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Background: Measurement of C-reactive protein(CRP), a marker of inflammation, is recommended to improve cardiovascular disease(CVD)risk stratification. However, no studies have collectively evaluated how inflammatory markers cluster empirically and relate to angiographic coronary artery disease and CVD events. Methods: From the WISE study, 580 women with fasting plasma samples of inflammatory m arkers(interleukin[IL]-6, IL-18, tumor necrosis factor α, transforming growth factor β, CRP, serum amyloid A[SAA], and intercellular adhesion molecules)were analyzed over a median of 4.7 years follow-up. All women were referred for coronary angiography(1996-2000)to evaluate suspected myocardial ischemia. Results: In factor analysis, a “proinflammation”factor(cluster)loaded on IL-6, CRP, and SAA(r=0.63-0.87); a “proinflammation and anti-inflammation”cluster loaded on IL-18 and tumor necrosis factor α(r=0.72, 0.77); and an “immunosuppressiv e”factor loaded singly on transforming growth factor β(r=0.96). No cluster was independently associated with angiographic coronary artery disease. However, quartile increases of the “proinflammation”cluster(IL-6, CRP, and SAA)yielded death rates of 2.6%, 7.2%, 13.1%, 26.6%, respectively(P< .0001). Women with ≥2 of 3 proinflammation markers in the upper quartile had an adjusted relative risk of death of 4.21(95%CI 1.91-9.25), a higher conferred risk than any single marker alone, all of which were roughly equally predictive. Conclusions: Altho ugh IL-6, CRP, and SAA all predict CVD risk in women, development of global mea sures of inflammation and simply counting the number of markers with high levels improve CVD risk stratification. In addition, results indicate that the adverse impact of inflammation may be largely through other mechanisms than promotion o f atherogenesis(ie, destabilization of vulnerable plaques).
Background: Measurement of C-reactive protein (CRP), a marker of inflammation, is recommended to improve cardiovascular disease (CVD) risk stratification. However, no studies have multiple as is inflammatory markers cluster empirically and relate to angiographic coronary artery disease and CVD Methods: From the WISE study, 580 women with fasting plasma samples of inflammatory m arkers (interleukin [IL] -6, IL-18, tumor necrosis factor alpha, transforming growth factor beta, CRP, serum amyloid A [SAA] All women were referred for coronary angiography (1996-2000) to evaluate suspected myocardial ischemia. Results: In factor analysis, a “proinflammation” factor (cluster) loaded a “proinflammation and anti-inflammation” cluster loaded on IL-18 and tumor necrosis factor α (r = 0.72, 0.77); and an “immunosuppressiv” on IL-6, CRP, and SAA (r = 0.63-0.87) factor loaded singly on transforming gro However, quartile increases of the “proinflammation” cluster (IL-6, CRP, and SAA) yielded death rates of 2.6%, 7.2% Women with ≥ 2 of 3 proinflammation markers in the upper quartile had an adjusted relative risk of death of 4.21 (95% CI 1.91-9.25), a higher conferred risk than any Conclusions: Altho ugh IL-6, CRP, and SAA all predict CVD risk in women, development of global mea sures of inflammation and simply counting the number of markers with high levels improve CVD In addition, results indicate that the adverse impact of inflammation may be substantially through other mechanisms than promotion of atherogenesis (ie, destabilization of vulnerable plaques).