Effect of obesity on the relationship between plasma C-reactive protein and coronary artery stenosis in patients with stable angina.

INTRODUCTION: The association between plasma C-reactive protein (CRP) and the extent of coronary artery disease (CAD) in patients with stable angina remains controversial. Obesity is strongly associated with elevated CRP levels, potentially confounding the relationship between CRP and CAD severity. METHODS AND RESULTS: We studied 830 subjects without CAD and 218 patients with CAD undergoing elective coronary angiography. Geometric means of CRP were computed in a two-way analysis of covariance model in which study participants were stratified into nine groups according to CAD status (no CAD, single-vessel disease or multivessel disease) and tertiles of BMI. There was a significant interaction between CAD and categories of BMI with regard to CRP level (P=0.002). In the lower tertile of BMI, patients with CAD had markedly higher CRP concentration compared to control subjects (1.16, 1.80 and 2.82 mg/L in subjects without CAD, patients with single-vessel disease and patients with multivessel disease, respectively; P=0.003). However, the relationship between CRP and CAD became weaker for patients in the second BMI tertile (P=0.15), whereas no significant relationship was observed for patients in the third BMI tertile (P=0.75). In patients undergoing coronary angioplasty (n=195), BMI was independently related to the magnitude of the angioplasty-induced CRP elevations (P=0.002). CONCLUSION: The level of obesity is essential to the interpretation of the relationship between CRP and severity of CAD. The production of inflammatory mediators with increasing levels of obesity becomes the dominant determinant of plasma CRP levels and masks the vascular contribution due to CAD.

Preprocedural C-reactive protein levels predict myocardial necrosis after successful coronary stenting in patients with stable angina.

BACKGROUND: Myocardial necrosis as assessed by cardiac troponin elevation occurs frequently after coronary stenting and is associated with adverse clinical outcome. Mechanical factors have been implicated in this complication and the role of systemic inflammation is not known. METHODS: We prospectively studied 208 patients with chronic stable angina who underwent elective coronary stenting. All patients had normal troponin levels before the procedure. Blood samples for high-sensitivity C-reactive protein (CRP) were obtained before the procedure and analyzed using a high-sensitivity kit. Cardiac troponin T (cTnT) was obtained 24 hours after the procedure. RESULTS: Postprocedural cTnT elevations were observed in 46 (22%) patients. There were 11 (16%), 14 (20%), and 21 (30%) patients with elevated postprocedural cTnT in the first, second, and third CRP tertile, respectively (P for trend = .045). In a multivariate logistic regression model, adjusting for all the significant univariate predictors and for statin therapy, CRP remained a significant independent predictor of postprocedural cTnT elevation with an odds ratio of 2.6 in patients in the third CRP tertile compared with patients in the first CRP tertile (95% CI 1.1-6.0, P = .02). Patients in the third CRP tertile also had higher cTnT elevations compared with patients in the first and second CRP tertile (P = .03). CONCLUSIONS: Elevated baseline CRP levels are associated with higher risk of postprocedural troponin elevations in patients with stable angina undergoing uncomplicated coronary stenting. These results underscore the role of systemic inflammation in the pathogenesis of periprocedural myocardial injury.