Related Experiment Video
Updated: Aug 25, 2026

Murine Heterotopic Heart Transplant Technique
Published on: July 8, 2014
Platelet activation in heart transplant recipients
Aina Hognestad1, Annika Michelsen, Frank Brosstad
1Department of Cardiology, Rikshospitalet, University of Oslo, Oslo, Norway. aina.hognestad@klinmed.uio.no
Insights
Long-term heart transplant survivors show increased platelet activation, indicated by higher P-selectin and CD63 expression. This enhanced platelet activity may contribute to ongoing immune issues and complications post-transplant.
Area of Science:
- Immunology
- Cardiovascular Science
- Transplantation Medicine
Background:
- Persistent immune activation is linked to long-term complications after heart transplantation.
- Platelets are increasingly recognized for their role in inflammation beyond thrombosis.
Purpose of the Study:
- To investigate enhanced platelet activation in long-term heart transplant recipients.
- To determine if platelet activation markers correlate with clinical status.
Main Methods:
- Flow cytometry to assess platelet surface markers (P-selectin, CD63).
- Enzyme immunoassay to measure soluble CD40 ligand levels.
- Comparison between heart transplant recipients (n=52) and healthy controls (n=38).
Main Results:
- Heart transplant recipients exhibited higher P-selectin and CD63 expression on platelets.
- Increased levels of soluble CD40 ligand were found in patients.
- Elevated soluble P-selectin was detected in platelet-free plasma.
- Enhanced platelet activation was most prominent in hypertensive transplant recipients.
Conclusions:
- Long-term heart transplant survivors display heightened platelet activation.
- This platelet hyperactivity may contribute to persistent immune activation and clinical issues.
- Hypertension exacerbates platelet activation in heart transplant patients.
Abstract:
An inappropriate and persistent immune activation has been suggested to contribute to long-term mortality and morbidity after heart transplantation. Several lines of evidence suggest that platelets do not only promote thrombus formation, but also act as inflammatory cells. In the present study, we investigated if long-time survivors of heart transplantation (mean time since transplantation 6.5 yr) were characterized by enhanced platelet activation as assessed by different experimental approaches. Our main findings when comparing heart transplant recipients (n = 52) and age- and sex-matched healthy controls (n = 38) were: (i) platelets from heart transplant recipients showed enhanced expression of both P-selectin and CD63 as assessed by flow cytometry; (ii) platelets from these patients also contained significantly increased levels of soluble CD40 ligand and tended to release higher levels of this cytokine upon SFLLRN stimulation as assessed by enzyme immunoassay; (iii) heart transplant recipients had increased levels of soluble P-selectin in platelet-free plasma; and (iv) the enhanced platelet activation after heart transplantation was most pronounced in those with concomitant hypertension. These findings suggest that long-term survivors of heart transplantation are characterized by enhanced activation of platelets, possibly contributing to the persistent immune activation and clinical complications in these patients.
