Vitamin K reduces bleeding in left ventricular assist device recipients.
BACKGROUND
Despite advances in left ventricular assist device (LVAD) design that permit support without anticoagulation, LVAD recipients often suffer profound bleeding complications. This bleeding diathesis may be attributable to pre-operative right-ventricular failure with concomitant hepatic dysfunction. The purpose of this study was to characterize coagulation abnormalities in LVAD recipients and determine the impact of pre-operative vitamin K administration on the incidence of postoperative bleeding.


METHODS
Hemostatic and liver function profiles were obtained in 66 recipients of the Heartmate LVAD; 39 of these patients received perioperative vitamin K.


RESULTS
During LVAD support, hepatic synthetic function improved as evidenced by increases in clotting factors II, V, VII, XI. There was ongoing fibrinolysis with elevation of fibrinopeptide A and D-dimers and diminution of fibrinogen; however, plasminogen levels did not decline suggesting that systemic disseminated intravascular coagulation (DIC) did not occur. Bleeding requiring re-exploration more than 48 hours postimplantation occurred in 9 of 66 patients (13.6%). Prior to implantation, patients that bled had decreased levels of factor II (52.2 +/- 27.1% vs 69.7 +/- 26.6%; p = 0.048) and prolonged prothrombin times (16.5 +/- 2.4 seconds vs 13.8 +/- 3.1 seconds; p = 0.005) compared to patients that did not bleed. Seven of 27 patients (25.9%) not treated with vitamin K bled, while only 2 of 39 (5.1%) patients treated with vitamin K required re-exploration for bleeding (p = 0.026).


CONCLUSIONS
We conclude that: (1) Liver synthetic function improves during LVAD support resulting in increased levels of circulating coagulation factors; (2) ongoing fibrinolysis occurs but likely only represents remodeling of fibrin on the LVAD surface; (3) perioperative vitamin K reduces nonsurgical bleeding in LVAD recipients.
Kaplon
R J
RJ
Department of Thoracic and Cardiovascular Surgery, Cleveland Clinic Foundation, Ohio 44195, USA.
Gillinov
A M
AM
Smedira
N G
NG
Kottke-Marchant
K
K
Wang
I W
IW
Goormastic
M
M
McCarthy
P M
PM
D004211:Disseminated Intravascular Coagulation / Q000517:prevention & control; D005165:Factor V / Q000032:analysis; D005167:Factor VII / Q000032:analysis; D005172:Factor XI / Q000032:analysis; D005260:Female; D005338:Fibrin Fibrinogen Degradation Products / Q000032:analysis; D005340:Fibrinogen / Q000032:analysis; D005342:Fibrinolysis / Q000502:physiology; D005344:Fibrinopeptide A / Q000032:analysis; D006353:Heart-Assist Devices; D006487:Hemostasis / Q000502:physiology; D006801:Humans; D015994:Incidence; D008099:Liver / Q000378:metabolism; D017093:Liver Failure / Q000150:complications; D008297:Male; D008875:Middle Aged; D010958:Plasminogen / Q000032:analysis; D019106:Postoperative Hemorrhage / Q000517:prevention & control*; D011292:Premedication; D011516:Prothrombin / Q000032:analysis; D011517:Prothrombin Time; D012086:Reoperation; D018497:Ventricular Dysfunction, Right / Q000150:complications; D016277:Ventricular Function, Left; D014812:Vitamin K / Q000008:administration & dosage / Q000627:therapeutic use*
D005338:Fibrin Fibrinogen Degradation Products; C036309:fibrin fragment D; D014812:Vitamin K; D005344:Fibrinopeptide A; D005165:Factor V; D005167:Factor VII; D011516:Prothrombin; D005340:Fibrinogen; D010958:Plasminogen; D005172:Factor XI