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Hemostatic changes in heart transplant recipients and their relationship to accelerated coronary sclerosis
Insights
Heart transplant recipients (HTRs) exhibit altered hemostasis with a prothrombotic tendency. These changes, particularly fibrinogen levels, can help distinguish HTRs from healthy individuals and those with ischemic heart disease.
Area of Science:
- Cardiology
- Hematology
- Transplantation Medicine
Background:
- Heart transplant recipients (HTRs) often experience complications related to hemostasis.
- Understanding hemostatic profiles in HTRs is crucial for managing post-transplant health and preventing thrombotic events.
Purpose of the Study:
- To assess hemostasis in steady-state HTRs.
- To compare hemostatic parameters between HTRs, healthy controls, and patients with ischemic heart disease (IHD).
- To identify key hemostatic factors that differentiate these groups and explore associations with accelerated coronary sclerosis (ACS).
Main Methods:
- Hemostasis was evaluated in 115 HTRs, 23 healthy controls, and 21 IHD patients.
- Measurements included fibrinogen, factor VIIC, von Willebrand factor antigen, antithrombin III, protein C, total and free protein S.
- Stepwise discriminant analysis was used to identify discriminating hemostatic variables.
Main Results:
- HTRs showed significantly increased levels of fibrinogen, factor VIIC, and von Willebrand factor antigen compared to controls.
- HTRs also had increased antithrombin III and protein C activity, but decreased total protein S.
- Fibrinogen was the best discriminator between HTRs, IHD patients, and controls. HTRs transplanted for IHD exhibited more prothrombotic changes, particularly those with ACS.
Conclusions:
- HTRs possess a perturbed hemostatic system with a net prothrombotic effect.
- Specific hemostatic alterations in HTRs warrant further investigation, especially concerning their link to accelerated coronary sclerosis.
- Fibrinogen levels are a key indicator of hemostatic changes in HTRs.
Abstract:
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.