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Related Experiment Video

Updated: Jun 26, 2026

Utilizing Percutaneous Ventricular Assist Devices in Acute Myocardial Infarction Complicated by Cardiogenic Shock

Utilizing Percutaneous Ventricular Assist Devices in Acute Myocardial Infarction Complicated by Cardiogenic Shock

Published on: June 12, 2021

Platelet dysfunction in outpatients with left ventricular assist devices.

Barbara Steinlechner¹, Martin Dworschak, Beatrice Birkenberg

¹Division of Cardiothoracic and Vascular Anesthesia and Intensive Care, Medical University of Vienna, Vienna, Austria. barbara.steinlechner@meduniwien.ac.at

The Annals of Thoracic Surgery

|December 23, 2008

Summary

Patients with left ventricular assist devices show impaired platelet function, particularly under high shear rates. This dysfunction, resembling acquired von Willebrand syndrome, contributes to bleeding risks.

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Utilizing Percutaneous Ventricular Assist Devices in Acute Myocardial Infarction Complicated by Cardiogenic Shock

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Published on: June 12, 2021

In Vitro Thrombosis Test for Ventricular Assist Devices

In Vitro Thrombosis Test for Ventricular Assist Devices

Published on: March 21, 2025

Area of Science:

Cardiology
Hematology
Biomedical Engineering

Background:

Left ventricular assist devices (LVADs) are crucial for heart failure management but pose risks of bleeding and clotting.
Balancing anticoagulation and procoagulation is vital for LVAD patients.
Current coagulation tests overlook platelet function, a critical factor in LVAD complications.

Purpose of the Study:

To differentially evaluate platelet function in LVAD outpatients using four point-of-care devices.
To identify specific platelet function defects in LVAD patients.

Main Methods:

Cross-sectional study comparing 12 LVAD outpatients and 12 healthy volunteers.
Assessment of platelet function using thrombelastography platelet mapping, thromboelastometry, platelet function analyzer, and Multiplate whole blood aggregometer.
Evaluation of platelet response to collagen, adenosine diphosphate, and ristocetin.

Main Results:

LVAD patients exhibited significantly prolonged clotting times and compromised platelet function under high shear stress (collagen/ADP).
Despite elevated von Willebrand factor antigen, ristocetin-induced aggregation was reduced, indicating impaired glycoprotein Ib-von Willebrand factor axis function.
Abnormal von Willebrand factor multimer patterns were observed in LVAD patients.

Conclusions:

Multimodal monitoring reveals significant platelet dysfunction in LVAD patients.
Impaired platelet function under high shear and abnormal ristocetin aggregation are partly due to reduced von Willebrand factor activity.
These findings suggest an acquired von Willebrand syndrome in LVAD patients, potentially explaining bleeding complications.