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Donor or recipient hepatitis B seropositivity is associated with allograft vasculopathy
Showkat A Haji1, Robin K Avery, Mohamad H Yamani
1Department of Cardiology, Tulane University Medical Center, New Orleans, Louisiana 70112, USA. Shaji@tulane.edu
Insights
Hepatitis B virus (HBV) infection in heart transplant recipients may accelerate cardiac allograft vasculopathy. This study found a higher incidence of vasculopathy in HBV-seropositive patients compared to controls.
Area of Science:
- Cardiology
- Transplantation Immunology
- Hepatology
Background:
- Viral triggers for cardiac allograft vasculopathy (CAV) are of increasing interest.
- Hepatitis C virus (HCV) seropositivity is linked to accelerated CAV.
- The role of hepatitis B virus (HBV) in CAV requires investigation.
Purpose of the Study:
- To investigate the association between hepatitis B virus (HBV) seropositivity and accelerated cardiac allograft vasculopathy (CAV).
Main Methods:
- Sixty-six heart transplant recipients were analyzed using intravascular ultrasound at 6 weeks and 12 months post-transplant.
- Patients were categorized into an HBV Group (donor or recipient HBcAb positive, n=13) and a Control Group (neither positive, n=53).
Main Results:
- The HBV Group showed a significantly greater increase in average intimal area per vessel length compared to controls (1.59 vs 0.46 mm², p=0.01).
- CAV incidence at 1 year was higher in the HBV group (46% vs 24%, p=0.05 for >0.50 mm intimal thickness increase).
- Using a >0.30 mm intimal thickness increase, CAV occurred in 31% of the HBV group versus 5% of controls (p=0.01).
Conclusions:
- HBV seropositivity in either the donor or recipient is associated with an increased risk of developing cardiac allograft vasculopathy.
- These findings suggest HBV as a potential risk factor for accelerated CAV post-heart transplantation.
Background:
Increasing interest has focused on possible viral triggers of cardiac allograft vasculopathy. Although much interest has centered on cytomegalovirus, it has recently been noted that donor hepatitis C seropositivity is associated with risk for accelerated vasculopathy. The current study hypothesized that hepatitis B (HBV) might be associated with accelerated vasculopathy.
Methods:
Sixty-six patients who received heart transplants between September 1998 and July 2000 were analyzed by intravascular ultrasound within 6 weeks and again at 12 months after transplantation. These patients were divided into 2 groups: the HBV Group (n = 13) in which either the donor or recipient was seropositive for hepatitis B core antibody (HBcAb), and a Control Group (n = 53) in which neither donor nor recipient was positive for HBcAb.
Results:
Baseline characteristics of the 2 groups were similar. The HBV Group had significant increase in the change in average intimal area (1.59 +/- 1.4 vs 0.46 +/- 0.4 mm2, p = 0.01) per mm length of the vessel compared with controls. Allograft vasculopathy at 1 year (defined as largest maximal intimal thickness increase of > or =0.50 mm) occurred in 46% of the HBV group compared with 24% of the control group (p = 0.05). When measured as an average maximal intimal thickness increase of >0.30 mm, allograft vasculopathy at 1 year occurred in 31% of the HBV Group compared with 5% of Controls (p = 0.01).
Conclusions:
These preliminary results suggest that HBV seropositivity in donor or recipient may be associated with an increased risk for cardiac allograft vasculopathy.
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