Novel Biomarkers for Coronary Restenosis Occurrence After Drug-Eluting Stent Implantation in Patients With Diabetes Having Stable Coronary Artery Disease
Jazyk angličtina Země Spojené státy americké Médium print-electronic
Typ dokumentu klinické zkoušky, časopisecké články
PubMed
29716394
PubMed Central
PMC6714775
DOI
10.1177/1076029618771752
Knihovny.cz E-zdroje
- Klíčová slova
- CD45+ platelet count, coronary artery disease, diabetes mellitus, drug-eluting stents, neutrophil to lymphocyte ratio, restenosis,
- MeSH
- antigeny CD45 krev MeSH
- biologické markery krev MeSH
- diabetes mellitus 2. typu krev patologie chirurgie MeSH
- diabetické angiopatie krev patologie chirurgie MeSH
- koronární restenóza krev patologie MeSH
- lidé středního věku MeSH
- lidé MeSH
- nemoci koronárních tepen krev patologie chirurgie MeSH
- počet trombocytů MeSH
- senioři MeSH
- stenty uvolňující léky * MeSH
- trombocyty metabolismus patologie MeSH
- Check Tag
- lidé středního věku MeSH
- lidé MeSH
- mužské pohlaví MeSH
- senioři MeSH
- ženské pohlaví MeSH
- Publikační typ
- časopisecké články MeSH
- klinické zkoušky MeSH
- Názvy látek
- antigeny CD45 MeSH
- biologické markery MeSH
- PTPRC protein, human MeSH Prohlížeč
The purpose of the study was to assess whether the occurrence of restenosis is associated with CD45+ platelet count and neutrophil to lymphocyte ratio in patients with type 2 diabetes mellitus (DM) after drug-eluting stent (DES) implantation for stable coronary artery disease (CAD). The study comprised 126 patients, including 55 patients with type 2 DM and stable CAD who underwent elective coronary artery stenting with DES and follow-up angiography within 6 to 12 months. Blood samples were collected from each patient on the morning of the coronary angiography procedure. The variables related to in-stent restenosis were selected by logistic regression analysis. The logistic regression analysis showed that 2 inflammatory factors, CD45+ platelet count (odds ratio [OR] = 4.51, 95% confidence interval [CI]: 1.50-13.50, P = .007) and neutrophil to lymphocyte ratio (OR = 3.09, 95% CI: 1.05-9.10, P = .04), were significantly associated with the risk of in-stent restenosis after stenting with DES in patients with stable CAD and type 2 DM. A receiver operator characteristic curve analysis indicated that the area under the curve was 0.83% (0.05%; P < .001), which showed that the logistic model had good predictive accuracy (based on CD45+ platelet count and neutrophil to lymphocyte ratio) for the risk of in-stent restenosis development in DES in patients with CAD and type 2 DM. Two novel biomarkers of restenosis, CD45+ platelet count and neutrophil to lymphocyte ratio, may be effectively used to predict in-stent restenosis after DES implantation in patients with CAD and type 2 DM.
1st Department of Internal Medicine Faculty of Medicine Comenius University Bratislava Slovakia
Department of Cardiology East Slovak Institute of Cardiovascular Diseases Kosice Slovakia
Department of Internal Medicine Brothers of Mercy Hospital Brno Czech Republic
Faculty of Medicne University of Oviedo Central University Hospital of Asturias Oviedo Spain
Institute of Biomedical Problems of Russian Academy of Sciences Moscow Russian Federation
Russian Cardiology Research and Production Complex Moscow Russian Federation
Zobrazit více v PubMed
Costa MA, Simon DI. Molecular basis of restenosis and drug-eluting stents. Circulation. 2005;111(17):2257–2273. PubMed
Wessely R, Kastrati A, Schomig A. Late restenosis in patients receiving a polymer-coated sirolimus-eluting stent. Ann Intern Med. 2005;143(5):392–394. PubMed
Virmani R, Liistro F, Stankovic G, et al. Mechanism of late in-stent restenosis after implantation of a paclitaxel derivate-eluting polymer stent system in humans. Circulation. 2002;106(21):2649–2651. PubMed
Park DW, Hong MK, Mintz GS, et al. Two-year follow-up of the quantitative angiographic and volumetric intravascular ultrasound analysis after nonpolymeric paclitaxel-eluting stent implantation: late “catch-up” phenomenon from ASPECT study. J Am Coll Cardiol. 2006;48(12):2432–2249. PubMed
Claessen BE, Stone GW, Mehran R, et al. Relationship between biomarkers and subsequent clinical and angiographic restenosis after paclitaxel-eluting stents for treatment of STEMI: a HORIZONS-AMI substudy. J Thromb Thrombolysis. 2012;34(2):165–179. PubMed
Niccoli G, Montone RA, Ferrante G, Crea F. The evolving role of inflammatory biomarkers in risk assessment after stent implantation. J Am Coll Cardiol. 2010;56(22):1783–1793. PubMed
