Cardiovascular implant calcification: a survey and update

Levy, Robert J.; Schoen, Frederick J.; Anderson, H. Clarke; Harasaki, H; Koch, T H; Brown, W. E.; Lian, Jane B.; Cumming, Robert E.; Gavin, J.B.

doi:10.1016/0142-9612(91)90017-5

Cited by 70 publications

(38 citation statements)

References 46 publications

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“…Despite this success, tissue valves still fail, primarily because of structural degradation and dystrophic calcification. 3,4 Glutaraldehyde fixation may have a role in both modes of failure. One contributing factor in structural degradation seems to be tissue buckling, with the stiffer and more constrained glutaraldehydetreated materials being more susceptible.…”

Section: Introductionmentioning

confidence: 98%

“…1,2 The durability of these materials is limited by structural deterioration, which is, in part, attributed to dystrophic calcification of the collagenous matrix. 3,4 However, to their advantage, and as opposed to mechanical valves, tissue valves have a lower rate of thromboembolism and thus do not require permanent anticoagulation therapy. In addition, the flow and hemodynamic characteristics of tissue valves are more similar to native valves.…”

Section: Introductionmentioning

confidence: 99%

“…7,8 Glutaraldehyde has also been linked to calcification and cytotoxicity in numerous studies. 3,4,9,10 A number of different strategies have been used to reduce/prevent the calcification of tissue including new crosslinking chemistries and various prefixation and postfixation chemical treatments. [11][12][13][14][15][16][17][18][19][20][21][22][23][24] Based on this body of work, a number of hypotheses 12,13,24 and a simple alcohol (ethanol) to alter the confirmation of collagen and perhaps remove lipids and excess glutaraldehyde as well.…”

Section: Introductionmentioning

confidence: 99%

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Treatment of bioprosthetic heart valve tissue with long chain alcohol solution to lower calcification potential

Pathak¹,

Adams²,

Simpson³

et al. 2004

J Biomedical Materials Res

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The use of glutaraldehyde-treated biological tissue in heart valve substitutes is an important option in the treatment of heart valve disease. These devices have limited durability, in part, because of tissue calcification and subsequent tearing of the valve leaflets. Components thought to induce calcification include lipids, cell remnants, and residual glutaraldehyde. We hypothesized that treatment of glutaraldehyde-treated bioprosthetic heart valve material using a short and long chain alcohol (LCA) combination, composed of 5% 1,2-octanediol in an ethanolic buffered solution, would reduce phospholipid content and subsequently lower the propensity of these tissues to calcify in vivo. Phospholipid content of glutaraldehyde-treated porcine valve leaflets and bovine pericardium was found to be 10.1 +/- 4.3 (n = 7) and 3.9 +/- 0.48 (n = 2) microg/mg dry tissue, respectively, which was reduced to 0.041 +/- 0.06 (n = 7) and 0.21 +/- 0.05 (n = 4) microg/mg dry tissue, respectively, after LCA treatment. Calcification potential of the treated tissues was assessed using a rat subcutaneous implant model. After 60 days of implantation, calcium levels were found to be 171 +/- 32 (n = 11) and 83 +/- 70 (n = 12) mg/g dry weight for glutaraldehyde-treated porcine leaflets and bovine pericardium, respectively, whereas prior LCA treatment resulted in reduced calcium levels of 1.1 +/- 0.6 (n = 12) and 0.82 +/- 0.1 (n = 12) mg/g dry weight, respectively. These data, taken together, support the notion that treatment of glutaraldehyde-treated tissue with a short and long chain alcohol combination will reduce both extractable phospholipids and the propensity for in vivo calcification.

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Section: Introductionmentioning

confidence: 98%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Treatment of bioprosthetic heart valve tissue with long chain alcohol solution to lower calcification potential

Pathak¹,

Adams²,

Simpson³

et al. 2004

J Biomedical Materials Res

View full text Add to dashboard Cite

show abstract

“…Calcification is especially problematic in children, who often require valve replacement 2-5 years postimplantation. 3,4 The mechanism of this degenerative valve calcification in both children and adults is poorly understood, thus making it difficult to formulate an effective treatment or prevention strategy.…”

Section: Introductionmentioning

confidence: 99%

“…[1][2][3][4] In adults, valve replacement is necessary, on average, 10-12 years postimplantation. Calcification is especially problematic in children, who often require valve replacement 2-5 years postimplantation.…”

