Abstract 2841: Elevated C-Reactive Protein Levels are Associated With Rapid Progression of Non-culprit Complex Lesion in Non-ST-segment Elevation Acute Coronary Syndromes
Inflammation plays an important role in the vulnerability and progression of atheromatous plaque. We examined the relation of elevated baseline inflammatory activity and enhanced inflammatory response to percutaneous coronary intervention (PCI) to non-culprit plaque progression in non-ST-segment elevation acute coronary syndrome (NSTE-ACS).
Methods We measured high sensitivity C-reactive protein (CRP) levels in 100 patients with NSTE-ACS treated with PCI. Baseline and follow-up (mean interval, 6 months) coronary angiographic data were examined. Rapid progression was defined as ≥10% diameter reduction of a pre-existing stenosis ≥50% or ≥30% diameter reduction of a stenosis <50%. Elevated CRP at admission (admission CRP↑) was defined as CRP level >0.140 mg/dl (median value), and elevated CRP after PCI (post-PCI CRP↑) was defined as CRP level 2days after PCI >1.800 mg/dl (median value).
Results: Both admission CRP↑ and post-PCI CRP↑ were associated with a higher frequency of non-culprit complex lesion and a higher rate of rapid progression of these lesions, but no relationship was found with regard to non-culprit smooth lesion. In multivariate analysis, both admission CRP↑ (OR 22.6, p<0.01) and post-PCI CRP↑ (OR 39.9, p<0.01) were strong predictors of rapid progression of non-culprit complex lesion. Combination of these markers showed a stepwise increase in the frequency of non-culprit complex lesion and the rate of rapid progression of these lesions.
Conclusions: Enhanced inflammatory response to PCI in addition to elevated baseline inflammatory activity may be involved in the pathogenesis of non-culprit complex plaque progression in NSTE-ACS.