Hemostatic changes in heart transplant recipients and their relationship to accelerated coronary sclerosis.
Hemostasis was assessed in 115 steady-state heart transplant recipients (HTRs) and compared with that of 23 age-matched healthy controls and 21 age-matched patients with ischemic heart disease (IHD). Compared with the controls, the HTRs had increased levels of fibrinogen (mean and 95% confidence limits of 4.50 [4.32-4.68] g/L versus 3.47 [3.07-3.87] g/L, P < 0.001), factor VIIC (1.16 [0.98-1.21] IU/ml versus 0.99 [0.89-1.10] IU/ml, P < 0.001), and von Willebrand factor antigen (1.72 [1.58-1.88] IU/ml versus 1.00 [0.80-1.26] IU/ml, P < 0.001). HTRs had increased antithrombin III activity (P = 0.002) and protein C activity (P = 0.002), with a decrease in total protein S levels (P < 0.001) but no change in free protein S levels. Stepwise discriminant analysis of hemostatic variables showed that fibrinogen was the best discriminator of the three groups, classifying 55.6% of HTR, 40% of IHD, and 66.7% of the controls. More marked prothrombotic changes were found in HTRs transplanted for IHD than for other causes; this reached significance for prothrombin (P = 0.048), factor IX (P = 0.003), and poor fibrinolytic activity as measured by euglobulin clot lysis time (P = 0.008). The HTRs with accelerated coronary sclerosis (ACS) tended to have the most prothrombotic changes; this reached significance with factor IX (P = 0.03). In conclusion, HTRs have perturbed hemostasis; the net effects of these changes are prothrombotic. The relationship between prothrombotic changes and ACS merits further studies.
Hunt
B J
BJ
Research Haematology Group, Harefield Hospital, Middlesex, England.
Segal
H
H
Yacoub
M
M
D000328:Adult; D000368:Aged; D003324:Coronary Artery Disease / Q000209:etiology*; D005260:Female; D005340:Fibrinogen / Q000032:analysis; D016027:Heart Transplantation / Q000009:adverse effects*; D006487:Hemostasis / Q000502:physiology*; D006801:Humans; D007165:Immunosuppression Therapy; D008297:Male; D008875:Middle Aged; D017202:Myocardial Ischemia / Q000097:blood; D017395:Plasminogen Activator Inhibitor 1 / Q000096:biosynthesis; D014841:von Willebrand Factor / Q000032:analysis
D017395:Plasminogen Activator Inhibitor 1; D014841:von Willebrand Factor; D005340:Fibrinogen