Section: Introductionmentioning

confidence: 99%

Identification of specific calcium-binding noncollagenous proteins associated with glutaraldehyde-preserved bovine pericardium in the rat subdermal model

Gura

Wright

Veis

et al. 1997

J. Biomed. Mater. Res.

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Calcification of glutaraldehyde-preserved bioprosthetic heart valves (BHVs) results in their clinical failure. The mechanism of this pathologic calcification is not well defined. Since serum proteins are known to be taken up in mineralized tissue, we hypothesized that serum proteins derived from several calcium-binding noncollagenous proteins (NCPs) of bone and teeth also may be associated with pathologically mineralized BHVs. Using a rat subdermal model of BHV calcification, glutaraldehyde-preserved bovine pericardium (GPBP) was implanted for 1, 3, 14, and 60 days, and then subjected to an extraction procedure designed to isolate only NCPs tightly bound to the mineral phase. Gel electrophoresis and Coomassie Brilliant Blue staining demonstrated that these proteins became associated with GPBP over time, paralleling reported calcium uptake by the tissue. Stains-All staining demonstrated a marked accumulation of highly acidic, phosphorylated NCPs associated with 60-day GPBP extracts. Some of these proteins were detected in rat serum but were absent from extracts of GPBP incubated in rat serum in vitro. Western blotting with antibodies to three NCPs found in bone and teeth-bone acidic glycoprotein 75 (BAG 75), osteopontin, and SPARC-demonstrated that these NCPs were tightly bound to the mineral phase of calcified GPBP. A fourth NCP, bone sialoprotein II (BSP II) was barely detectable. Thus each identified NCP showed a different pattern of GPBP association relative to mineral deposition, suggesting unique roles for each in pathologic calcification. SPARC increased within 3 days of GPBP implantation but decreased by 2 weeks. BAG 75 and osteopontin uptake was detected in the initial mineral deposits and increased mineralization proceeded. BSP II never increased significantly over the entire-period. Further studies, which should include immunohistochemistry, will be important for delineating the source, location, and function of these three NCPs and for identifying others that also may be involved in this pathological process. Most important, the new insights into the mechanism of pathologic calcification described here present exciting opportunities for novel approaches to BHV calcification prevention.

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Shrinkage temperature versus protein extraction as a measure of stabilization of photooxidized tissue

Moore¹,

Chen²,

Phillips³

et al. 1996

J. Biomed. Mater. Res.

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A rise in thermal denaturation temperature has been utilized as an indication of stabilization of collagen-containing materials such as pericardial tissue and porcine heart-valve leaflets following treatment with glutaraldehyde, Denacol, or other chemical agents. In contrast, stabilization of bovine pericardial tissue by dye-mediated photooxidation does not result in a significant rise in shrinkage temperature comparable with these treated materials. It was therefore hypothesized that a rise in shrinkage temperature is not a necessary indication for tissue stabilization. A sensitive protein extraction assay has been developed which can be used to monitor the stabilization of pericardial tissue by a variety of treatment methods, including photooxidation. A reduction in extractable protein, as analyzed by polyacrylamide gel electrophoresis, is noted for pericardial tissue treated with photooxidation, glutaraldehyde, or Denacol. Loss of extractable protein, as a function of treatment time, correlates well with a significant rise in shrinkage temperature for pericardium treated with glutaraldehyde or Denacol but not with photooxidation. This difference is attributed to the stabilization processes of glutaraldehyde and Denacol, which involve extensive crosslinking and polymer formation within and in addition to the native pericardial matrix, leading to a rise in matrix complexity and thermal stability. In contrast, photooxidation is a catalytic process involving modification and crosslink formation within existing matrix components, resulting in a material with little added matrix complexity.

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Cardiovascular implant calcification: a survey and update

Cited by 70 publications

References 46 publications

Treatment of bioprosthetic heart valve tissue with long chain alcohol solution to lower calcification potential

Treatment of bioprosthetic heart valve tissue with long chain alcohol solution to lower calcification potential

Identification of specific calcium-binding noncollagenous proteins associated with glutaraldehyde-preserved bovine pericardium in the rat subdermal model

Shrinkage temperature versus protein extraction as a measure of stabilization of photooxidized tissue

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