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      Biocompatibility of Coronary Stents

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          Abstract

          Cardiovascular disease is the dominant cause of mortality in developed countries, with coronary artery disease (CAD) a predominant contributor. The development of stents to treat CAD was a significant innovation, facilitating effective percutaneous coronary revascularization. Coronary stents have evolved from bare metal compositions, to incorporate advances in pharmacological therapy in what are now known as drug eluting stents (DES). Deployment of a stent overcomes some limitations of balloon angioplasty alone, but provides an acute stimulus for thrombus formation and promotes neointimal hyperplasia. First generation DES effectively reduced in-stent restenosis, but profoundly delay healing and are susceptible to late stent thrombosis, leading to significant clinical complications in the long term. This review characterizes the development of coronary stents, detailing the incremental improvements, which aim to attenuate the major clinical complications of thrombosis and restenosis. Despite these enhancements, coronary stents remain fundamentally incompatible with the vasculature, an issue which has largely gone unaddressed. We highlight the latest modifications and research directions that promise to more holistically design coronary implants that are truly biocompatible.

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          Sirolimus-eluting stents versus standard stents in patients with stenosis in a native coronary artery.

          Jeffrey W Moses, Martin Leon, Jeffrey J. Popma … (2003)
          Preliminary reports of studies involving simple coronary lesions indicate that a sirolimus-eluting stent significantly reduces the risk of restenosis after percutaneous coronary revascularization. We conducted a randomized, double-blind trial comparing a sirolimus-eluting stent with a standard stent in 1058 patients at 53 centers in the United States who had a newly diagnosed lesion in a native coronary artery. The coronary disease in these patients was complex because of the frequent presence of diabetes (in 26 percent of patients), the high percentage of patients with longer lesions (mean, 14.4 mm), and small vessels (mean, 2.80 mm). The primary end point was failure of the target vessel (a composite of death from cardiac causes, myocardial infarction, and repeated percutaneous or surgical revascularization of the target vessel) within 270 days. The rate of failure of the target vessel was reduced from 21.0 percent with a standard stent to 8.6 percent with a sirolimus-eluting stent (P<0.001)--a reduction that was driven largely by a decrease in the frequency of the need for revascularization of the target lesion (16.6 percent in the standard-stent group vs. 4.1 percent in the sirolimus-stent group, P<0.001). The frequency of neointimal hyperplasia within the stent was also decreased in the group that received sirolimus-eluting stents, as assessed by both angiography and intravascular ultrasonography. Subgroup analyses revealed a reduction in the rates of angiographic restenosis and target-lesion revascularization in all subgroups examined. In this randomized clinical trial involving patients with complex coronary lesions, the use of a sirolimus-eluting stent had a consistent treatment effect, reducing the rates of restenosis and associated clinical events in all subgroups analyzed. Copyright 2003 Massachusetts Medical Society
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            Early and late coronary stent thrombosis of sirolimus-eluting and paclitaxel-eluting stents in routine clinical practice: data from a large two-institutional cohort study.

            Joost Daemen, Peter Wenaweser, Keiichi Tsuchida … (2007)
            Stent thrombosis is a safety concern associated with use of drug-eluting stents. Little is known about occurrence of stent thrombosis more than 1 year after implantation of such stents. Between April, 2002, and Dec, 2005, 8146 patients underwent percutaneous coronary intervention with sirolimus-eluting stents (SES; n=3823) or paclitaxel-eluting stents (PES; n=4323) at two academic hospitals. We assessed data from this group to ascertain the incidence, time course, and correlates of stent thrombosis, and the differences between early (0-30 days) and late (>30 days) stent thrombosis and between SES and PES. Angiographically documented stent thrombosis occurred in 152 patients (incidence density 1.3 per 100 person-years; cumulative incidence at 3 years 2.9%). Early stent thrombosis was noted in 91 (60%) patients, and late stent thrombosis in 61 (40%) patients. Late stent thrombosis occurred steadily at a constant rate of 0.6% per year up to 3 years after stent implantation. Incidence of early stent thrombosis was similar for SES (1.1%) and PES (1.3%), but late stent thrombosis was more frequent with PES (1.8%) than with SES (1.4%; p=0.031). At the time of stent thrombosis, dual antiplatelet therapy was being taken by 87% (early) and 23% (late) of patients (p<0.0001). Independent predictors of overall stent thrombosis were acute coronary syndrome at presentation (hazard ratio 2.28, 95% CI 1.29-4.03) and diabetes (2.03, 1.07-3.83). Late stent thrombosis was encountered steadily with no evidence of diminution up to 3 years of follow-up. Early and late stent thrombosis were observed with SES and with PES. Acute coronary syndrome at presentation and diabetes were independent predictors of stent thrombosis.
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              Evidence for circulating bone marrow-derived endothelial cells.

