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a Division of Cardiothoracic and Vascular Anesthesia and Intensive Care, Medical University of Vienna, Vienna, Austria
b Division of Cardiothoracic Surgery, Medical University of Vienna, Vienna, Austria
c Institute of Medical and Chemical Laboratory Diagnostics, Medical University of Vienna, Vienna, Austria
d Department of Clinical Pharmacology, Medical University of Vienna, Vienna, Austria
Accepted for publication October 14, 2008.
* Address correspondence to Dr Steinlechner, Division of Cardiothoracic and Vascular Anesthesia and Intensive Care, Medical University of Vienna, Waehringer Guertel 18-20, Vienna, A-1090, Austria (Email: barbara.steinlechner{at}meduniwien.ac.at).
Background: Thromboembolic and bleeding complications in outpatients with a left ventricular assist device are common and can be detrimental. A meticulous balance between anticoagulant and procoagulant factors is therefore crucial. However, in contrast to routinely performed plasmatic coagulation tests, platelet function is hardly ever monitored although recent reports indicated platelet dysfunction. We therefore differentially evaluated platelet function with four commonly used point-of-care devices.
Methods: In a cross-sectional design platelet function was assessed in 12 outpatients and 12 healthy matched volunteers using thrombelastography platelet mapping, thromboelastometry, platelet function analyzer, and a new whole blood aggregometer (Multiplate).
Results: Phenprocoumon produced an international normalized ratio of 3.5. It was associated with a twofold prolongation in the thromboelastometry clotting time (p < 0.001). Platelet function under high shear was severely compromised: collagen adenosine diphosphate closure times were 2.5-fold longer in patients than in volunteers (p < 0.001), and 50% of patients had maximal collagen adenosine diphosphate closure time values. Although antigen levels of von Willebrand factor were 80% higher in patients (p < 0.001), von Willebrand factor–ristocetin was subnormal in 5 of 12 patients. Ristocetin-induced aggregation was also threefold higher in volunteers (p < 0.001), indicating an additional functional defect of platelets affecting the glycoprotein Ib–von Willebrand factor axis. The von Willebrand factor multimer pattern in patients also appeared abnormal.
Conclusions: Multimodal antiplatelet monitoring showed markedly impaired platelet function in patients with a left ventricular assist device. Platelet dysfunction under high shear rates and abnormal ristocetin-induced aggregation is only partly attributable to low von Willebrand factor activity. These findings resemble the acquired von Willebrand syndrome that is associated with microaggregate formation and enhanced bleeding.
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Ann. Thorac. Surg. 2009 87: 137-138.
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