Prevalence and persistence of heparin/platelet factor 4 antibodies in patients with heparin coated and noncoated ventricular assist devices

Citation
A. Koster et al., Prevalence and persistence of heparin/platelet factor 4 antibodies in patients with heparin coated and noncoated ventricular assist devices, ASAIO J, 46(3), 2000, pp. 319-322
Citations number
12
Categorie Soggetti
Research/Laboratory Medicine & Medical Tecnology
Journal title
ASAIO JOURNAL
ISSN journal
10582916 → ACNP
Volume
46
Issue
3
Year of publication
2000
Pages
319 - 322
Database
ISI
SICI code
1058-2916(200005/06)46:3<319:PAPOHF>2.0.ZU;2-B
Abstract
Thromboembolism is a major complication in patients with ventricular assist devices (VAD). Anticoagulation with heparin, coumarin, and anti-platelet a gents, particularly the development of biocompatible surfaces such as inner pseudoendothelial layers or a coating with heparin, are intended to reduce these complications. However, the administration of heparin can lead to he parin induced thrombocytopenia type II (HIT ii). Predominantly heparin/plat elet factor 4 (HPF4) antibodies are responsible for the development of HIT Il. The goal of the present investigation was to assess the prevalence of t hese antibodies in patients with heparin coated and noncoated VADs. Fifty-f ive patients were enrolled in the investigation. A heparin coated system wa s implanted in 30 patients, and a noncoated system was implanted in 25 pati ents. Antibodies were evaluated before, on days 7 and 14, and 3 months afte r implantation. Testing was performed with the Heparin/Platelet factor 4 en zyme-linked immunosorbent assay (ELISA) (Stago, France). In 40 of the 55 pa tients, the formation of HPF4 antibodies was observed (73%). In 35 of these patients (88%), HPF4 antibodies were present before surgery. There were no differences between the groups. In 11 patients (equal from both groups), t he antibodies disappeared after termination of systemic heparinization. We conclude that in a rather high percentage of patients with VADs HPF4 antibo dies are found. This finding may be explained by the repetitive and prolong ed exposure of these patients to heparin. Immobilized heparin, as presently used in the carmeda coating, seems not to influence the formation and pers istence of HPF4 antibodies. Further studies will have to prove whether HPF4 antibodies contribute to thromboembolic complications in these patients.