Inflammatory response after intervention assessed by serial C-reactive protein measurements correlates with restenosis in patients treated with coronary stenting.
OBJECTIVE
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 (Delta) between highest CRP values after intervention and CRP values before intervention was calculated. Patients were grouped into tertiles according to DeltaCRP values. The primary end point was angiographic restenosis (diameter stenosis > or = 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 DeltaCRP values >11.8 mg/L, 25.3% in the middle tertile with DeltaCRP values 3.0-11.8 mg/L, and 21.5% in the lower tertile with DeltaCRP 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.
Dibra
Alban
A
Deutsches Herzzentrum and 1. Medizinische Klinik rechts der Isar, Technische Universität, Munich, Germany. dibra@dhm.mhn.de
Mehilli
Julinda
J
Braun
Siegmund
S
Hadamitzky
Martin
M
Baum
Hannsjörg
H
Dirschinger
Josef
J
Schühlen
Helmut
H
Schömig
Albert
A
Kastrati
Adnan
A
D000077284:Abciximab; D000368:Aged; D000787:Angina Pectoris / Q000097:blood / Q000628:therapy; D000789:Angina, Unstable / Q000097:blood / Q000628:therapy; D015906:Angioplasty, Balloon, Coronary; D000911:Antibodies, Monoclonal / Q000627:therapeutic use; D000925:Anticoagulants / Q000008:administration & dosage / Q000627:therapeutic use; D001241:Aspirin / Q000008:administration & dosage / Q000627:therapeutic use; D015415:Biomarkers; D002097:C-Reactive Protein / Q000032:analysis*; D000077144:Clopidogrel; D017023:Coronary Angiography; D023903:Coronary Restenosis / Q000097:blood* / Q000000981:diagnostic imaging; D023921:Coronary Stenosis / Q000097:blood* / Q000628:therapy; D005260:Female; D006493:Heparin / Q000008:administration & dosage / Q000627:therapeutic use; D006801:Humans; D007140:Immunoglobulin Fab Fragments / Q000627:therapeutic use; D007249:Inflammation; D008297:Male; D008875:Middle Aged; D011184:Postoperative Period; D011292:Premedication; D015607:Stents; D013988:Ticlopidine / Q000008:administration & dosage / Q000031:analogs & derivatives / Q000627:therapeutic use; D000077466:Tirofiban; D014443:Tyrosine / Q000031:analogs & derivatives / Q000627:therapeutic use
D000911:Antibodies, Monoclonal; D000925:Anticoagulants; D015415:Biomarkers; D007140:Immunoglobulin Fab Fragments; D014443:Tyrosine; D006493:Heparin; D002097:C-Reactive Protein; D000077144:Clopidogrel; D000077466:Tirofiban; D013988:Ticlopidine; D001241:Aspirin; D000077284:Abciximab