Elevated Plasma High Sensitivity C-reactive Protein (hs-CRP) Level is a Predictor of Periprocedural Myocardial Injury during Percutaneous Coronary Intervention (PCI)

Abstract

Background: Elevated high sensitivity C-reactive protein (hs-CRP) has been well known as a biomarker reflecting inflammatory process for prediction of ischemic events among patients with coronary artery disease. Relatively small studies have identified a heightened and sustained inflammatory response after percutaneous coronary intervention (PCI) to be a predictor of periprocedural events after coronary angioplasty and a marker of increased restenosis risk among patients undergoing coronary stenting. Embolization of atherosclerotic and thrombotic debris can induce myocardial necrosis during PCI. This study was designed to evaluate whether pre procedural hs-CRP level is associated with procedure related distal microembolization producing myocardial injury (assessed by CK-MB level) after PCI.

Methods: A total of 310 patients with chronic stable angina and unstable angina, who would undergo elective PCI were evaluated in National Institute of Cardiovascular Disease (NICVD), Dhaka with a view to evaluate the relationship between preprocedural hs-CRP and rise of CK-MB level, before and after PCI. Patients were divided in 2 groups according to hs-CRP: Group I = hs-CRP <3 mg/ L, Group II = hs-CRP >3 mg/L.

Results: A total of 310 patients were divided into two groups: Normal CRP group (n = 131) and elevated CRP group (n= 179). Following PCI, CK-MB level rose from baseline in both groups. In normal CRP group, there was no significant elevation of CK-MB level after PCI (Pre-procedural vs. Post-procedural: 18.6 ± 5.4 vs. 29.1 ± 5.6 mg/L, p= ns). In elevated CRP group, there was significant elevation of CK-MB level after PCI (Preprocedural vs. Post-procedural: 19.1 ± 6.7 vs. 52.46 ± 9.4 mg/L, p < 0.01). The mean rise of CK-MB level was higher in group II than group I (33.06±11.62U/L vs. 11.52±9.60 U/L). The findings were statistically significant between the study groups (p>0.05). Also there was a positive linear correlation between preprocediral hsCRP level and rise of CKMB (r=0.22) following procedure and it was statistically significant (p<0.05). Multivariate logistic regression analysis was done among traditional predictors of PCI outcome including advanced age (>50 years), female gender, diabetes mellitus, BMI, hypertension, smoking, dylipidaemia, type C lesion, multiple stents, post dilatation and hsCRP. After removing the effects of the all other variables, hs- CRP was independent predictor of periprocedural myocardial injury during PCI, assessed by CK-MB elevation with OR 1.57 and p=0.001.

Conclusion: The inflammatory activity, as represented by hs-CRP level, is associated with procedure related microvascular injury as assessed by CK-MB elevation after PCI. Measurement of hs-CRP levels could provide a rationale for risk stratification before coronary intervention and may be a useful tool to target aggressive antiaggregatory or anti-inflammatory therapy to patients that are exposed to the highest risk for ischemic complications. As distal microembolization is a determinant of short and long term mortality after PCI, specific strategies may be developed to minimize myocardial injury in subjects with elevated hs-CRP level.

Bangladesh Heart Journal 2015; 30(1) : 5-12