Key result
Viral endomyocardial infection in the first year post-cardiac transplant was associated with increased allograft inflammation compared to virus-free patients.
Why the study?
Does viral endomyocardial infection increase allograft inflammation in children who have undergone cardiac transplant?
Cohort (n=59)
No
Does viral endomyocardial infection increase allograft inflammation in children who have undergone cardiac transplant?
Viral endomyocardial infection in the first year post-transplant is associated with increased allograft inflammation and rejection episodes in pediatric heart transplant recipients, despite similar hemodynamics.
Answers are grounded in this paper and cite their sources.
May support viral surveillance in pediatric heart transplant recipients; hypothesis-generating for antiviral strategies to reduce rejection.
BACKGROUND: Viral genome in cardiac allograft has been associated with early graft loss in children who have undergone cardiac transplant from unknown mechanisms. METHODS: This study is a retrospective review of children who have undergone cardiac transplant at a single institution from 1/2004 to 5/2008. Patients underwent cardiac catheterisations with endomyocardial biopsies to evaluate for rejection--graded on Texas Heart Institute scale--and the presence of virus by polymerase chain reaction. Patients with virus identified during the first year post transplant were compared at 1 year post transplant with virus-free patients. RESULTS: The cohort comprised 59 patients, and the median age at transplant was 5.1 years. Viral genomes were isolated from 18 (31%) patients. The PCR + group had increased inflammation on endomyocardial biopsies, with a median score of 4 (ISHLT IR) versus 1 (ISHLT 1R) in the PCR--group (p = 0.014). The PCR + group had a similar cardiac index (median 3.7 ml/min/m(2)), pulmonary capillary wedge pressure (median 10 mmHg), and pulmonary vascular resistance index (median 1.7 U m(2)) comparatively. PCR + patients were more likely to have experienced an episode of rejection (p = 0.004). CONCLUSIONS: Children who developed viral endomyocardial infections after a cardiac transplant have increased allograft inflammation compared with virus-free patients. However, the haemodynamic profile is similar between the groups. The ongoing subclinical inflammation may contribute to the early graft loss associated with these patients.
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Molina et al. (2013) conducted a cohort in Cardiac transplant (n=59). Viral endomyocardial infection vs. Virus-free patients was evaluated on Inflammation on endomyocardial biopsies (ISHLT IR score) (p=0.014). Viral endomyocardial infection in the first year post-cardiac transplant was associated with increased allograft inflammation compared to virus-free patients.
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