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Pre-Transplant Toxoplasma gondiiSeropositivity Among Heart Transplant Recipients Is Associated With an Increased Risk of All-Cause and Cardiac Mortality

Authors :
A.K. Andreassen
Odd Geiran
Svein Simonsen
S. Arora
Lars Gullestad
Halvor Rollag
Pål A. Jenum
Pål Aukrust
E. Gude
Arnt E. Fiane
Source :
Journal of the American College of Cardiology. 50:1967-1972
Publication Year :
2007
Publisher :
Elsevier BV, 2007.

Abstract

Objectives We evaluated the risk of mortality, development of cardiac allograft vasculopathy (CAV), and acute cellular rejection among Toxoplasma gondii (T. gondii ) seropositive heart transplant (HTx) recipients and the 4 donor/recipient seropairing groups. Background Chronic T. gondii infection is known to trigger potentially adverse immunoregulatory changes, but the long-term implication for HTx recipients has not been assessed previously. Methods Frozen pre-HTx serum samples of 288 recipients and 246 donors were evaluated for T. gondii serostatus using Platelia immunoglobulin G immunoassay. Patients had undergone prospective serotesting using alternative assays, and results determined by the 2 methods were compared. Data regarding mortality, CAV, and acute cellular rejection were available for all patients. Results Overall, 211 recipients (73%) were seronegative and 77 (27%) were seropositive. In total, 82 recipients died, 76 developed CAV, and 82 had 1 or more episode of treated cellular rejection. Recipient seropositivity was associated with a significantly higher risk of all-cause (hazard ratio [HR] 1.9, 95% confidence interval [CI] 1.1 to 3.4; p = 0.02) and CAV mortality (HR 4.4, 95% CI 1.3 to 15.6; p = 0.02) and a higher risk of developing advanced CAV (HR 2.7, 95% CI 1.2 to 5.8; p = 0.01). Seropositivity did not influence the number of rejection episodes, and donor/recipient seropairing was not a risk factor for any end point. Conclusions T. gondii seropositivity among HTx recipients is associated with an increased risk of all-cause and CAV mortality and of development of advanced CAV. This may be mediated via immunoregulatory changes triggered by chronic T. gondii infection and needs to be explored further.

Details

ISSN :
07351097
Volume :
50
Database :
OpenAIRE
Journal :
Journal of the American College of Cardiology
Accession number :
edsair.doi.dedup.....a5d4e609cde99607e142eb97fe7534f5
Full Text :
https://doi.org/10.1016/j.jacc.2007.07.068