Increased C-reactive protein levels in patients with in-stent restenosis and its implications

Elevated Preprocedural High-Sensitivity C-Reactive Protein Levels are Associated With Neointimal Hyperplasia and Restenosis Development After Successful Coronary Artery Stenting

“…Angioi et al reported that patients with reste- nosis had significantly higher levels of CRP than those without restenosis (0.68 mg/dl vs 0.21 mg/dl, p<0.001) and when the patient population was divided by tertiles of CRP, the incidence of restenosis significantly increased from the first to the third tertiles (restenosis rate: 17% vs 42% vs 72%, p<0.003). 30 In our previous study performed in patients with acute myocardial infarction, we reported that the incidence of cardiogenic shock was higher in the elevated CRP group than in the normal CRP group (3/86, 3.5% vs 15/122, 12.3%, p=0.026) and the 1-year survival rate was significantly lower in the elevated CRP group than in the normal CRP group (96.5% vs 86.9%, p=0.018). 31 In the present study, the pre-interventional lesion P&M CSA was significantly larger in the elevated CRP group and the plaque burden was significantly greater, and a significant positive correlation was found between preinterventional CRP levels and pre-interventional P&M CSA and plaque burden.…”

Inflammation, Neointimal Hyperplasia, and Restenosis

“…7 These observations are further supported by recent evidence suggesting an increased risk of restenosis in humans when systemic markers of inflammation such as C-reactive protein or MCP-1 are elevated. 5,20,21 Furthermore, results from experimental and clinical trials that have shown markedly reduced rates of in-stent restenosis with local delivery of rapamycin (a potent antiproliferative and antiinflammatory drug) via drug-eluting stents have also helped corroborate this hypothesis. 22 Second, one needs to consider how well this strategy for inhibition of neointimal hyperplasia can be translated to the clinical setting.…”

Understanding and managing in-stent restenosis: a review of clinical data, from pathogenesis to treatment

“…Atherosclerosis is characterized by a sequence of processes which induce vasoconstriction and the initial endothelial dysfunction resulting in the mechanism of ER and vascular remodelling, enhanced by an inflammatory process triggered by vessel injury, as evidenced by the increase in C-reactive protein or MCP-1 in patients at increased risk of restenosis (20).…”