Inflammatory response after intervention assessed by serial C-reactive protein measurements correlates with restenosis in patients treated with coronary stenting

Alban Dibra, Julinda Mehilli, Siegmund Braun, Martin Hadamitzky, Hannsjörg Baum, Josef Dirschinger, Helmut Schühlen, Albert Schömig, Adnan Kastrati

Research output: Contribution to journalArticlepeer-review

65 Scopus citations

Abstract

Objectives: We hypothesized that a higher degree of inflammatory response to coronary stenting, as measured by the change in C-reactive protein (CRP) levels after intervention in patients with stable or unstable angina, would be related to a higher risk of in-stent restenosis. Methods: We studied 1800 consecutive patients with stable or unstable angina treated with coronary stenting. C-reactive protein levels were serially measured before and after the intervention. The difference (Δ) between highest CRP values after intervention and CRP values before intervention was calculated. Patients were grouped into tertiles according to ΔCRP values. The primary end point was angiographic restenosis (diameter stenosis ≥50% at 6-month angiography). The secondary end point was clinical restenosis, defined as target vessel revascularization performed in the presence of angiographic restenosis and symptoms or signs of ischemia. Results: No relationship was found between CRP values at baseline and angiographic restenosis (P = .88). On the other hand, the change between baseline and peak postintervention CRP values strongly correlated with angiographic restenosis (30.5% in the upper tertile with ΔCRP values >11.8 mg/L, 25.3% in the middle tertile with ΔCRP values 3.0-11.8 mg/L, and 21.5% in the lower tertile with ΔCRP values <3.0 mg/L, P = .002) as well as with clinical restenosis (P = .01). Patients in the upper tertile had the highest risk of restenosis even after adjustment for other covariates. Conclusions: The inflammatory response to coronary stenting as assessed by the change in CRP correlates with the development of in-stent restenosis. These findings provide strong support for the role of inflammation in restenosis.

Original languageEnglish
Pages (from-to)344-350
Number of pages7
JournalAmerican Heart Journal
Volume150
Issue number2
DOIs
StatePublished - Aug 2005
Externally publishedYes

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