Inflammatory response and re-stenosis after percutaneous coronary intervention in heart transplant recipients and patients with native atherosclerosis.
BACKGROUND
The clinical benefit of percutaneous coronary intervention (PCI) in heart transplant recipients (HTRs) with coronary allograft vasculopathy (CAV) has been questioned. We investigated the degree of inflammatory reaction during PCI in CAV compared to patients with native atherosclerosis, and the possible relationship between PCI-induced inflammation and the degree of re-stenosis in these 2 patient groups.


METHODS
In 11 CAV patients and 10 patients with native atherosclerosis, blood samples were drawn before and 24 hours and 6 months after PCI, and analyzed with regard to hsCRP, MCP-1, components of complement activation, von Willebrand factor (vWf), soluble L-selectin and ICAM-1. Quantitative angiography was performed before and after PCI, and at 6-month follow-up.


RESULTS
Baseline levels of hsCRP, vWf and MCP-1 were significantly elevated and levels of L-selectin and ICAM-1 and activation products of the alternative pathway of the complement system were decreased in CAV patients compared to those with native atherosclerosis. PCI induced significant increases of hsCRP in both groups as well as an increase in vWf in native atherosclerosis, whereas a decrease in L-selectin was observed in native atherosclerosis. Plasma levels of MCP-1 correlated with percent stenosis at follow-up in both groups, whereas a correlation between hsCRP and percent stenosis was evident only in patients with native atherosclerosis. There were no differences in rates of re-stenosis between the 2 groups.


CONCLUSIONS
HTRs with CAV and patients with native atherosclerosis are characterized by different profiles of immune activation and respond differently to PCI. Nevertheless, an inappropriate inflammatory reactivity may predispose to re-stenosis after PCI in both groups of patients, with pre-procedural inflammation being of particular importance in CAV.
Hognestad
Aina
A
Department of Cardiology, Rikshospitalet, University of Oslo, Norway. aina.hognestad@klinmed.uio.no
Endresen
Knut
K
Wergeland
Ragnhild
R
Mellembakken
Jan R
JR
Mollnes
Tom E
TE
Omland
Torbjørn
T
Kjekshus
John K
JK
Aukrust
Pål
P
Andreassen
Arne K
AK
D000368:Aged; D015906:Angioplasty, Balloon, Coronary / Q000009:adverse effects* / Q000379:methods; D002097:C-Reactive Protein / Q000378:metabolism; D016022:Case-Control Studies; D018932:Chemokine CCL2 / Q000032:analysis / Q000378:metabolism; D003324:Coronary Artery Disease / Q000000981:diagnostic imaging / Q000628:therapy*; D023903:Coronary Restenosis / Q000000981:diagnostic imaging / Q000628:therapy; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D005434:Flow Cytometry; D005500:Follow-Up Studies; D006084:Graft Rejection; D006085:Graft Survival; D016027:Heart Transplantation / Q000009:adverse effects* / Q000379:methods; D006801:Humans; D007249:Inflammation / Q000097:blood / Q000175:diagnosis*; D018836:Inflammation Mediators / Q000097:blood*; D018799:Intercellular Adhesion Molecule-1 / Q000032:analysis / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D010865:Pilot Projects; D011237:Predictive Value of Tests; D011336:Probability; D011859:Radiography; D012016:Reference Values; D018570:Risk Assessment; D012720:Severity of Illness Index
D018932:Chemokine CCL2; D018836:Inflammation Mediators; D018799:Intercellular Adhesion Molecule-1; D002097:C-Reactive Protein