![]() ![]() ![]() The PF4/heparin EIA was strongly positive (OD 1.73), but the HIPA was negative.Īt day −20, the 59-year-old female patient had an ST-segment elevation myocardial infarction and cardiac arrest. ![]() “HIT test” denotes the time point at which a blood sample was taken for HIT diagnosis test results are shown below the graph. The patient was discharged at day 25 and has remained stable. In addition, abciximab and clopidogrel were given. All heparins were stopped, and anticoagulation was switched to argatroban. Heparin-induced thrombocytopenia was suspected the 4T score was 7. Three days later, the patient was transferred to the hospital of 1 of the authors (C.P.) with a further myocardial infarction (MI) due to in-stent thrombosis of the right coronary artery. Anticoagulation was switched to dalteparin (5000 aFXaU twice a day subcutaneously). Severe pulmonary embolism (PE) occurred at day 6, and the platelet count had decreased to 114 per microliter. Therapeutic-dose low molecular weight heparin was started at day 0 upon diagnosis of a deep vein thrombosis (DVT) of the right leg (enoxaparin 1 mg/kg body weight twice a day subcutaneously). No thrombosis prophylaxis was given because of the anticipated risk of bleeding after liver injury. Resuscitation was complicated by liver laceration requiring surgery. She required cardiopulmonary resuscitation during which a bolus of unfractionated heparin was given, followed by placement of 3 drug-eluting stents in the right coronary artery. A total of 500 μL of HIPA + sera spiked with ticagrelor was incubated with 20 mg of pulverized activated charcoal tablets (Kohle-Hevert, Hevert Arzneimittel, Berlin, Germany) for 5 minutes, then centrifuged, and the supernatant was used.Īt day −20, the 59-year-old female patient had an ST-segment elevation myocardial infarction and cardiac arrest. Serum from the index patient ( Figure 1) and ticagrelor-spiked known HIPA + sera were incubated for 30 minutes with 100 μg/mL the ticagrelor antidote PB2452 (kindly provided by PhaseBio, Malvern, PA). The IgG fraction from patient sera was prepared using protein G sepharose (optical density 2.20 in the PF4/heparin EIA). Confirmed HIT + sera were spiked with ticagrelor (final concentrations: 15.6, 31.3, 62.5, 125, 250, 500, and 1000 ng/mL in vivo range, 227-770 ng/mL 1% dimethyl sulfoxide was used as carrier control). 9,13,14 Aggregation in ≥3 of 4 donors’ test cells in the presence of low molecular weight heparin (0.2 aFXaU/mL) within 35 minutes was defined as HIT +. The in-house anti-PF4/heparin-immunoglobulin G (IgG) EIA and HIPA tests were performed as previously described. When we observed a patient with a clinical course typical for HIT, a positive anti-PF4/heparin enzyme immunoassay (EIA) but a negative HIPA test ( Figure 1), we systematically assessed whether ticagrelor may lead to a false-negative HIPA test. Platelet activation by HIT antibodies is caused via the platelet FcγRIIA receptor and depends on cosignaling via the P2Y 12 ADP receptor, 12 which is blocked by ticagrelor. ![]()
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