BACKGROUND: Mechanisms of instability in patients affected by unstable angina and who exhibit low levels of C-reactive protein (CRP) on admission are unclear. We compared levels of markers of thrombin generation [thrombin-antithrombin complexes (TAT), of fibrinolysis [plasmin-antiplasmin complexes (PAP)], and angiographic severity and extent of coronary atherosclerosis in patients with severe unstable angina and high or low systemic levels of CRP. METHODS: Forty consecutive patients (age 59.7+/-8.7, 76% males) admitted to our coronary care unit with severe unstable angina (Braunwald class IIIB) were included in the present study. We assayed TAT and PAP using commercially available ELISA assays and CRP with high sensitivity nephelometry. The evaluation of atherosclerotic disease severity and extent was performed. Patients were divided in two groups according to CRP levels: G1=CRP>3 mg/L and G2=CRP<3 mg/L. RESULTS: Number of diseased vessels and number of stenoses plus occlusion were similar between the two groups (1.8+/-0.9 in G1 vs 2.2+/-0.9 in G2, p=NS and 2.6+/-1.9 in G1 vs 2.7+/-1.3 in G2, p=NS, respectively), as well as extent score and index (8.4+/-4.5 in G1 vs 9.2+/-3.1 in G2, p=NS and 0.6+/-0.3 in G1 vs 0.6+/-0.27 in G2, p=NS, respectively). Episodic activation of thrombin generation, as assessed by TAT was more frequent in G1 than in G2 (85% vs 47%, p=0.03). Episodic activation of the fibrinolysis was more frequent in G1 than in G2 (80% vs 40%, p=0.01). CONCLUSION: Patients with coronary instability and systemic evidence of inflammation exhibit more frequent activation of the thrombin/fibrinolysis system than patients with a similar clinical presentation but no evidence of systemic inflammation, whereas the coronary atherosclerotic burden is similar. The mechanisms of coronary instability in the absence of systemic evidence of inflammation need to be elucidated by future studies.
BACKGROUND: Mechanisms of instability in patients affected by unstable angina and who exhibit low levels of C-reactive protein (CRP) on admission are unclear. We compared levels of markers of thrombin generation [thrombin-antithrombin complexes (TAT), of fibrinolysis [plasmin-antiplasmin complexes (PAP)], and angiographic severity and extent of coronary atherosclerosis in patients with severe unstable angina and high or low systemic levels of CRP. METHODS: Forty consecutive patients (age 59.7+/-8.7, 76% males) admitted to our coronary care unit with severe unstable angina (Braunwald class IIIB) were included in the present study. We assayed TAT and PAP using commercially available ELISA assays and CRP with high sensitivity nephelometry. The evaluation of atherosclerotic disease severity and extent was performed. Patients were divided in two groups according to CRP levels: G1=CRP>3 mg/L and G2=CRP<3 mg/L. RESULTS: Number of diseased vessels and number of stenoses plus occlusion were similar between the two groups (1.8+/-0.9 in G1 vs 2.2+/-0.9 in G2, p=NS and 2.6+/-1.9 in G1 vs 2.7+/-1.3 in G2, p=NS, respectively), as well as extent score and index (8.4+/-4.5 in G1 vs 9.2+/-3.1 in G2, p=NS and 0.6+/-0.3 in G1 vs 0.6+/-0.27 in G2, p=NS, respectively). Episodic activation of thrombin generation, as assessed by TAT was more frequent in G1 than in G2 (85% vs 47%, p=0.03). Episodic activation of the fibrinolysis was more frequent in G1 than in G2 (80% vs 40%, p=0.01). CONCLUSION:Patients with coronary instability and systemic evidence of inflammation exhibit more frequent activation of the thrombin/fibrinolysis system than patients with a similar clinical presentation but no evidence of systemic inflammation, whereas the coronary atherosclerotic burden is similar. The mechanisms of coronary instability in the absence of systemic evidence of inflammation need to be elucidated by future studies.