Thromboelastography characterized CD36 null subjects as slow clot formation and indicative of hypocoagulability.

Background: Platelet CD36 is the receptor for oxidized low-density lipoprotein and collagen. The conventional platelet test cannot distinguish CD36-null subjects from normal expression subjects. Thromboelastography (TEG) testing can analyze global hemostasis. TEG testing data on CD36-null subjects are not available. Methods: Our subjects were 40 apheresis platelet donors, including 8 CD36-null individuals. We grouped the donors according to the platelet CD36 expression levels to assess the effects of platelet CD36 expression levels on TEG measurement variables. Results: The whole blood TEG test revealed that CD36-null subjects had prolonged reaction time of fibrin formation (TEG R time) and a slower rate to build up cross-linked fibrin (TEG a angle). The final maximal amplitudes of clot formation showed little difference between CD36-null individuals and normal expression individuals. Correlation analysis showed that CD36 expression levels were negatively correlated with TEG R time (r=-0.342, p= 0.031) and positively correlated with the TEG a angle (0.379, p= 0.016). TEG testing on apheresis platelet samples with diminished heterocellular interaction did not reveal differences between CD36null and normal expression individuals. A subanalysis of the data of a group of healthy subjects showed that platelet CD36 levels correlated positively with platelet-monocyte aggregates (PMAs). Low PMA can diminish heterocellular interaction and likely explain the abnormal TEG results observed in CD36-null individuals. Conclusion: TEG distinguishes CD36-null subjects from normal CD36 expression subjects as having a slower rate of fibrin formation and reassessment of TEG-based diagnostic monitoring is necessary for CD36 null subjects.