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Paradoxical arterial and venous thromboembolism during heparin therapy is considered to be caused by type II heparin-induced thrombocytopenia (HIT) mediated by anti-heparin-platelet factor 4 antibodies (HIT antibodies).1 The antibodies activate platelets and endothelial cells, resulting in excessive thrombin generation and intravascular coagulation. Half of HIT patients initially present with thromboembolism.1 We describe a heparinized patient who suddenly developed thrombus in a cerebral artery during catheter angiography without a simultaneous thrombocytopenic reaction, and who was later diagnosed with HIT.
Case report.
A 75-year-old woman with combined valvular heart disease and atrial fibrillation was admitted to our hospital for severe congestive heart failure. Fifty-six days after diagnostic cardiac catheterization and angiography, she underwent aortic valve replacement, mitral valve plasty, and right coronary artery bypass surgery with cardiopulmonary bypass using heparin as an anticoagulant. Immediately after surgery, the platelet count declined from 159 × 103 to 40 × 103 cells/μL, and then returned to 168 × 103 cells/μL after platelet concentrate transfusion. Since the patient was enrolled in a multicenter, prospective …
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