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Ann Thorac Surg 1990;49:714-723
© 1990 The Society of Thoracic Surgeons
a Departments of Surgery and Anesthesiology, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, USA
b Berlex Laboratories, Inc, Wayne, New Jersey, USA
* Address reprint requests to Dr Addonizio, Department of Surgery, Temple University School ot Medicine, Broad and Ontario Sts, Philadelphia, PA 19140.
For 11 patients with confirmed heparin-induced thrombocytopenia, we used reversible platelet inhibition with iloprost, a stable prostacyclin analogue, to permit safe heparin administration for cardiac (n = 9) or vascular (n = 2) operations. In vitro, iloprost (0.01 µmol/L) prevented both heparin-induced platelet aggregation and 14C-serotonin release in all patients. Therefore, intraoperatively, a continuous infusion of iloprost was started before administration of heparin and was continued until 15 minutes after administration of protamine. For cardiac patients, after heparin administration, the whole Mood platelet count did not change (171,000 ± 29,000/gmL versus 174,000 ± 29,000/gmL, mean ± standard error of the mean); no spontaneous platelet aggregation was observed, and plasma levels of the α-granule constituents platelet factor 4 and β-thromboglobulin increased from 38 ± 14 and 140 ± 18 ng/mL to 591 ± 135 and 235 ± 48 ng/mL, respectively. Fibrinopeptide A levels actually decreased from 287 ± 150 to 27 ± 6 ng/mL. Furthermore, adenosine diphosphate-induced platelet activation was preserved, postoperative bleeding times wen unchanged, and no heparin-related deaths occurred. Similar results were obtained in both vascular patients. We conclude that temporary platelet inhibition with iloprost now permits safe heparin administration in all patients with heparin-induced thrombocytopenia who require a cardiac or vascular operation.
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