Figure 7.
Figure 7. Schematic representation of HIT model. The situation shown in the top panel is more common. Patients have low or normal levels of total platelet PF4, and if they have atherosclerosis or other causes of vascular injury leading to platelet activation and PF4 release, they have relatively low levels of surface PF4 expression. When these patients are heparinized, PF4 is removed, fewer antigenic complexes remain, and there is less likelihood of platelet activation if HIT antibodies develop. These patients are at low risk of HIT. The bottom panel shows the smaller subset of patients with high levels of total PF4 who have suffered significant vascular injury and/or significant platelet activation and have high surface PF4 levels. Upon heparinization, they form and retain significant amounts of antigenic complexes on the platelet surface. If they develop HIT antibodies, they are at high risk of developing HIT.

Schematic representation of HIT model. The situation shown in the top panel is more common. Patients have low or normal levels of total platelet PF4, and if they have atherosclerosis or other causes of vascular injury leading to platelet activation and PF4 release, they have relatively low levels of surface PF4 expression. When these patients are heparinized, PF4 is removed, fewer antigenic complexes remain, and there is less likelihood of platelet activation if HIT antibodies develop. These patients are at low risk of HIT. The bottom panel shows the smaller subset of patients with high levels of total PF4 who have suffered significant vascular injury and/or significant platelet activation and have high surface PF4 levels. Upon heparinization, they form and retain significant amounts of antigenic complexes on the platelet surface. If they develop HIT antibodies, they are at high risk of developing HIT.

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