Evaluation of Coronary Stents in the Animal Model: A Review

Wieneke, Heinrich; Haude, Michael; Knocks, M.; Gutersohn, Achim; Birgelen, Clemens von; Baumgart, Dietrich; Erbel, Raimund

doi:10.1002/(sici)1521-4052(199912)30:12<809::aid-mawe809>3.0.co;2-3

Cited by 6 publications

(9 citation statements)

References 40 publications

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“…Nevertheless, this response also depends on the intensity of the mechanical damage and hence it is necessary to further study how different stent designs and deployment parameters influence the development of in-stent restenosis. In this context, when the extent of vascular injury increases, causing laceration to the external elastic lamina and adventitia, the neointimal thickness significantly increases and could necessitate repeat surgical intervention (Wieneke et al, 1999). In addition, endothelial denudation and disruption is observed following stent deployment which has implications for in-stent restenosis given that endothelial cells synthesise nitric oxide which is directly implicated in inducing and maintaining the contractile and quiescent phenotype in VSMC (Lemson et al, 2000).…”

Section: Resultsmentioning

confidence: 99%

“…Close correlation has been observed between the degree of inflammation and neo-intimal thickness which suggests that inflammation caused by the arterial injury plays a central role in the formation of in-stent restenosis (Wieneke et al, 1999;Welt et al, 2002;Mitra et al, 2006). After stent deployment, vessel injury by the stent struts leads to the activation of thrombocytes and the formation of mural thrombus at the injury site.…”

Section: The Mechanism Of In-stent Restenosismentioning

confidence: 99%

“…This change of phenotype is followed by a chemotactic migration and proliferation of dedifferentiated medial VSMC towards the lumen and lesion formation, see Figure 1. The cytokines produced by the inflammatory cells not only serve as mitogens for VSMC but also upregulate synthesis of extracellular matrix by the synthetic VSMC (Wieneke et al, 1999;Babapulle and Eisenberg, 2002;Welt et al, 2002;Mitra et al, 2006).…”

Section: The Mechanism Of In-stent Restenosismentioning

confidence: 99%

“…The stent induced lesions are invaded by VSMC with mainly a synthetic phenotype. These cells produce extracellular matrix (ECM) components such as collagen, elastin and proteoglycans which constitute the neointimal tissue and the process usually takes up to 6 months, after which further luminal loss is minimal (Wieneke et al, 1999, Sousa et al, 2005. Intimal hyperplasia is found to be present at increasing thicknesses following injury and lacerations to the internal elastic lamina (IEL), the media, external elastic lamina (EEL) and adventitia (Wieneke et al, 1999;Lowe et al, 2002).…”

Section: The Mechanism Of In-stent Restenosismentioning

confidence: 99%

See 3 more Smart Citations

Vascular Stent Design Optimisation Using Numerical Modelling Techniques

Zahedmanesh¹,

Cahill²,

Lally³

2012

Applied Biological Engineering - Principles and Practice

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Section: Resultsmentioning

confidence: 99%

Section: The Mechanism Of In-stent Restenosismentioning

confidence: 99%

Section: The Mechanism Of In-stent Restenosismentioning

confidence: 99%

Section: The Mechanism Of In-stent Restenosismentioning

confidence: 99%

See 2 more Smart Citations

Vascular Stent Design Optimisation Using Numerical Modelling Techniques

Zahedmanesh¹,

Cahill²,

Lally³

2012

Applied Biological Engineering - Principles and Practice

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“…Animal studies, however, are a valuable tool and much of what is known about restenosis and the healing response after stent implantation has been gathered from the study of both healthy and atherosclerotic animal models (Touchard and Schwartz 2006;Schwartz, Chronos and Virmani 2004;Wieneke, et al 1999).…”

Section: In Vivo Animal Modelsmentioning

confidence: 99%

Design and Optimization of a Blood Vessel Mimic Bioreactor System for the Evaluation of Intravascular Devices in Simple and Complex Vessel Geometries

Leifer¹

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Coronary artery disease affects millions of people and the ability to detect and treat the disease is advancing at a rapid rate. As a result, the development of intravascular technologies is the focus of many medical device manufacturers. Specifically, coronary stent implantation is being performed in an increasing number of patients and a number of new stent designs have been introduced to the market, resulting in the need for improved preclinical testing methods. An in vitro tissue engineered "blood vessel mimic" (BVM) system has previously been established and its feasibility for the initial testing of newly emerging intravascular technology has been demonstrated. There are limitations that exist with this original design, however, and the focus of this thesis was to both improve and expand upon the original model. Therefore, research was conducted based on two specific aims. The first aim was to develop a more ideal BVM system to accommodate a wider range of stent lengths and diameters, while allowing for easy graft insertion and seal-ability. The second aim was to develop next generation BVM systems, v focused on future needs and technology, such as long, angulated and bifurcated geometries.The work described in this thesis demonstrates that a BVM chamber can be created which has the advantages of easy graft insertion and seal-ability, as well as the ability to accommodate varying sizes of vessel scaffolds, all while maintaining the needs of a tissue engineering bioreactor system. The next generation BVM systems presented demonstrate that the BVM concept can be expanded to meet the needs of long, angulated and bifurcated geometries. Overall, the work in this thesis describes the design and optimization of an in vitro blood vessel mimic bioreactor system for the evaluation of intravascular devices, specifically coronary stents, in simple and complex vessel geometries.vi ACKNOWLEDGEMENTS First, I would like to acknowledge and thank the members of my thesis committee: Dr. Kristen O'Halloran Cardinal, Dr. Trevor Cardinal and Dr. Lily Laiho. Thanks for all your guidance and input and for providing assistance and ideas throughout the project.

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Multiscale Modeling in Vascular Disease and Tissue Engineering

Zahedmanesh

Lally

2012

Multiscale Computer Modeling in Biomechanics and Biomedical Engineering

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The human body, and hence the vascular system, is by its very nature a dynamic multiscale hierarchial system. This multiscale nature encompasses different length scales, from molecular and cellular levels to the tissue and organ level, as well as different physical phenomena, such as mechanical, biological and chemical processes. In arteries, vascular cells alter their growth, phenotype and extracellular matrix production in response to macro mechanical changes. These cell level events can in turn accumulate and emerge at the tissue level as pathological conditions such as atherosclerosis and intimal hyperplasia. These cardiovascular diseases evolve through adaptation of cells and tissues over days to months also demonstrating the multiscale nature of vascular diseases with respect to time. The challenge in vascular multiscale modelling is to create a framework which can incorporate the key mechanical, biological and chemical characteristics of this complex system at these various space and time scales to successfully capture the long-term behaviour of the system. Such a framework can then be used to gain additional insights with regards to pathological conditions within the vascular system and to improve the design of medical devices used to treat such pathologies. In the following chapter, a review will be presented of some relevant studies reported in literature which have used multiscale modelling approaches to elucidate the growth and remodelling mechanisms underlying vascular diseases, such as atherosclerosis, in-stent restenosis and intimal hyperplasia.

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Evaluation of Coronary Stents in the Animal Model: A Review

Cited by 6 publications

References 40 publications

Vascular Stent Design Optimisation Using Numerical Modelling Techniques

Vascular Stent Design Optimisation Using Numerical Modelling Techniques

Design and Optimization of a Blood Vessel Mimic Bioreactor System for the Evaluation of Intravascular Devices in Simple and Complex Vessel Geometries

Multiscale Modeling in Vascular Disease and Tissue Engineering

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