Abstract 3037: Immuno-inflammatory Cascade Activation and Restenosis in Stable and Unstable Angina Patients Undergoing Coronary Interventions
Background: Inflammation is an important feature of atherosclerotic lesions and associated with the development of restenosis after coronary angioplasty. The purpose of this study was to investigate whether “active” coronary plaque disruption during percutaneous coronary intervention (PCI), further provokes the activation of immuno-inflammatory cascade and predisposes to restenosis, in stable and unstable angina patients.
Methods and Results: We assessed the levels of soluble intercellular adhesion molecule (s-ICAM-1), vascular adhesion molecule (s-VCAM-1), metalloproteinase (MMP-9), metalloproteinase inhibitor (TIMP-2), monocyte chemoattractant proteine-1 (MCP-1), T cells chemoattractant proteine IP-10, interleukine-6 (IL-6), C-reactive proteine (CRP) and anti-inflammatory marker IL-10, in 43 stable angina (SA) and 46 unstable angina (UA) patients, before, 12 h and 40 h after PCI. As a control group, we studied 19 SA and 20 UA patients, after coronary angiography. After PCI, serum levels of VCAM-1, MMP-9, IL-6 and CRP increased significantly in both groups, in SA (p<0.01) and UA (p<0.001), while levels of ICAM-1, MCP-1, IP-10, TIMP and IL-10, did not change significantly. After diagnostic angiography, a significant elevation in CRP was observed in SA patients (p=0.04), while no difference in any inflammatory marker was detected in UA patients. At 6 months follow-up, 27 out of 89 pts underwent re-angiography because of:
positive stress test in 25 pts and
UA in 2 pts.
Restenosis (lumen diameter stenosis ≥50%) was observed in 12 pts (14%). A positive correlation (p=0.04) was found between IL-10 levels at 12h post-PCI and in stent restenosis (Relative risk [RR]=1.14, 95% CI 1.006 –1.2933). We found no correlation between in-stent restenosis and all the other inflammatory markers.
Conclusion: Our results provide further evidence of the role of iatrogenic plaque disruption inducing immunoinflammatory responses detectable in systemic circulation, especially in UA patients. The elevation of anti-inflammatory cytokine IL-10 after PCI is associated with in-stent restenosis. This anti-inflammatory marker, strong indicator of an activated inflammatory process, could probably be used as independent predictor of in-stent restenosis.