Alterations in coagulation after implantation of a pulsatile Novacor LVAD and the axial flow micromed DeBakey LVAD

• Published in: The Annals of thoracic surgery Vol. 70; no. 2; pp. 533 - 537
• Main Authors: Koster, Andreas, Loebe, Matthias, Hansen, Roland, Potapov, Evgenij V, Noon, George P, Kuppe, Hermann, Hetzer, Roland
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier Inc 01.08.2000
• Subjects: Adult; alpha-2-Antiplasmin - analysis; Antithrombin III - analysis; Antithrombins; beta-Thromboglobulin - analysis; Blood Coagulation; Blood Coagulation Factors - analysis; Equipment Design; Female; Heart-Assist Devices; Humans; Male; Middle Aged; Peptide Hydrolases - analysis; Platelet Factor 4 - analysis; Postoperative Period
• ISSN: 0003-4975; 1552-6259
• DOI: 10.1016/S0003-4975(00)01404-1

Background. The MicroMed DeBakey left ventricular assist device (LVAD) is a chamber and valveless axial flow blood pump. We investigated parameters of the coagulation system in patients after implantation of the axial flow LVAD and patients following implantation of a pulsatile Novacor LVAD. Methods. Six consecutive patients of both groups were investigated over a period of 6 weeks after implantation. β-Thromboglobulin, platelet factor 4, factor XIIa, thrombin/antithrombin complexes, plasmin/α 2-antiplasmin complexes, and D-Dimer levels were measured. Results. With the exception of the plasmin/α 2-antiplasmin levels in the Novacor group, all parameters were elevated in both groups. The levels of β-thromboglobulin, platelet factor 4, factor XIIa, and plasmin/α 2-antiplasmin were significantly increased in the axial flow LVAD group. Conclusions. The axial flow LVAD strongly influences the systems of contact activation and fibrinolysis. The elevation of platelet proteins appears to follow platelet damage. Although no thromboembolic events were observed in both groups, elevation of thrombin/antithrombin complexes provides convincing evidence of an increased activation of the coagulation system and the concomitant risk for the development of thromboembolism.