Gabbasov ZA, Kozlov SG, Imaeva AE, et al. In-stent restenosis after revascularization of myocardium with drug-eluting stents is accompanied by elevated level of blood plasma eosinophil cationic protein. Can J Physiol Pharmacol. 2011;89(6):413–448. PubMed
Park DW, Lee CW, Yun SC, et al. Prognostic impact of preprocedural C reactive protein levels on 6-month angiographic and 1-year clinical outcomes after drug-eluting stent implantation. Heart. 2007;93(9):1087–1092. PubMed PMC
Dibra A, Ndrepepa G, Mehilli J, et al. Comparison of C-reactive protein levels before and after coronary stenting and restenosis among patients treated with sirolimus-eluting versus bare metal stents. Am J Cardiol. 2005;95(10):1238–1240. PubMed
Kang WC, Ahn TH, Moon CI, et al. Comparison of inflammatory markers and angiographic outcomes after implantation of sirolimus and paclitaxel-eluting stents. Heart. 2009;95(12):970–975. PubMed
Gaspardone A, Versaci F, Tomai F, et al. C-reactive protein, clinical outcome, and restenosis rates after implantation of different drug-eluting stents. Am J Cardiol. 2006;97(9):1311–1316. PubMed
Cui S, Li K, Ang L, et al. Plasma phospholipids and sphingolipids identify stent restenosis after percutaneous coronary intervention. JACC Cardiovasc Interv. 2017;10(13):1307–1316. PubMed
Fujimoto H, Suzuki T, Aizawa K, et al. Processed B-type natriuretic peptide is a biomarker of postinterventional restenosis in ischemic heart disease. Clin Chem. 2013;59(9):1330–1337. PubMed
Gabbasov Z, Kozlov S, Byazrova S, et al. Blood level of CD45+ platelets and development of restenosis after drug-eluting stent implantation in patients with stable coronary artery disease. Wien Klin Wochenschr. 2016;128(23-24):898–905. PubMed
Peduzzi P, Concato J, Kemper E, Holford TR, Feinstein AR. A simulation study of the number of events per variable in logistic regression analysis. J Clin Epidemiol. 1996;49(12):1373–1379. PubMed
Angelillo-Scherrer A. Leukocyte-derived microparticles in vascular homeostasis. Circ Res. 2012;110(2):356–363. PubMed
Osterud B, Bjorklid E. Tissue factor in blood cells and endothelial cells. Front Biosci (Elite Ed). 2012;4:289–299. PubMed
Owens AP, 3rd, Mackman N. Microparticles in hemostasis and thrombosis. Circ Res. 2011;108(10):1284–1297. PubMed PMC
Totani L, Evangelista V. Platelet–leukocyte interactions in cardiovascular disease and beyond. Arterioscler Thromb Vasc Biol. 2010;30(12):2357–2361. PubMed PMC
Gabbasov Z, Ivanova O, Kogan-Yasny V, et al. Activated platelet chemiluminescence and presence of CD45+ platelets in patients with acute myocardial infarction. Platelets. 2014;25(6):405–408. PubMed
Papa A, Emdin M, Passino C, Michelassi C, Battaglia D, Cocci F. Predictive value of elevated neutrophil–lymphocyte ratio on cardiac mortality in patients with stable coronary artery disease. Clin Chim Acta. 2008;395(1-2):27–31. PubMed
Uthamalingam S, Patvardhan EA, Subramanian S, et al. Utility of the neutrophil to lymphocyte ratio in predicting long-term outcomes in acute decompensated heart failure. Am J Cardiol. 2011;107(3):433–438. PubMed
Balli M, Taşolar H, Çetin M, et al. Use of the neutrophil to lymphocyte ratio for prediction of in-stent restenosis in bifurcation lesions. Eur Rev Med Pharmacol Sci. 2015;19(10):1866–1873. PubMed
Duffy BK, Gurm HS, Rajagopal V, et al. Usefulness of an elevated neutrophil to lymphocyte ratio in predicting long-term mortality after percutaneous coronary intervention. Am J Cardiol. 2006;97(7):993–996. PubMed
Turak O, Ozcan F, Isleyen A. Usefulness of the neutrophil-to-lymphocyte ratio to predict bare-metal stent restenosis. Am J Cardiol. 2012;110(10):1405–1410. PubMed
Thiele JR, Habersberger J, Braig D, et al. The dissociation of pentameric to monomeric C-reactive protein localises and aggravates inflammation: in vivo proof of a powerful pro-inflammatory mechanism and a new anti-inflammatory strategy. Circulation. 2014;130(1);35–50. PubMed
Li HY, Wang J, Wu YX, et al. Topological localization of monomeric C-reactive protein determines proinflammatory endothelial cell responses. J Biol Chem. 2014;289(20):14283–14290. PubMed PMC
Khreiss T, József L, Potempa LA, Filep JG. Conformational rearrangement in C-reactive protein is required for proinflammatory actions on human endothelial cells. Circulation. 2004;109(16):2016–2022. PubMed
Habersberger J, Strang F, Scheichl A, et al. Circulating microparticles generate and transport monomeric C-reactive protein in patients with myocardial infarction. Cardiovascular Res. 2012;96(1):64–72. PubMed
Eisenhardt SU, Habersberger J, Murphy A, et al. Dissociation of pentameric to monomeric C-reactive protein on activated platelets localizes inflammation to atherosclerotic plaques. Circ Res. 2009;105(2):128–137. PubMed