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      Predictors of stent thrombosis and their implications for clinical practice

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          Abstract

          Stent thrombosis (ST) is a rare but severe complication of coronary procedures with high mortality, high relapse rate and a very complex pathophysiology. An individual's susceptibility to ST is multifactorial and results from interactions between clinical factors, endothelial biology, hypersensitivity and/or inflammatory reactions, blood rheology, platelet reactivity, clotting factors, physical and mechanical properties of the stent and from the effects of these different factors on the fluid dynamics of blood flow. Since the introduction of stents 32 years ago, continuous improvements in our understanding of the pathophysiology of ST have triggered important advances, including new therapies, new technologies and an increased awareness of the implications of implantation techniques. Furthermore, advances in medical imaging and in the mathematical processing of this information have allowed a more detailed assessment of the mechanisms of ST at the time of its onset. Evidence shows that addressing the risk factors for ST leads to a substantial reduction in its incidence, both early and late after stent implantation. A better knowledge of the mechanisms of this complication is, however, necessary to direct the choice of the most appropriate strategy for its prevention and treatment.

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          Most cited references138

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          Derivation and validation of the predicting bleeding complications in patients undergoing stent implantation and subsequent dual antiplatelet therapy (PRECISE-DAPT) score: a pooled analysis of individual-patient datasets from clinical trials

          Dual antiplatelet therapy (DAPT) with aspirin plus a P2Y12 inhibitor prevents ischaemic events after coronary stenting, but increases bleeding. Guidelines support weighting bleeding risk before the selection of treatment duration, but no standardised tool exists for this purpose.
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            Stent thrombogenicity early in high-risk interventional settings is driven by stent design and deployment and protected by polymer-drug coatings.

            Stent thrombosis is a lethal complication of endovascular intervention. Concern has been raised about the inherent risk associated with specific stent designs and drug-eluting coatings, yet clinical and animal support is equivocal. We examined whether drug-eluting coatings are inherently thrombogenic and if the response to these materials was determined to a greater degree by stent design and deployment with custom-built stents. Drug/polymer coatings uniformly reduce rather than increase thrombogenicity relative to matched bare metal counterparts (0.65-fold; P=0.011). Thick-strutted (162 μm) stents were 1.5-fold more thrombogenic than otherwise identical thin-strutted (81 μm) devices in ex vivo flow loops (P<0.001), commensurate with 1.6-fold greater thrombus coverage 3 days after implantation in porcine coronary arteries (P=0.004). When bare metal stents were deployed in malapposed or overlapping configurations, thrombogenicity increased compared with apposed, length-matched controls (1.58-fold, P=0.001; and 2.32-fold, P<0.001). The thrombogenicity of polymer-coated stents with thin struts was lowest in all configurations and remained insensitive to incomplete deployment. Computational modeling-based predictions of stent-induced flow derangements correlated with spatial distribution of formed clots. Contrary to popular perception, drug/polymer coatings do not inherently increase acute stent clotting; they reduce thrombosis. However, strut dimensions and positioning relative to the vessel wall are critical factors in modulating stent thrombogenicity. Optimal stent geometries and surfaces, as demonstrated with thin stent struts, help reduce the potential for thrombosis despite complex stent configurations and variability in deployment.
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              Guided de-escalation of antiplatelet treatment in patients with acute coronary syndrome undergoing percutaneous coronary intervention (TROPICAL-ACS): a randomised, open-label, multicentre trial

              Current guidelines recommend potent platelet inhibition with prasugrel or ticagrelor for 12 months after an acute coronary syndrome managed with percutaneous coronary intervention (PCI). However, the greatest anti-ischaemic benefit of potent antiplatelet drugs over the less potent clopidogrel occurs early, while most excess bleeding events arise during chronic treatment. Hence, a stage-adapted treatment with potent platelet inhibition in the acute phase and de-escalation to clopidogrel in the maintenance phase could be an alternative approach. We aimed to investigate the safety and efficacy of early de-escalation of antiplatelet treatment from prasugrel to clopidogrel guided by platelet function testing (PFT).
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                Author and article information

                Journal
                Nature Reviews Cardiology
                Nat Rev Cardiol
                Springer Nature
                1759-5002
                1759-5010
                December 5 2018
                Article
                10.1038/s41569-018-0118-5
                30518952
                42accc4b-2385-4135-aee6-3195e51bf3b8
                © 2018

                http://www.springer.com/tdm

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