PHYSICOCHEMICAL PROPERTIES OF CALCIFIC DEPOSITS ISOLATED FROM PORCINEBIOPROSTHETIC HEART-VALVES REMOVED FROM PATIENTS FOLLOWING 2-13 YEARSFUNCTION

Citation
Bb. Tomazic et al., PHYSICOCHEMICAL PROPERTIES OF CALCIFIC DEPOSITS ISOLATED FROM PORCINEBIOPROSTHETIC HEART-VALVES REMOVED FROM PATIENTS FOLLOWING 2-13 YEARSFUNCTION, Journal of biomedical materials research, 28(1), 1994, pp. 35-47
Citations number
50
Categorie Soggetti
Engineering, Biomedical","Materials Science, Biomaterials
ISSN journal
00219304
Volume
28
Issue
1
Year of publication
1994
Pages
35 - 47
Database
ISI
SICI code
0021-9304(1994)28:1<35:PPOCDI>2.0.ZU;2-9
Abstract
The purpose of this study was to characterize the physicochemical prop erties of calcific deposits that cause the failure of tissue-derived h eart valve bioprostheses. This was done in an effort to understand the mechanism of pathologic biomineralization in the cardiovascular syste m and potentially prevent deterioration of bioprostheses. Calcific dep osits taken from 10 failed bioprosthetic valves that had been implante d in patients for 2-13 years were characterized by chemical analysis, x-ray diffraction, FTIR spectroscopy, scanning electron microscopy, po larized light microscopy, and solubility measurements. The combined re sults identified the biomineral as an apatitic calcium phosphate salt with substantial incorporation of sodium, magnesium and carbonate. The average Ca/PO4 ratio for this ''young'' pathologic biomineral was sim ilar to 1.3, considerably lower than similar to 1.7 found in mature at herosclerotic plaque biomineral and mature skeletal biomineral, both o f which approximate hydroxyapatite in composition. Deproteinated calci fic deposits from bioprostheses had thermodynamic solubilities compara ble to those of both atherosclerotic plaque, typical pathologic biomin eral and hydrolyzed octacalcium phosphate (OCP, Ca4H(PO4)(3).2.5 H2O), a proposed precursor phase to biomineral apatite. This later finding, together with chemical composition and structural details of the biop rostetic deposits themselves, supports a mechanism of cardiovascular c alcification in which OCP plays a crucial role in the formation of the final apatitic phase. This suggests an approach toward prevention of bioprosthetic tissue calcification through control of the formation of the kinetically favored OCP precursor and/or its transformation into bioapatite. (C) 1994 John Wiley and Sons, Inc.