Sevelamer Attenuates Bioprosthetic Heart Valve Calcification

Meng, Zhen; Li, Zhe; Zhang, Erli; Zhang, Li; Liu, Qingrong; Wu, Yongjian

doi:10.3389/fcvm.2021.740038

Cited by 5 publications

(2 citation statements)

References 23 publications

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“…Given the well-recognized association between end-stage renal disease, diabetes mellitus, hyperparathyroidism and BHV calcification, aggressive treatment should be applied. Notably, sevelamer hydrochloride, a phosphate binder used to treat hyperphosphatemia in patients with chronic kidney disease, has been showing the ability to decrease BHV calcification (Meng et al, 2021).…”

Section: Potential Drug Therapymentioning

confidence: 99%

Mechanisms and Drug Therapies of Bioprosthetic Heart Valve Calcification

et al. 2022

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Valve replacement is the main therapy for valvular heart disease, in which a diseased valve is replaced by mechanical heart valve (MHV) or bioprosthetic heart valve (BHV). Since the 2000s, BHV surpassed MHV as the leading option of prosthetic valve substitute because of its excellent hemocompatible and hemodynamic properties. However, BHV is apt to structural valve degeneration (SVD), resulting in limited durability. Calcification is the most frequent presentation and the core pathophysiological process of SVD. Understanding the basic mechanisms of BHV calcification is an essential prerequisite to address the limited-durability issues. In this narrative review, we provide a comprehensive summary about the mechanisms of BHV calcification on 1) composition and site of calcifications; 2) material-associated mechanisms; 3) host-associated mechanisms, including immune response and foreign body reaction, oxidative stress, metabolic disorder, and thrombosis. Strategies that target these mechanisms may be explored for novel drug therapy to prevent or delay BHV calcification.

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Section: Potential Drug Therapymentioning

confidence: 99%

Mechanisms and Drug Therapies of Bioprosthetic Heart Valve Calcification

et al. 2022

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“…The persistently unbound residual aldehyde groups in BHVs might directly bind with calcium ions to form calcification sites ( Gong et al, 1991 ; Levy, 1994 ), and then can also induce cell lysis around the xenografts, leading to the release of cellular debris and phospholipid cell membrane debris ( Thiene and Valente, 2011 ), and inhibiting endothelialization ( Hoffman et al, 1992 ). Serum calcium reacts with residual phosphorus in cell debris to generate calcium phosphate apatite crystals, which allows the formation of some potential calcification sites ( Pettenazzo et al, 2008 ; Meng et al, 2021 ).…”

Section: Introductionmentioning

confidence: 99%

Free-aldehyde neutralized and oligohyaluronan loaded bovine pericardium with improved anti-calcification and endothelialization for bioprosthetic heart valves

Liu

Chen

et al. 2023

Front. Bioeng. Biotechnol.

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The number of patients with valvular heart disease is increasing yearly, and valve replacement is the most effective treatment, during which bioprosthetic heart valves (BHVs) are the most widely used. Commercial BHVs are mainly prepared with glutaraldehyde (Glut) cross-linked bovine pericardial or porcine aortic valves, but the residual free aldehyde groups in these tissues can cause calcification and cytotoxicity. Moreover, insufficient glycosaminoglycans (GAGs) in tissues can further reduce biocompatibility and durability. However, the anti-calcification performance and biocompatibility might be improved by blocking the free aldehyde groups and increasing the GAGs content in Glut-crosslinked tissues. In our study, adipic dihydrazide (ADH) was used to neutralize the residual free aldehyde groups in tissues and provide sites to blind with oligohyaluronan (OHA) to increase the content of GAGs in tissues. The modified bovine pericardium was evaluated for its content of residual aldehyde groups, the amount of OHA loaded, physical/chemical characteristics, biomechanical properties, biocompatibility, and in vivo anticalcification assay and endothelialization effects in juvenile Sprague-Dawley rats. The results showed that ADH could completely neutralize the free aldehyde groups in the Glut-crosslinked bovine pericardium, the amount of OHA loaded increased and the cytotoxicity was reduced. Moreover, the in vivo results also showed that the level of calcification and inflammatory response in the modified pericardial tissue was significantly reduced in a rat subcutaneous implantation model, and the results from the rat abdominal aorta vascular patch repair model further demonstrated the improved capability of the modified pericardial tissues for endothelialization. Furthermore, more α-SMA+ smooth muscle cells and fewer CD68+ macrophages infiltrated in the neointima of the modified pericardial patch. In summary, blocking free-aldehydes and loading OHA improved the anti-calcification, anti-inflammation and endothelialization properties of Glut-crosslinked BHVs and in particularly, this modified strategy may be a promising candidate for the next-generation of BHVs.

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