A fatal complication after repair of post-infarction ventric
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Heparin-induced thrombocytopenia (HIT) is a rare but potentially devastating and life-threatening complication of heparin therapy. HIT not only causes thrombocytopenia, but it also carries an increased risk for both arterial and venous thrombotic complications, despite the administration of heparin as an anticoagulating agent.1

HIT is associated with antibodies to a complex of heparin–platelet factor 4 (H-PF4). HIT-associated antibodies are generally detected after open-heart surgery.2,3 Post-infarction ventricular septal rupture (PI-VSR) following acute myocardial infarction has a high mortality rate and surgical repair also presents a high risk of mortality.

In this report, we describe the case of a patient in whom fatal HIT developed after successful surgical repair of a posterior PI-VSR on cardiopulmonary bypass (CPB). This is rare, and a limited number of cases have been reported following surgical repair of a PI-VSR.

Case report
A 74-year-old man presented with chest pain to a local hospital, from where he was transferred to our institution, with a PI-VSR. He had been anticoagulated with unfractioned heparin (UFH) (1 000 IU/h daily) for three days since the myocardial infarction (MI) had occurred.

On admission, his heart rate was 92 beats/min, blood pressure was 90/50 mmHg and weight was 85 kg. Physical examination showed a systolic murmur at the left sternal border. Cardiac catheterisation was performed, during which a single intravenous dose of 2 500 units of heparin was administered. Coronary angiography showed critical stenoses in the mid segment of the left anterior descending artery and ostium of the second diagonal branch, and occlusion in the distal segment of the right coronary artery. The time between the onset of acute MI and surgery was three days.....