No abstract

The implantation of a ventricular assist device (VAD) is associated with a stimulation of the inflammatory system. We compared changes in the inflammatory response after implantation of a pulsatile Novacor left (L) VAD and the axial flow MicroMed DeBakey VAD. Six consecutive patients after implantation of a Novacor LVAD (NC) and six patients after implantation of a MicroMed DeBakey VAD (MD) were included in the investigation. Patients received LVADs for medically non treatable end-stage heart failure. Tumor necrosis factor alpha (TNF), C3a, C5a, interleukin 6 (IL-6), and neutrophil elastase were measured twice a week over a period of 3 months after implantation of the device. All tests were performed with an enzyme-linked immunosorbent assay. There was no significant difference in the clinical course of the two groups. All inflammatory parameters were elevated in both groups during the entire period of the investigation. There was no difference in TNF, polynuclear leukocyte elastase, or C3a levels between the two groups; however, IL-6 (NC: 23.6+/-37.6 pg/ml vs. MD: 63+/-114 pg/ml, p < 0.001) and C5a (NC: 708+/-352 microg/L vs. MD: 1,745+/-1,305 microg/L, p < 0.001) were increased significantly more in patients following implantation of the axial flow MicroMed DeBakey VAD. Compared with the pulsatile Novacor device, the implantation of the axial flow MicroMed DeBakey LVAD seems to be associated with an increased stimulation of one part of the inflammatory system. Further investigations are necessary for evaluation of the pathophysiologic mechanism and clinical implications of these findings.

No abstract

Thromboembolism is a major complication in patients with ventricular assist devices (VAD). Anticoagulation with heparin, coumarin, and anti-platelet agents, particularly the development of biocompatible surfaces such as inner pseudo-endothelial layers or a coating with heparin, are intended to reduce these complications. However, the administration of heparin can lead to heparin induced thrombocytopenia type II (HIT II). Predominantly heparin/platelet factor 4 (HPF4) antibodies are responsible for the development of HIT II. The goal of the present investigation was to assess the prevalence of these antibodies in patients with heparin coated and noncoated VADs. Fifty-five patients were enrolled in the investigation. A heparin coated system was implanted in 30 patients, and a noncoated system was implanted in 25 patients. Antibodies were evaluated before, on days 7 and 14, and 3 months after implantation. Testing was performed with the Heparin/Platelet factor 4 enzyme-linked immunosorbent assay (ELISA) (Stago, France). In 40 of the 55 patients, 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), the antibodies disappeared after termination of systemic heparinization. We conclude that in a rather high percentage of patients with VADs HPF4 antibodies are found. This finding may be explained by the repetitive and prolonged exposure of these patients to heparin. Immobilized heparin, as presently used in the carmeda coating, seems not to influence the formation and persistence of HPF4 antibodies. Further studies will have to prove whether HPF4 antibodies contribute to thromboembolic complications in these patients.

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