TY - JOUR
T1 - Hemolysate-mediated platelet aggregation
T2 - An additional risk mechanism contributing to thrombosis of continuous flow ventricular assist devices
AU - Tran, Phat L.
AU - Pietropaolo, Maria Grazia
AU - Valerio, Lorenzo
AU - Brengle, William
AU - Wong, Raymond K.
AU - Kazui, Toshinobu
AU - Khalpey, Zain I.
AU - Redaelli, Alberto
AU - Sheriff, Jawaad
AU - Bluestein, Danny
AU - Slepian, Marvin J.
N1 - Publisher Copyright:
© 2016 SAGE Publications.
PY - 2016/7/1
Y1 - 2016/7/1
N2 - Despite the clinical success and growth in the utilization of continuous flow ventricular assist devices (cfVADs) for the treatment of advanced heart failure, hemolysis and thrombosis remain major limitations. Inadequate and/or ineffective anticoagulation regimens, combined with high pump speed and non-physiological flow patterns, can result in hemolysis which often is accompanied by pump thrombosis. An unexpected increase in cfVADs thrombosis was reported by multiple major VAD implanting centers in 2014, highlighting the association of hemolysis and a rise in lactate dehydrogenase (LDH) presaging thrombotic events. It is well established that thrombotic complications arise from the abnormal shear stresses generated by cfVADs. What remains unknown is the link between cfVAD-associated hemolysis and pump thrombosis. Can hemolysis of red blood cells (RBCs) contribute to platelet aggregation, thereby, facilitating prothrombotic complications in cfVADs? Herein, we examine the effect of RBC-hemolysate and selected major constituents, i.e., lactate dehydrogenase (LDH) and plasma free hemoglobin (pHb) on platelet aggregation, utilizing electrical resistance aggregometry. Our hypothesis is that elements of RBCs, released as a result of shear-mediated hemolysis, will contribute to platelet aggregation. We show that RBC hemolysate and pHb, but not LDH, are direct contributors to platelet aggregation, posing an additional risk mechanism for cfVAD thrombosis.
AB - Despite the clinical success and growth in the utilization of continuous flow ventricular assist devices (cfVADs) for the treatment of advanced heart failure, hemolysis and thrombosis remain major limitations. Inadequate and/or ineffective anticoagulation regimens, combined with high pump speed and non-physiological flow patterns, can result in hemolysis which often is accompanied by pump thrombosis. An unexpected increase in cfVADs thrombosis was reported by multiple major VAD implanting centers in 2014, highlighting the association of hemolysis and a rise in lactate dehydrogenase (LDH) presaging thrombotic events. It is well established that thrombotic complications arise from the abnormal shear stresses generated by cfVADs. What remains unknown is the link between cfVAD-associated hemolysis and pump thrombosis. Can hemolysis of red blood cells (RBCs) contribute to platelet aggregation, thereby, facilitating prothrombotic complications in cfVADs? Herein, we examine the effect of RBC-hemolysate and selected major constituents, i.e., lactate dehydrogenase (LDH) and plasma free hemoglobin (pHb) on platelet aggregation, utilizing electrical resistance aggregometry. Our hypothesis is that elements of RBCs, released as a result of shear-mediated hemolysis, will contribute to platelet aggregation. We show that RBC hemolysate and pHb, but not LDH, are direct contributors to platelet aggregation, posing an additional risk mechanism for cfVAD thrombosis.
KW - hemolysis
KW - lactate dehydrogenase (LDH)
KW - multiplate analyzer
KW - platelet aggregation
KW - thrombosis
KW - ventricular assist devices
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U2 - 10.1177/0267659115615206
DO - 10.1177/0267659115615206
M3 - Article
C2 - 26590166
AN - SCOPUS:84976448539
SN - 0267-6591
VL - 31
SP - 401
EP - 408
JO - Perfusion (United Kingdom)
JF - Perfusion (United Kingdom)
IS - 5
ER -