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Review
. 2020 Aug 21;8(16):4383-4395.
doi: 10.1039/d0bm00226g. Epub 2020 Jul 9.

Current understanding of intimal hyperplasia and effect of compliance in synthetic small diameter vascular grafts

Affiliations
Review

Current understanding of intimal hyperplasia and effect of compliance in synthetic small diameter vascular grafts

YeJin Jeong et al. Biomater Sci. .

Abstract

Despite much effort, synthetic small diameter vascular grafts still face limited success due to vascular wall thickening known as intimal hyperplasia (IH). Compliance mismatch between graft and native vessels has been proposed to be one of a key mechanical factors of synthetic vascular grafts that could contribute to the formation of IH. While many methods have been developed to determine compliance both in vivo and in vitro, the effects of compliance mismatch still remain uncertain. This review aims to explain the biomechanical factors that are responsible for the formation and development of IH and their relationship with compliance mismatch. Furthermore, this review will address the current methods used to measure compliance both in vitro and in vivo. Lastly, current limitations in understanding the connection between the compliance of vascular grafts and the role it plays in the development and progression of IH will be discussed.

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Conflict of interest statement

Conflict of interest

The authors declare no conflict of interest

Figures

Figure 1.
Figure 1.
Photomicrographs by Costa et al. showing the nuclei of smooth muscle cells in intimal hyperplasia (↔), stained in blue. Irradiated group in A (21 days) and B image analysed by the computer system; control group in C (21 days) and D image analysed. (hematoxylin and eosin – 10x magnification).
Figure 2.
Figure 2.
Locations of intimal hyperplasia formation in synthetic vascular grafts. IH in synthetic vascular grafts occur mainly at the floor of the native blood vessel and the toe, and heel and toe around the distal anastomoses.
Figure 3.
Figure 3.
Factors that influence intimal hyperplasia formation. WS – wall stress, EC – endothelial cells, VSMC – vascular smooth muscle cells, PDGF – platelet-derived growth factors, MMP – metalloproteinase, TNF-α – tumor necrosis factor-α, and eNOS – endothelial nitric oxide synthase.
Figure 4.
Figure 4.
Vascular vessel wall remodelling due to alteration in wall shear stress.
Figure 5.
Figure 5.
Summary of the techniques used for calculation of compliance of vascular grafts in vitro.
Figure 6.
Figure 6.
Summary of current progress in understanding intimal hyperplasia formation in synthetic vascular grafts.

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