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Risk factors for Chagas' disease reactivation after heart transplantation
Sílvia V Campos1, Tânia Mara V Strabelli, Vicente Amato Neto
1Department of Infectious and Parasitic Diseases, University of São Paulo Medical School, São Paulo, Brazil. silviavcampos@uol.com.br
Insights
Reactivation of Chagas' disease after heart transplantation is linked to increased immunosuppression, specifically from rejection episodes and neoplasms. Early diagnosis and preemptive therapy are crucial for managing this risk.
Area of Science:
- Cardiology
- Infectious Diseases
- Transplantation Immunology
Background:
- Chagas' disease, caused by Trypanosoma cruzi, remains endemic in Latin America.
- Heart transplantation is a vital option for end-stage Chagas' cardiomyopathy.
- Post-transplant reactivation of Chagas' disease can lead to severe complications.
Purpose of the Study:
- To identify risk factors for Chagas' disease reactivation after heart transplantation.
- To understand the determinants of post-transplant Chagas' disease reactivation.
Main Methods:
- Retrospective cohort study of heart transplant recipients with Chagas' disease (1985-2004).
- Review of clinical, microbiologic, and histopathologic data.
- Statistical analysis using SPSS software.
Main Results:
- 17 out of 64 patients (26.5%) experienced Chagas' disease reactivation.
- Independent risk factors for reactivation included multiple rejection episodes, development of neoplasms, and use of mycophenolate mofetil.
- Age, gender, cytomegalovirus infection, and mortality did not show significant association.
Conclusions:
- Increased immunosuppression, indicated by rejection episodes and neoplasms, elevates the risk of Chagas' disease reactivation.
- Physicians should be vigilant for early diagnosis and consider preemptive treatment.
- While reactivation causes significant morbidity, mortality risk is low.
Background:
Chagas' disease is the illness caused by the protozoan Trypanosoma cruzi and it is still endemic in Latin America. Heart transplantation is a therapeutic option for patients with end-stage Chagas' cardiomyopathy. Nevertheless, reactivation may occur after transplantation, leading to higher morbidity and graft dysfunction. This study aimed to identify risk factors for Chagas' disease reactivation episodes.
Methods:
This investigation is a retrospective cohort study of all Chagas' disease heart transplant recipients from September 1985 through September 2004. Clinical, microbiologic and histopathologic data were reviewed. Statistical analysis was performed with SPSS (version 13) software.
Results:
Sixty-four (21.9%) patients with chronic Chagas' disease underwent heart transplantation during the study period. Seventeen patients (26.5%) had at least one episode of Chagas' disease reactivation, and univariate analysis identified number of rejection episodes (p = 0.013) and development of neoplasms (p = 0.040) as factors associated with Chagas' disease reactivation episodes. Multivariate analysis showed that number of rejection episodes (hazard ratio = 1.31; 95% confidence interval [CI]: 1.06 to 1.62; p = 0.011), neoplasms (hazard ratio = 5.07; 95% CI: 1.49 to 17.20; p = 0.009) and use of mycophenolate mofetil (hazard ratio = 3.14; 95% CI: 1.00 to 9.84; p = 0.049) are independent determinants for reactivation after transplantation. Age (p = 0.88), male gender (p = 0.15), presence of rejection (p = 0.17), cytomegalovirus infection (p = 0.79) and mortality after hospital discharge (p = 0.15) showed no statistically significant difference.
Conclusions:
Our data suggest that events resulting in greater immunosuppression status contribute to Chagas' disease reactivation episodes after heart transplantation and should alert physicians to make an early diagnosis and perform pre-emptive therapy. Although reactivation led to a high rate of morbidity, a low mortality risk was observed.
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