Abstract
Von Willebrand Factor (VWF) plays a major role in thrombosis and hemostasis and its thrombogenicity is controlled by ADAMTS13. Whereas increasing evidence shows a clear association between VWF levels and acute ischemic stroke, little is known about a correlation with ADAMTS13. Therefore, the aim of this study was to compare plasma levels of ADAMTS13 between 85 healthy volunteers (HV), 104 patients with acute ischemic stroke and 112 patients with a chronic cerebrovascular disease (CCD). In this case-control study, plasma ADAMTS13 antigen levels were measured by ELISA and plasma VWF levels, measured previously, were next used to calculate VWF:ADAMTS13 ratios. ADAMTS13 levels and VWF:ADAMTS13 ratios were subsequently correlated with key demographic and clinical parameters. ADAMTS13 levels were significantly lower in acute ischemic stroke patients (82.6 ± 21.0%) compared with HV (110.6 ± 26.9%). Also, CCD patients (99.6 ± 24.5%) had significantly lower ADAMTS13 levels compared with HV however these were still higher than in acute stroke patients. Furthermore, when assessing the VWF:ADAMTS13 ratios, an even greater difference was revealed between stroke patients (2.7 ± 1.9), HV (1.1 ± 0.5) and CCD patients (1.7 ± 0.7). The VWF:ADAMTS13 ratio was significantly associated with stroke severity and modality. In conclusion, both in acute and chronic cerebrovascular disease patients, ADAMTS13 levels were significantly decreased, with the lowest ADAMTS13 levels found in acute stroke patients. This difference was even more distinct when the ratio of VWF:ADAMTS13 was considered. These results demonstrate the potentially important involvement of the VWF/ADAMTS13 axis in ischemic stroke.
Highlights
Ischemic stroke is one of the leading causes of death and sustained disability in the Western world
We report that patients with acute or chronic cerebrovascular disease have significantly lower ADAMTS13 levels
These results further add to the notion that reduced ADAMTS13 activity is a risk factor for ischemic stroke.[10,11,12,13,14,15]
Summary
Ischemic stroke is one of the leading causes of death and sustained disability in the Western world. The detrimental role of von Willebrand factor (VWF) in ischaemic stroke has gained increasing attention.[1] VWF. VWF promotes inflammation thereby creating a thrombo-inflammatory environment.[2] The activity of VWF is controlled by the metalloproteinase ADAMTS13 (A Disintegrin And Metalloproteinase with Thrombospondin type 1 motif, member 13). ADAMTS13 cleaves ultra-large, highly reactive VWF multimers into smaller, less active ones, preventing spontaneous platelet-thrombus formation and reducing inflammation.[3] Preclinical animal studies have shown that absence of VWF is protective in ischemic stroke whereas absence of ADAMTS13 worsens disease outcome.[4,5,6] Increasing clinical evidence demonstrates a clear association between high VWF-levels and acute ischaemic stroke in patients. We performed a case-control study to investigate levels of ADAMTS13 in patients during the acute phase of ischemic stroke
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