OBJECTIVE: The concentration of the complex between activated protein C (APC) and protein C inhibitor (PCI) is a measure of thrombin generation. We studied whether it can provide information useful for the diagnosis and treatment of arterial vascular disease. METHODS: Blood was obtained from 429 vascular patients admitted consecutively during September 2004 to March 2005. The APC-PCI complex was measured by using a sandwich immunofluorometric method. The patients were divided into cohorts according to the planned treatment and compared with a control group of healthy individuals. RESULTS: The APC-PCI complex concentration varied from 0.08 to 2.50 microg/L. In the cohort of patients with aortic aneurysms (n = 78), the median APC-PCI value was 0.45 (10th to 90th percentile, 0.24-1.47), and values were clearly increased compared with all other cohorts (P < .0001). Patients with carotid disease (n = 73) yielded a median of 0.22 (10th to 90th percentile, 0.15-0.48). The median for claudicants (n = 74) was 0.26 microg/L (10th to 90th percentile, 0.15-0.75), which was higher than in those (n = 97) with critical ischemia (0.20; 10th to 90th percentile, 0.13-0.36; P < .0023). The cohort with other forms of atherosclerotic disease (n = 40) had a median of 0.23 (10th to 90th percentile, 0.14-0.42), whereas the value for a cohort of 21 patients with venous disease was 0.19 (10th to 90th percentile, 0.10-0.34). The median was 0.15 (10th to 90th percentile, 0.10-0.23) for the control group (n = 121). CONCLUSIONS: Patients with atherosclerosis had an increased APC-PCI concentration that corresponded to increased generation of thrombin. Patients with aortic aneurysm had a threefold higher median concentration than the control group. We suggest that this remarkable increase is caused by the local activation of coagulation, and we surmise that APC-PCI measurements can be used as a screening tool to identify patients with aortic aneurysms.
OBJECTIVE: The concentration of the complex between activated protein C (APC) and protein C inhibitor (PCI) is a measure of thrombin generation. We studied whether it can provide information useful for the diagnosis and treatment of arterial vascular disease. METHODS: Blood was obtained from 429 vascular patients admitted consecutively during September 2004 to March 2005. The APC-PCI complex was measured by using a sandwich immunofluorometric method. The patients were divided into cohorts according to the planned treatment and compared with a control group of healthy individuals. RESULTS: The APC-PCI complex concentration varied from 0.08 to 2.50 microg/L. In the cohort of patients with aortic aneurysms (n = 78), the median APC-PCI value was 0.45 (10th to 90th percentile, 0.24-1.47), and values were clearly increased compared with all other cohorts (P < .0001). Patients with carotid disease (n = 73) yielded a median of 0.22 (10th to 90th percentile, 0.15-0.48). The median for claudicants (n = 74) was 0.26 microg/L (10th to 90th percentile, 0.15-0.75), which was higher than in those (n = 97) with critical ischemia (0.20; 10th to 90th percentile, 0.13-0.36; P < .0023). The cohort with other forms of atherosclerotic disease (n = 40) had a median of 0.23 (10th to 90th percentile, 0.14-0.42), whereas the value for a cohort of 21 patients with venous disease was 0.19 (10th to 90th percentile, 0.10-0.34). The median was 0.15 (10th to 90th percentile, 0.10-0.23) for the control group (n = 121). CONCLUSIONS:Patients with atherosclerosis had an increased APC-PCI concentration that corresponded to increased generation of thrombin. Patients with aortic aneurysm had a threefold higher median concentration than the control group. We suggest that this remarkable increase is caused by the local activation of coagulation, and we surmise that APC-PCI measurements can be used as a screening tool to identify patients with aortic aneurysms.
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