Levels and values of inflammatory markers in patients with angina pectoris.

Inflammation plays an important pathogenic role in the initiation and progression of atherosclerotic plaque lesions. C-reactive protein (CRP), which directly participates in plaque inflammation, induces vascular cell adhesion molecule-1 (VCAM-1) expression in endothelial cells. However, the levels and values of high-sensitivity (hs)-CRP, white blood cell (WBC) count, and VCAM-1 in both stable and unstable angina pectoris (AP) have not been fully investigated. This study examines the levels and values of these inflammatory markers in patients with stable or unstable AP. From March 2003 to December 2003, a prospective cohort study was conducted in 128 consecutive patients, including unstable AP patients (class I: n = 59; combined class II and III: n = 16) and stable AP patients (n = 53) undergoing elective coronary stenting. Blood samples for hs-CRP, WBC count, and VCAM-1 were obtained in the catheterization laboratory before coronary angiography. The circulating levels of hs-CRP and VCAM-1 were also evaluated in 40 healthy volunteers. The circulating levels of these three inflammatory markers were substantially higher in patients than in healthy volunteers (all P values < 0.0001). Additionally, circulating levels of hs-CRP and the WBC count were significantly higher in patients with unstable AP than in patients with stable AP (all P value < 0.0001). However, only those patients with class II and III unstable AP had significantly higher circulating levels of VCAM-1 than patients with stable AP (P < 0.0001). On the other hand, the circulating levels of VCAM-1 did not differ between patients with class I unstable AP and patients with stable AP (P = 0.782). Multiple stepwise logistic regression analysis showed that only hs-CRP level was independently associated with unstable AP (P = 0.0002). In conclusion, circulating levels of hs-CRP, WBC count, and VCAM-1 were significantly increased in patients with AP. The circulating level of hs-CRP was strongly associated with the clinical setting of unstable AP.