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Updated: May 16, 2026

Utilizing Percutaneous Ventricular Assist Devices in Acute Myocardial Infarction Complicated by Cardiogenic Shock
Published on: June 12, 2021
Left ventricular assist device-induced coagulation and platelet activation and effect of the current anticoagulant
Michael Ashbrook1, Jeanine M Walenga, Jeffrey Schwartz
1Department of Thoracic & Cardiovascular Surgery, Loyola University Medical Center, Maywood, IL 60153, USA.
Insights
Left ventricular assist devices (LVADs) suppress platelet and coagulation activation. Pharmacotherapy in LVAD patients yields a profile similar to warfarin therapy alone.
Area of Science:
- Cardiology
- Biomedical Engineering
- Hematology
Background:
- Left ventricular assist devices (LVADs) are crucial for managing advanced heart failure.
- Understanding the impact of LVADs on hemostasis is vital for patient management.
Purpose of the Study:
- To evaluate platelet and coagulation activation in LVAD patients on warfarin and aspirin.
- To compare hemostatic profiles of LVAD patients with healthy controls and warfarin-only patients.
Main Methods:
- Assessed platelet aggregation (collagen, arachidonate, ADP) in 7 LVAD patients.
- Utilized thrombelastography to analyze clot initiation and formation.
- Measured von Willebrand Factor (vWF) antigen and propeptide levels.
Main Results:
- LVAD patients showed significantly inhibited platelet aggregation compared to controls.
- Thrombelastography revealed longer clot initiation times and stronger clot formation in LVAD patients.
- Increased vWF degradation was observed in LVAD patients, though not statistically significant.
Conclusions:
- Pharmacotherapy in LVAD patients suppresses LVAD-induced coagulation and platelet activation.
- The hemostatic profile in LVAD patients on antiplatelet and anticoagulant therapy resembles that of patients on warfarin alone.
Abstract:
Left ventricular assist devices (LVADs) are mechanical pumps that enhance cardiac function in patients with heart failure. In all, 7 patients with an LVADs (1.8 international normalized ratio warfarin, 81 mg aspirin) were evaluated monthly for 3 months for platelet and coagulation activation (controls: 5 healthy adults and 5 patients having warfarin). Platelet works revealed greater inhibition of collagen (31.8% vs 7.9%; P = .004), arachidonate- (30.9% vs 8.2%; P = .001), and adenosine diphosphate- (10.9% vs 6.1%; P = .004)-induced platelet aggregation for LVADs. Thrombelastography (recalcified whole blood) showed inhibition of clot initiation time (R; 8.81 vs 6.02 min; P = .001) and stronger clot formation (maximum amplitude; 69.1 vs 64.9 mm; P = .016). Platelet function determined by plateletMapping and flow cytometry was within the normal range. The LVADs had increased ratio of von Willebrand Factor (vWF) antigen and vWF propeptide, indicating increased degradation of vWF (2.04 vs 1.44; P = .144). Coagulation and platelet activation caused by LVAD is suppressed by pharmacotherapy, yielding a profile similar to that of patients on warfarin alone.
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