Serum levels of cardiac troponin I (cTnI) are frequently measured in the evaluation of potential heart donors. However, the utility of cTnI levels for predicting recipient outcomes remains controversial. This study was performed to determine whether donor cardiac cTnI levels exceeding 1.0 microg/liter are associated with adverse recipient outcomes.All donors managed by the California Transplant Donor Network between January 2001 and July 2002 with consent for donor evaluation and at least 1 measured cTnI level were included in the study if 1-year recipient mortality data were available. Each study subject was classified as having elevated cTnI if any level exceeded 1.0 microg/liter. Donor variables, recipient risk of 30-day and 1-year mortality, and recipient need for mechanical circulatory support were compared between the 2 groups.A total of 263 potential donors were evaluated, and 98 had elevated cTnI levels. Of these potential donors, 139 were accepted for transplantation. The cTnI levels were normal in 96 and elevated in 43. Most donors (77%) with elevated cTnI levels had levels of less than 10 microg/liter. Donor cardiopulmonary resuscitation was associated with cTnI elevations. Donors with elevated cTnI levels did not require higher doses of inotropic drugs before transplantation and had similar hemodynamic profiles compared with donors with normal cTnI levels. Although there was a trend towards longer post-transplant hospitalization in recipients of grafts from donors with elevated cTnI levels (17 days vs 15 days, p = 0.044), there was no significant difference in the recipient need for mechanical circulatory support or 30-day and 1-year mortality between the 2 groups.In this study, a modestly elevated donor cTnI was not associated with a higher risk of recipient mortality or need for post-transplant mechanical circulatory support. A potential donor heart should not be discarded solely because the troponin level is elevated.
View details for DOI 10.1016/j.healun.2007.07.026
View details for Web of Science ID 000250268900013
View details for PubMedID 17919626