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Autoimmune heparin-induced thrombocytopenia following cardiac surgery
Rosanne St Bernard1, Ishac Nazy2,3, Theodore Earl Warkentin4
1Department of Medicine, Grand River Hospital, Kitchener, Ontario, Canada.
An elderly man underwent cardiac surgery with heparin anticoagulation; postoperatively, the platelet counts steadily fell, reaching 50×109/L on postoperative day 5 (POD5), prompting testing for heparin-induced thrombocytopenia (HIT) antibodies; brain imaging showed parietal stroke. Screening immunoassay for HIT antibodies yielded a strong-positive result; the platelet activation test (serotonin-release assay) gave an atypical profile (strong serotonin release at 0, 0.1 and 0.3 U/mL heparin with only partial inhibition by a platelet Fc receptor-blocking monoclonal antibody). Anticoagulation was changed to argatroban plus high-dose intravenous immunoglobulin. Persisting hypercoagulability prompted a switch to fondaparinux, with gradual platelet count recovery (155×109/L, POD62); neurological abnormalities resolved. Laboratory evaluation confirmed HIT antibodies with heparin-independent platelet-activating properties, indicating autoimmune HIT (aHIT). Besides profound thrombocytopenia (platelet count nadir, 13×10⁹/L), novel aspects of this case of aHIT include early postoperative onset (before POD5) resulting from preoperative heparin exposure and a unique laboratory aHIT antibody profile with partial resistance to Fc receptor blockade.
An elderly man underwent cardiac surgery with heparin anticoagulation; postoperatively, the platelet counts steadily fell, reaching 50×109/L on postoperative day 5 (POD5), prompting testing for heparin-induced thrombocytopenia (HIT) antibodies; brain imaging showed parietal stroke. Screening immunoassay for HIT antibodies yielded a strong-positive result; the platelet activation test (serotonin-release assay) gave an atypical profile (strong serotonin release at 0, 0.1 and 0.3 U/mL heparin with only partial inhibition by a platelet Fc receptor-blocking monoclonal antibody). Anticoagulation was changed to argatroban plus high-dose intravenous immunoglobulin. Persisting hypercoagulability prompted a switch to fondaparinux, with gradual platelet count recovery (155×109/L, POD62); neurological abnormalities resolved. Laboratory evaluation confirmed HIT antibodies with heparin-independent platelet-activating properties, indicating autoimmune HIT (aHIT). Besides profound thrombocytopenia (platelet count nadir, 13×10⁹/L), novel aspects of this case of aHIT include early postoperative onset (before POD5) resulting from preoperative heparin exposure and a unique laboratory aHIT antibody profile with partial resistance to Fc receptor blockade.
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