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Interaction Between vWF Levels and Aspirin Resistance in Ischemic Stroke Patients

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Abstract

The von Willebrand factor (vWF) levels increase in acute-phase ischemic stroke because of endothelial dysfunction and thrombus formation and may reduce acetylsalicylic acid (ASA) efficiency in hemostatic cascade. The aim of the study is to investigate the relationship between vWF levels and ASA resistance in ischemic stroke patients. Fifty acute ischemic stroke patients (mean age 66.3 ± 13 years, 34 males) were given 300 mg/day aspirin for at least 10 days, and 25 healthy volunteers as a control group were compared using platelet function analyzer-100 test. All risk factors were investigated for a correlation to ASA resistance. ASA resistance was apparent in 32 % of the study group and in 20 % of the control group (p = 0.140). vWF levels were elevated in only ASA nonresponders and the ischemic stroke group that showed a statistically significant association with aspirin resistance (p ≤ 0.05). vWF levels increase in ASA nonresponders and ischemic stroke group in acute phase. High vWF levels may relate to ASA resistance and recurrent strokes.

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Acknowledgments

The PFA-100 test financial support was provided by government hospital funding. None of the authors have any conflict of interest to disclose. Experiments were undertaken with the understanding and written consent of each subject. This study conducted in accordance with The Code of Ethics of the World Medical Association (Helsinki Declaration of 1975, as revised in 1983).

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Authors and Affiliations

  1. Neurology Clinic, İzmir Tepecik Education and Research Hospital, Yenişehir Mah, 35120, Konak, Izmir, Turkey

    Yıldız Arslan & Yaşar Zorlu

  2. Neurology Clinic, Ankara Dişkapi Education and Research Hospital, Ankara, Turkey

    Tahir Kurtuluş Yoldaş

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  1. Yıldız Arslan
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  2. Tahir Kurtuluş Yoldaş
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  3. Yaşar Zorlu
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Correspondence to Yıldız Arslan.

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Arslan, Y., Yoldaş, T.K. & Zorlu, Y. Interaction Between vWF Levels and Aspirin Resistance in Ischemic Stroke Patients. Transl. Stroke Res. 4, 484–487 (2013). https://doi.org/10.1007/s12975-013-0259-0

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  • DOI: https://doi.org/10.1007/s12975-013-0259-0

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