Abstract 520: Changes in Plasma Von Willebrand Factor-cleaving Protease(ADAMTS13) Levels in Patients with Unstable Angina
Background: Increased plasma levels of von Willebrand factor (VWF) has been reported in acute myocardial infarction (AMI), which indicates the injured endothelial damage in occluded coronary arteries. The larger VWF multimers are known to be more active biologically, and are more potent mediators of platelet thromubus formations. Recently, a metalloprotease that cleaves VWF multimers has been identified, namely, VWF-cleaving protease (ADAMTS13). We recently reported reduced ADAMTS13 activity in AMI patients and the importance of this protease in the prognosis after AMI. However, whether ADAMTS13 may affect the pathogenesis of unstable angina (UA) has not been fully elucidated. The purpose of this study is to examine changes in plasma VWF and ADAMTS13 levels in patients with UA.
Methods and Results: Plasma VWF and ADAMTS13 levels (mU/ml) were measured in 39 patients with UA, 55 patients with stable exertional angina (SEA) and 47 patients with chest pain syndrome (CPS) at the time of coronary angiography by enzyme-linked immunosorbent assay. We measured these antigen levels after 6 months follow-up period in patients with UA. Plasma VWF antigen levels (mU/ml) increased significantly in patients with UA compared with SEA and CPS (2118.5 ± 810.5, 1571.8 ± 494.2 and 1536.0 ± 526.4, respectively; P < 0.0001 in UA vs. SEA or CPS). Plasma ADAMTS13 antigen levels (mU/ml) decreased significantly in patients with UA than SEA or CPS (741.2 ± 150.9, 875.3 ± 229.0 and 877.3 ± 199.7mU/ml, respectively; P < 0.01 in UA vs. SEA or CPS). Furthermore, there were significant inverse correlations between VWF and ADAMTS13 antigen levels (r = −0.320, P < 0.0001). Plasma VWF and ADAMTS13 antigen levels did not change compared to each level in acute phase in 15 UA patients that the blood samples could be obtained at 6 months follow-up periods.
Conclusions: These findings suggested the prolonged endothelial damage in UA and tendency toward platelet thrombus formation at the injury sites after the attacks in patients with UA. The long-term antithrombotic therapy might be needed in those patients.