              Q Shi, S. RAFII, M. Wu … (1998)
              It has been proposed that hematopoietic and endothelial cells are derived from a common cell, the hemangioblast. In this study, we demonstrate that a subset of CD34(+) cells have the capacity to differentiate into endothelial cells in vitro in the presence of basic fibroblast growth factor, insulin-like growth factor-1, and vascular endothelial growth factor. These differentiated endothelial cells are CD34(+), stain for von Willebrand factor (vWF), and incorporate acetylated low-density lipoprotein (LDL). This suggests the possible existence of a bone marrow-derived precursor endothelial cell. To demonstrate this phenomenon in vivo, we used a canine bone marrow transplantation model, in which the marrow cells from the donor and recipient are genetically distinct. Between 6 to 8 months after transplantation, a Dacron graft, made impervious to prevent capillary ingrowth from the surrounding perigraft tissue, was implanted in the descending thoracic aorta. After 12 weeks, the graft was retrieved, and cells with endothelial morphology were identified by silver nitrate staining. Using the di(CA)n and tetranucleotide (GAAA)n repeat polymorphisms to distinguish between the donor and recipient DNA, we observed that only donor alleles were detected in DNA from positively stained cells on the impervious Dacron graft. These results strongly suggest that a subset of CD34+ cells localized in the bone marrow can be mobilized to the peripheral circulation and can colonize endothelial flow surfaces of vascular prostheses.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Materials (Basel)
                Journal ID (iso-abbrev): Materials (Basel)
                Journal ID (publisher-id): Materials
                Title: Materials
                Publisher: MDPI
                ISSN (Electronic): 1996-1944
                Publication date Collection: February 2014
                Publication date (Electronic): 28 January 2014
                Volume: 7
                Issue: 2
                Pages: 769-786
                Affiliations
                [1 ]The Heart Research Institute, Sydney NSW 2042, Australia; E-Mails: thamarasee.jeewandara@ 123456hri.org.au (T.M.J.); wises@ 123456hri.org.au (S.G.W.)
                [2 ]Sydney Medical School, University of Sydney, Sydney NSW 2006, Australia
                [3 ]School of Molecular Bioscience, University of Sydney, Sydney NSW 2006, Australia
                [4 ]Department of Cardiology, Royal Prince Alfred Hospital, University of Sydney, Sydney NSW 2050, Australia
                Author notes
                [* ]Author to whom correspondence should be addressed; E-Mail: mkcng@ 123456med.usyd.edu.au ; Tel.: +64-2-8208-8900; Fax: +61-2-9565-5584.
                Article
                Publisher ID: materials-07-00769
                DOI: 10.3390/ma7020769
                PMC ID: 5453068
                SO-VID: ac613fcb-86e1-40e4-8fe8-a22f2d8dc652
                Copyright © © 2014 by the authors.
                License:

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution license ( http://creativecommons.org/licenses/by/3.0/).

                History
                Date received : 24 December 2013
                Date revision received : 20 January 2014
                Date accepted : 20 January 2014
                Categories
                Subject: Review

                Keywords: coronary artery disease,biofunctionalization,stent,thrombosis,restenosis
                Data availability:
                Keywords: coronary artery disease, biofunctionalization, stent, thrombosis, restenosis

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