Conclusion: Current evidence suggests that HIT is mediated by antibodies that react with heparin and platelet factor 4. The heparin, platelet factor 4, and antibodies form immune complexes, which activate platelets and the coagulation cascade, resulting in a hypercoagulable state. This can result in the development of arterial and venous thrombosis at multiple sites. The reported incidence of venous and arterial thrombosis in HIT ranges from 39% to 53%.Internal mammary and saphenous vein (SV) graft occlusion rates in the setting of HIT are unknown. In this study, the graft patency of post-CABG patients with HIT was assessed and compared with graft patency of non-HIT post-CABG patients
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