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      Management of Stent Thrombosis Post-Percutaneous Coronary Intervention and Associated Rare Complications

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      Author(s): 1 , , 1 , 1 , 2 , 3
      Editor(s): ,
      Publication date (Electronic, pub):
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      Journal: Cureus
      Publisher: Cureus
      Keywords: very late stent thrombosis, subacute stent thrombosis, thrombosis, stents, pci

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          Abstract

          Stent thrombosis is a devastating complication of percutaneous coronary intervention (PCI) associated with significant morbidity and mortality. Progressive technical advancements from balloon angioplasty to bare-metal stent and drug-eluting stent placement have reduced the incidence of stent thrombosis. Definitive management and preventive methods are still negligible. Here, we describe two cases of definite subacute stent thrombosis of the right coronary complicated by pericarditis and very late left anterior descending stent thrombosis after the intervention in the right coronary artery. In both cases, antiplatelet treatment with clopidogrel showed excellent compliance. Therefore, after successful PCI, we switched both cases from clopidogrel to potentially more potent antiplatelet treatment, such as ticagrelor, to reduce the occurrence of stent thrombosis in the future.

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          A randomized comparison of coronary-stent placement and balloon angioplasty in the treatment of coronary artery disease. Stent Restenosis Study Investigators.

          David L Fischman, Martin Leon, Donald S Baim … (1994)
          Coronary-stent placement is a new technique in which a balloon-expandable, stainless-steel, slotted tube is implanted at the site of a coronary stenosis. The purpose of this study was to compare the effects of stent placement and standard balloon angioplasty on angiographically detected restenosis and clinical outcomes. We randomly assigned 410 patients with symptomatic coronary disease to elective placement of a Palmaz-Schatz stent or to standard balloon angioplasty. Coronary angiography was performed at base line, immediately after the procedure, and six months later. The patients who underwent stenting had a higher rate of procedural success than those who underwent standard balloon angioplasty (96.1 percent vs. 89.6 percent, P = 0.011), a larger immediate increase in the diameter of the lumen (1.72 +/- 0.46 vs. 1.23 +/- 0.48 mm, P < 0.001), and a larger luminal diameter immediately after the procedure (2.49 +/- 0.43 vs. 1.99 +/- 0.47 mm, P < 0.001). At six months, the patients with stented lesions continued to have a larger luminal diameter (1.74 +/- 0.60 vs. 1.56 +/- 0.65 mm, P = 0.007) and a lower rate of restenosis (31.6 percent vs. 42.1 percent, P = 0.046) than those treated with balloon angioplasty. There were no coronary events (death; myocardial infarction; coronary-artery bypass surgery; vessel closure, including stent thrombosis; or repeated angioplasty) in 80.5 percent of the patients in the stent group and 76.2 percent of those in the angioplasty group (P = 0.16). Revascularization of the original target lesion because of recurrent myocardial ischemia was performed less frequently in the stent group than in the angioplasty group (10.2 percent vs. 15.4 percent, P = 0.06). In selected patients, placement of an intracoronary stent, as compared with balloon angioplasty, results in an improved rate of procedural success, a lower rate of angiographically detected restenosis, a similar rate of clinical events after six months, and a less frequent need for revascularization of the original coronary lesion.
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            Vascular inflammation and repair: implications for re-endothelialization, restenosis, and stent thrombosis.

            Teruo Inoue, Kevin Croce, Toshifumi Morooka … (2011)
            The cellular and molecular processes that control vascular injury responses after percutaneous coronary intervention involve a complex interplay among vascular cells and progenitor cells that control arterial remodeling, neointimal proliferation, and re-endothelialization. Drug-eluting stents (DES) improve the efficacy of percutaneous coronary intervention by modulating vascular inflammation and preventing neointimal proliferation and restenosis. Although positive effects of DES reduce inflammation and restenosis, negative effects delay re-endothelialization and impair endothelial function. Delayed re-endothelialization and impaired endothelial function are linked to stent thrombosis and adverse clinical outcomes after DES use. Compared with bare-metal stents, DES also differentially modulate mobilization, homing, and differentiation of vascular progenitor cells involved in re-endothelialization and neointimal proliferation. The effects of DES on vascular inflammation and repair directly impact clinical outcomes with these devices and dictate requirements for extended-duration dual antiplatelet therapy. Copyright © 2011 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.
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              Drug-eluting stent and coronary thrombosis: biological mechanisms and clinical implications.

              Gaku Nakazawa, Michael Joner, Renu Virmani … (2007)
              Although rare, stent thrombosis remains a severe complication after stent implantation owing to its high morbidity and mortality. Since the introduction of drug-eluting stents (DES), most interventional centers have noted stent thrombosis up to 3 years after implantation, a complication rarely seen with bare-metal stents. Some data from large registries and meta-analyses of randomized trials indicate a higher risk for DES thrombosis, whereas others suggest an absence of such a risk. Several factors are associated with an increased risk of stent thrombosis, including the procedure itself (stent malapposition and/or underexpansion, number of implanted stents, stent length, persistent slow coronary blood flow, and dissections), patient and lesion characteristics, stent design, and premature cessation of antiplatelet drugs. Drugs released from DES exert distinct biological effects, such as activation of signal transduction pathways and inhibition of cell proliferation. As a result, although primarily aimed at preventing vascular smooth muscle cell proliferation and migration (ie, key factors in the development of restenosis), they also impair reendothelialization, which leads to delayed arterial healing, and induce tissue factor expression, which results in a prothrombogenic environment. In the same way, polymers used to load these drugs have been associated with DES thrombosis. Finally, DES impair endothelial function of the coronary artery distal to the stent, which potentially promotes the risk of ischemia and coronary occlusion. Although several reports raise the possibility of a substantially higher risk of stent thrombosis in DES, evidence remains inconclusive; as a consequence, both large-scale and long-term clinical trials, as well as further mechanistic studies, are needed. The present review focuses on the pathophysiological mechanisms and pathological findings of stent thrombosis in DES.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Cureus
                Journal ID (iso-abbrev): Cureus
                Journal ID (issn): 2168-8184
                Title: Cureus
                Publisher: Cureus (Palo Alto (CA) )
                ISSN (Electronic): 2168-8184
                Publication date (Electronic, pub): 29 September 2021
                Publication date (Electronic, collection): September 2021
                Volume: 13
                Issue: 9
                Electronic Location Identifier: e18370
                Affiliations
                [1 ] Internal Medicine, Texas Tech University Health Sciences Center El Paso Paul L. Foster School of Medicine, El Paso, USA
                [2 ] Cardiovascular Medicine, Texas Tech University Health Sciences Center El Paso, El Paso, USA
                [3 ] Cardiology, Texas Tech University Health Sciences Center El Paso, El Paso, USA
                Author notes
                Article
                DOI: 10.7759/cureus.18370
                PMC ID: 8526071
                PubMed ID: 34692363
                SO-VID: 3d27f3f2-3a28-4a66-be4a-becf32c171bd
                Copyright © Copyright © 2021, Fadah et al.
                License:

                This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

                History
                Date accepted : 28 September 2021
                Categories
                Subject: Cardiology
                Subject: Internal Medicine

                Keywords: very late stent thrombosis,subacute stent thrombosis,thrombosis,stents,pci
                Data availability:
                Keywords: very late stent thrombosis, subacute stent thrombosis, thrombosis, stents, pci

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