Cytomegalovirus infection after heart transplantation

    Authors

    Keywords

    heart transplantation, cytomegalovirus infection, cardiac allograft vasculopathy

    DOI

    https://doi.org/10.15836/ccar2018.363

    Full Text

    Introduction : Cytomegalovirus (CMV) infection is known as an external trigger for cardiac allograft vasculopathy (CAV), due to the mechanisms that stimulate graft immunogenicity. ( 1 , 2 ) The aim of the study was to investigate different aspects of CMV infection and their effect on the development of CAV and cellular rejection (CS) after heart transplantation (HTx). Patients and methods : 123 patients after HTx performed in the period from 2005 to 2016 were included, with regular CMV monitoring by PCR method. Follow-up was 3 years (IQR 2-6 years). The presence of CAV was evaluated by coronary angiography and analyzed with respect to pretransplant CMV-immunization and the presence and form of CMV infection, time of the infection (early infection, which was permanently cured within 6 months after HTx, or late with persistence of viremia or viral reactivation after the first 6 months). All patients received CMV-prophylaxis for three months. Results : CMV infection was detected in 31.7% of patients, of which 64% had asymptomatic viremia, 25% pneumonitis, 10% enterocolitis and 2.5% myocarditis. There was no difference in CMV seropositivity (91% of patients) compared to later CAV development (p = 0.551) and no effect on reduction of CMV infection after HTx (p=0.485). Significantly higher CAV incidence was associated with higher prevalence of CMV infection (p = 0.013), however early CMV infection had a lower prevalence of CAV than late. The number of viral copies by PCR did not correlate with CAV incidence. Patients with CMV infection did not have a shorter survival rate than CMV-negative patients (p = 0.384) or higher frequency of significant cellular rejection. Conclusion : Pretransplant CMV-seropositivity did not affect the ultimate number of CMV infections. CMV infection was confirmed as the trigger for later development of CAV, but it was not related to increased mortality. The number of viral copies was not significant in predicting CAV incidence, but late CMV infection showed higher importance in CAV development than early CMV infection. Despite the high prevalence of CMV infection in our patients (32%), no higher incidence of CAV has been demonstrated, possibly due to effective prophylaxis and thus shorter duration of viremia. The CMV infection did not prove to be the cause of the more frequent cellular graft rejection.

    Cardiologia Croatica
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    Cytomegalovirus infection after heart transplantation

    Extended Abstract
    Issue11-12
    Published
    Pages363
    PDF via DOIhttps://doi.org/10.15836/ccar2018.363
    heart transplantation
    cytomegalovirus infection
    cardiac allograft vasculopathy

    Authors

    Jana Ljubas Maček*ORCIDUniversity Hospital Centre Zagreb, Zagreb, Croatia
    Boško SkorićUniversity Hospital Centre Zagreb, Zagreb, Croatia
    Marijan PašalićORCIDUniversity Hospital Centre Zagreb, Zagreb, Croatia
    Daniel LovrićORCIDUniversity Hospital Centre Zagreb, Zagreb, Croatia
    Jure SamardžićORCIDUniversity Hospital Centre Zagreb, Zagreb, Croatia
    Maja ČikešORCIDUniversity Hospital Centre Zagreb, Zagreb, Croatia
    Hrvoje JurinORCIDUniversity Hospital Centre Zagreb, Zagreb, Croatia
    Ivo PlanincORCIDUniversity Hospital Centre Zagreb, Zagreb, Croatia
    Nina JakušORCIDUniversity Hospital Centre Zagreb, Zagreb, Croatia
    Dora FabijanovićORCIDUniversity Hospital Centre Zagreb, Zagreb, Croatia
    Hrvoje GašparovićORCIDUniversity Hospital Centre Zagreb, Zagreb, Croatia
    Davor MiličićORCIDUniversity Hospital Centre Zagreb, Zagreb, Croatia

    Full Text

    Introduction : Cytomegalovirus (CMV) infection is known as an external trigger for cardiac allograft vasculopathy (CAV), due to the mechanisms that stimulate graft immunogenicity. ( 1 , 2 ) The aim of the study was to investigate different aspects of CMV infection and their effect on the development of CAV and cellular rejection (CS) after heart transplantation (HTx). Patients and methods : 123 patients after HTx performed in the period from 2005 to 2016 were included, with regular CMV monitoring by PCR method. Follow-up was 3 years (IQR 2-6 years). The presence of CAV was evaluated by coronary angiography and analyzed with respect to pretransplant CMV-immunization and the presence and form of CMV infection, time of the infection (early infection, which was permanently cured within 6 months after HTx, or late with persistence of viremia or viral reactivation after the first 6 months). All patients received CMV-prophylaxis for three months. Results : CMV infection was detected in 31.7% of patients, of which 64% had asymptomatic viremia, 25% pneumonitis, 10% enterocolitis and 2.5% myocarditis. There was no difference in CMV seropositivity (91% of patients) compared to later CAV development (p = 0.551) and no effect on reduction of CMV infection after HTx (p=0.485). Significantly higher CAV incidence was associated with higher prevalence of CMV infection (p = 0.013), however early CMV infection had a lower prevalence of CAV than late. The number of viral copies by PCR did not correlate with CAV incidence. Patients with CMV infection did not have a shorter survival rate than CMV-negative patients (p = 0.384) or higher frequency of significant cellular rejection. Conclusion : Pretransplant CMV-seropositivity did not affect the ultimate number of CMV infections. CMV infection was confirmed as the trigger for later development of CAV, but it was not related to increased mortality. The number of viral copies was not significant in predicting CAV incidence, but late CMV infection showed higher importance in CAV development than early CMV infection. Despite the high prevalence of CMV infection in our patients (32%), no higher incidence of CAV has been demonstrated, possibly due to effective prophylaxis and thus shorter duration of viremia. The CMV infection did not prove to be the cause of the more frequent cellular graft rejection.