Left ventricular assist devices (LVADs) have markedly improved the survival for patients with advanced heart failure but are plagued with significant morbidity, including pump thrombosis and bleeding. Better understanding of the platelet, and its role in the balance of bleeding and thrombosis, stands to impact the frequency and treatment of these significant complications.
In patients with LVADs, there is little consistency linking traditional biomarkers of platelet activation and clinical events. A number of innovative methods of assessing platelet functionality, including shedding of platelet receptors and formation of microparticle complexes as well as measuring mitochondrial membrane potentials, exist and appear to be clinically relevant. Acquired von Willebrand syndrome, while not explaining all bleeding events, is a central feature of mechanical support and offers a target for innovative therapies.
Although the platelet is only one component of impacting thrombosis and bleeding in patients supported with LVADs, it plays a central role in mediating these two opposing forces. Innovations in understanding platelet physiology as well as manipulating genomic and receptor interactions for an individual patient will be critical if we are to decrease these serious adverse events in the future.
aDivision of Cardiothoracic Surgery
bDepartment of Internal Medicine, University of Utah Health Sciences Center, Salt Lake City, Utah, USA
Correspondence to Craig H. Selzman, MD, Professor of Surgery, Division of Cardiothoracic Surgery, University of Utah Health Sciences Center, 30 N 1900 E; SOM 3C 127, Salt Lake City, UT 84132, USA. Tel: +1 801 581 5311; fax: +1 801 585 3935; e-mail: email@example.com