Abstract

BackgroundIn-stent restenosis remains an unresolved issue. Inflammation plays a pivotal role in the process of in-stent restenosis. Significant and positive associations were found between red blood cell distribution width (RDW) and inflammation. But whether there is a close relationship between higher RDW and in-stent restenosis is still not clarified.MethodsThis retrospective observational study investigated 214 consecutive patients with unstable angina pectoris who underwent successful percutaneous coronary interventions with drug-eluting stents. Patients were divided into three groups according to baseline RDW before percutaneous coronary interventions (low RDW group:≤12.5%; intermediate RDW group:> 12.5% and ≤ 13.5%; high RDW group:> 13.5%). The follow-up angiographies were routinely performed 9–12 months after the initial percutaneous coronary interventions. The multivariate logistic regression analysis was employed to determine the independent predictors of in-stent restenosis.ResultsThe in-stent restenosis rate was significantly higher in group with higher baseline RDW value (12.3, 19.7, 47.7% in low, intermediate, and high RDW groups respectively, P < 0.001). The baseline RDWs were significantly higher in patients with in-stent restenosis compared with those in patients without in-stent restenosis (13.7 ± 0.8% vs. 13.0 ± 0.8%, P < 0.001). For prediction of in-stent restenosis, the ROC (receiver operating characteristic) curve analysis demonstrated the optimal RDW cutoff value was 13.37 (sensitivity: 65.5%, specificity: 73.6%); the diagnosis cutoff value was 13.89 (sensitivity: 40.0%, specificity: 91.8%); the screening cutoff value was 12.99 (sensitivity: 83.6%, specificity: 49.1%). By multivariate logistic analysis, higher baseline RDW (odds ratio [OR], 5.179; 95% confidence interval [CI], 2.568 to 10.446; P<0.001) together with lower baseline indirect bilirubin (OR, 0.413; 95% CI, 0.305 to 0.559; P<0.001) and diabetes (OR, 4.077; 95% CI, 1.654 to 10.054; P = 0.002) were closely associated with in-stent restenosis at followup (11.1 ± 5.8 months).ConclusionsThe baseline RDW was closely associated with in-stent restenosis at follow-up. The patients with higher baseline RDW might have more chances to develop in-stent restenosis at followup.

Highlights

  • We explored whether the red blood cell distribution width (RDW) before Percutaneous coronary intervention (PCI) was associated with in-stent restenosis (ISR) and could be used as an independent predictor of ISR after PCI in patients with unstable angina pectoris

  • In the present study, we found that the baseline RDW, indirect bilirubin and diabetes before PCI were strongly associated with the occurrence of ISR and might be used as independent predictors of ISR in patients with unstable angina pectoris at followup

  • The baseline RDW was closely associated with in-stent restenosis at follow-up

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Summary

Introduction

Inflammation plays a pivotal role in the process of in-stent restenosis. The inflammation is believed to play a critical role in the process of ISR [4]. The pathophysiology of ISR, which is characterized by neo-intimal hyperplasia, is an overreaction of the woundhealing response after the vascular injury caused by balloon dilation (barotrauma) and stent placement during PCI [5]. Vascular mechanical injury caused by PCI leads to substantial inflammation reaction which stimulates vascular smooth muscle cell proliferation and extracellular matrix deposition, resulting in neo-intimal thickening and restenosis [4]. Walter et al found that higher tertiles of preprocedural C-type creative protein levels were independently associated with a higher risk of major adverse clinical events and angiographic restenoses after stenting [6]

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