Usefulness of Platelet Distribution Width and Fibrinogen in Predicting In-stent Restenosis With Stable Angina and Type 2 Patients With Diabetes Mellitus

Abstract

AimThe purpose of this study was to investigate the predicting value of platelet distribution width (PDW) and fibrinogen for in-stent restenosis (ISR) in patients with stable angina pectoris and type 2 diabetes mellitus (T2DM) after drug-eluting stent (DES) implantation.MethodsWe enrolled 161 patients who were readmitted with recurrent chest pain and successfully reviewed for coronary angiography and were divided into the ISR and non-ISR groups. We compared the levels of PDW and fibrinogen between the two groups. Logistic regression was used for analyzing independent predictors of ISR. The receiver operating characteristic (ROC) curve analysis was used to determine the optimum cutoff points of PDW and fibrinogen to predict ISR. The Kaplan–Meier survival curves for target lesion failure (TLF) by levels of PDW and fibrinogen.ResultsThe multivariate logistic regression analysis showed that PDW and fibrinogen were independent predictors of ISR [odds ratio (OR) = 1.209, 95% CI: 1.024–1.427, p = 0.025; OR = 1.006, 95% CI: 1.002–1.011, p = 0.010, respectively]. The ROC analyses showed that PDW ≥ 13.15% and fibrinogen ≥ 333.5 mg/dl were predictive of ISR in patients with stable angina pectoris and T2DM after DES implantation. However, the Kaplan–Meier estimate for TLF showed no statistical significance.ConclusionHigher levels of PDW and fibrinogen were associated with the incidence of ISR in patients with stable angina with T2DM after DES implantation, but were not independent predictors of TLF.

Development and validation of a nomogram for ISR within 2 years in patients after iliac or femoral artery stent placement

“…Fibrinogen is a new biomarker of oxidative stress and in ammation in recent years [11].Hyper brinogenemia is an independent risk factor for cardiovascular and cerebrovascular diseases and ISR after coronary stent implantation [12,13].Fibrinogen is mainly expressed in hepatocytes, and its synthesis is regulated by in ammatory factors, such as IL-6 derived by monocytes, macrophages and vascular endothelial cells [14,15].In our study, brinogen > 4g / L is de ned as hyper brinogenemia.Hyper brinogenemia suggests that the patient is in a hypercoagulable state and the risk of thrombosis is increased, which is one of the causes of in-stent restenosis.In addition, brinogen is an important in ammatory marker that plays an important role in platelet aggregation [16].After stent implantation, mechanical vascular injury occurred,which causing the aggregation of in ammatory cells and the production of cytokines.Fibrinogen also promotes endothelin-1(ET-1) secretion by endothelial cells and ET-1 can effectively constricts blood vessels [17].In addition, brinogen and its degradation products can stimulate the proliferation and migration of smooth muscle cells [18].These evidences indicate that hyper brinogenemia is one of the risk factors for ISR.…”

Risk investigation of in-stent restenosis after initial implantation of intracoronary drug-eluting stent in patients with coronary heart disease

“…Elevated fibrinogen levels are a recognized risk factor for adverse cardiovascular events in patients with coronary heart disease ( 28 , 29 ). Many studies have shown that fibrinogen levels are associated with the occurrence of ISR after PCI ( 30 – 32 ). Our study also confirmed that fibrinogen is an independent predictor of ISR.…”

“…Our study also confirmed that fibrinogen is an independent predictor of ISR. Chai et al suggested that fibrinogen and its metabolites can stimulate endothelial cell degeneration, increase the release of endothelial cell-derived growth factors, lead to endothelial dysfunction, and stimulate the growth of smooth muscle cells, ultimately leading to the occurrence of ISR ( 32 ).…”

Restenosis after Coronary Stent Implantation: Cellular Mechanisms and Potential of Endothelial Progenitor Cells (A Short Guide for the Interventional Cardiologist)

“…In an observational study of 161 patients with recurrent angina after coronary stenting, platelet distribution width, an easily accessible marker of platelet activation, was an independent predictor of stent restenosis (Odd's ratio 1.2 [1.02-1.4], p = 0.025) [15]. Following arterial injury, platelets rapidly adhere and release thromboxane A2; the glycoprotein (GP) IIb/IIIa complex binds to fibrinogen, leading to platelet aggregation and activation [16].…”