid is present in the apical region (see Fig. 3, B in the Dunmore-Buyze article 1), no specific region with higher propensity to calcification could be revealed in our study (Fig. 1).
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Fig. 1. Morphologic characteristics of calcification in a glutaraldehyde-treated whole porcine pulmonary valve implanted subcutaneously in a rat for 12 weeks. Massive calcific deposits (black) in the muscle wall, at the apical and basal regions of the leaflet, and in the pulmonary artery can be seen. (von Kossa stain; original magnification x10.)
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An opinion about the prevalence of pathogenic processes similar to coronary atherosclerosis in the calcification of bioprosthetic valves (oxidative modification of endogenous lipids of tissue
adinflammatory reactionadsecretion of matrix proteinadcalcification) has been expressed. 2 Dunmore-Buyze and associates 1 speculate that lipid extraction during the preparation of bioprosthetic materials or the avoidance of valves with high lipid concentrations might be an appropriate strategy for prevention of calcification. However, in preventing calcification, treatment of a tissue with a lipid-extracting agent before glutaraldehyde cross-linking is not as effective as treatment with the lipid-extracting agent after glutaraldehyde cross-linking. Thus this phenomenon suggests that the mechanism of action of lipid-extracting agent must be due to the interactions with glutaraldehyde. 3 Because endogenous lipid extraction does not completely prevent the calcification 3,4 of glutaraldehyde-treated bioprostheses, lipids cannot be considered a key factor in calcification of glutaraldehyde cross-linked bioprosthetic valves. Despite the discrepancy in lipid content, treatment with an anticalcificant can equally prevent the calcification of both porcine aortic and pulmonary valves without lipid extraction. 5
In our view, lipid may play a secondary role to glutaraldehyde or any other cross-linking agent in the calcification of bioprostheses. Nevertheless, lipid infiltration as one of the common pathologic features was observed in bioprosthetic heart valves that failed clinically. 6 Despite the adequate anticalcification treatment, the possibility of infiltrated lipid-induced calcification (similar to atherosclerosis) in the future cannot be ignored and may interfere with the long-term performances of bioprosthetic valves.
Department of Cardiovascular SurgeryAkita University School of Medicine,
Akita 010, Japan
References
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