BACKGROUND AND OBJECTIVES: von Willebrand factor (VWF) is stored in the Weibel-Palade bodies of endothelial cells and may be released in response to different secretion stimuli such as stress, physical exercise, adrenaline, DDAVP and thrombin. DESIGN AND METHODS: We found that fainting can also induce an acute increase in plasma VWF and factor FVIII (FVIII) concentrations, following observations in two patients with von Willebrand's disease (VWD) who experienced a fainting episode during venipuncture for blood collection. RESULTS: One patient was classified as having type Vicenza VWD, the other as type 1 VWD; both had normal platelet VWF content. After the fainting episode, FVIII and VWF levels were significantly higher than the levels in blood samples collected without stress; mean increases were 4.35-fold for FVIII, 4-fold for VWF:Ag and 5.3-fold for VWF:RCo, with values overshooting the upper limit of the normal range. Moreover, the post-fainting plasma VWF multimer pattern was characterized by a significant increase in all oligomers with the appearance of unusually large VWF multimers, similar to those observed following DDAVP infusion. INTERPRETATION AND CONCLUSIONS: These findings demonstrate that fainting acts as a stimulus capable of inducing the release of VWF from endothelial cells, and further highlight the role of stress in determining hemostatic states potentially favorable to the development of thrombotic complications.
BACKGROUND AND OBJECTIVES:von Willebrand factor (VWF) is stored in the Weibel-Palade bodies of endothelial cells and may be released in response to different secretion stimuli such as stress, physical exercise, adrenaline, DDAVP and thrombin. DESIGN AND METHODS: We found that fainting can also induce an acute increase in plasma VWF and factor FVIII (FVIII) concentrations, following observations in two patients with von Willebrand's disease (VWD) who experienced a fainting episode during venipuncture for blood collection. RESULTS: One patient was classified as having type Vicenza VWD, the other as type 1 VWD; both had normal platelet VWF content. After the fainting episode, FVIII and VWF levels were significantly higher than the levels in blood samples collected without stress; mean increases were 4.35-fold for FVIII, 4-fold for VWF:Ag and 5.3-fold for VWF:RCo, with values overshooting the upper limit of the normal range. Moreover, the post-fainting plasma VWF multimer pattern was characterized by a significant increase in all oligomers with the appearance of unusually large VWF multimers, similar to those observed following DDAVP infusion. INTERPRETATION AND CONCLUSIONS: These findings demonstrate that fainting acts as a stimulus capable of inducing the release of VWF from endothelial cells, and further highlight the role of stress in determining hemostatic states potentially favorable to the development of thrombotic complications.
Authors: Markus Kraemer; Markus Kuepper; Andrea Nebe-vom Stein; Ulrich Sorgenfrei; Rolf R Diehl Journal: Clin Auton Res Date: 2009-07-25 Impact factor: 4.435