Hemostatic abnormalities in total artificial heart patients as detected by specific blood markers.
We retrospectively evaluated the hemostatic system of 13 patients during implantation (2 to 35 days) of the Jarvik 7-70 total artificial heart (TAH). Although all patients were clinically manageable while on the TAH, 5 had excessive generalized bleeding. After the heart transplant procedure, 2 patients had neurological events and 1 patient, thrombosis of the leg. While the patients were supported by the TAH, the routine coagulation assays (prothrombin time, activated partial thromboplastin time, fibrinogen, factor assays, and platelet count) showed slight abnormalities but no correlation to hemorrhagic or thrombotic events. In contrast, plasma and cellular activation markers, which are highly sensitive and specific for hypercoagulability, fibrinolysis, or platelet activation, revealed activation in all patients. Most striking was the marked activation of the fibrinolytic system (p less than 0.05 to 0.001). Correlations of individual patient data compared with the average TAH group response could be made between excessive enhancement of fibrinolysis (increased D-dimer and tissue plasminogen activator and decreased plasminogen activator inhibitor) and bleeding. A hypercoagulable state (increased fibrinogen and thrombin-antithrombin complex and decreased antithrombin III and protein C), decreased fibrinolysis (decreased tissue plasminogen activator and D-dimer), activated platelets (increased thromboxane B2), or combinations of these were associated with thrombosis. The hemostatic activation returned to normal 1 day after removal of the TAH. These data suggest that the patient with a TAH requires more sophisticated laboratory monitoring and individualized treatment for excessive fibrinolysis, hypercoagulable state, or platelet activation to avoid thrombotic and hemorrhagic complications.
Walenga
J M
JM
Department of Thoracic and Cardiovascular Surgery, Loyola University Medical Center, Maywood, Illinois 60153.
Hoppensteadt
D
D
Fareed
J
J
Pifarré
R
R
D015121:6-Ketoprostaglandin F1 alpha / Q000097:blood; D000293:Adolescent; D000328:Adult; D001777:Blood Coagulation / Q000502:physiology; D005260:Female; D005342:Fibrinolysis / Q000502:physiology; D006354:Heart, Artificial; D006487:Hemostasis / Q000502:physiology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D008991:Monitoring, Physiologic; D015539:Platelet Activation / Q000502:physiology; D010976:Platelet Count; D010978:Platelet Factor 4 / Q000737:chemistry; D012189:Retrospective Studies; D015996:Survival Rate; D013929:Thromboxane B2 / Q000097:blood
D010978:Platelet Factor 4; D013929:Thromboxane B2; D015121:6-Ketoprostaglandin F1 alpha