Background-Both endothelial cell activation and macrophage activation play a significant role in atherogenesis and atheromatous plaque vulnerability and may determine rapid coronary artery disease (CAD) progression. We sought to assess the association between serum inflammatory markers and rapid CAD progression in patients with chronic stable angina pectoris. Methods and Results-We studied 124 chronic stable angina pectoris patients (84 men; mean age, 61Ϯ10 years) who were on a waiting list for coronary angioplasty for a mean time of 4.8Ϯ2.4 months. CAD progression was defined as Ն10% diameter reduction of a pre-existing stenosis Ն50%, Ն30% diameter reduction of a stenosis Ͻ50%, development of a new stenosis Ն30% in a previously normal segment, or progression of any stenosis to total occlusion. CAD progression occurred in 35 patients (28%). After adjustment with binary logistic regression, neopterin (PϽ0.001), high-sensitivity C-reactive protein (Pϭ0.017), matrix metalloproteinase-9 (Pϭ0.002), soluble intercellular adhesion molecule 1 (PϽ0.001), and previous history of unstable angina (Pϭ0.01) were independent predictors of rapid CAD progression. The association between rapid disease progression and inflammatory markers remained significant even when presence of complex lesions was introduced into the multivariate model. Conclusions-Rapid CAD progression in patients with stable angina pectoris is associated with increased C-reactive protein levels and raised concentrations of biochemical markers of endothelial and macrophage activation. (Circulation.

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This study showed for the first time that compared to control subjects, patients with CSX have higher hs-CRP serum levels, increased mean common carotid artery IMT and increased arterial stiffness. The role of these abnormalities in the pathogenesis of CSX deserves investigation.