Hemostatic profiles of HeartMate ventricular assist device recipients

• Published in: ASAIO journal (1992) Vol. 41; no. 3; p. M782
• Main Authors: Wang, I W, Kottke-Marchant, K, Vargo, R L, McCarthy, P M
• Format: Journal Article
• Language: English
• Published: United States 01.07.1995
• Subjects: Blood Coagulation Factors - metabolism; Cardiomyopathies - physiopathology; Cardiomyopathies - therapy; Heart Transplantation; Heart-Assist Devices - adverse effects; Hemorrhage - etiology; Hemostasis - physiology; Humans; Liver - physiopathology; Plasminogen - metabolism; Time Factors
• ISSN: 1058-2916; 1538-943X
• DOI: 10.1097/00002480-199507000-00120

Candidates for ventricular assist devices often have hepatic dysfunction and concomitant coagulation abnormalities. Factors II, V, VII, XI, plasminogen, fibrinopeptide A (FpA), and D-dimers were measured in 19 HeartMate (ThermoCardiosystems, Inc., Woburn, MA) patients before device implantation; at 6 hr, 24 hr, and 2 weeks postimplantation; and before explantation. Ten patients had entry hepatic dysfunction (total bilirubin > 2 mg/dl; aspartate and alanine aminotransferases > 60 U/L); nine had normal hepatic function. All except one patient received perioperative aprotinin; all received only aspirin and dipyridamole after surgery. At preimplant, both patient groups had subnormal factor II, V, VII, XI, and plasminogen with elevated FpA and D-dimer. By 2 weeks postimplant, these factor levels had normalized, except for FpA and D-dimer levels, which suggest ongoing remodeling of fibrin deposits on the device surfaces. No statistically significant differences in the assayed hemostatic markers were observed between the two patient groups. Clinically, 15/19 (79%) patients survived to cardiac transplantation; 3/19 (16%) patients required reoperation for early bleeding. All three had low factor VII and XI; two of three also had hepatic dysfunction and subnormal levels of factor II and V. Most patients with entry hepatic dysfunction improve after device implantation; all four deaths were in patients with persistent hepatic dysfunction despite circulatory support.