Time-dependent cardiac structural and functional changes after kidney transplantation: a multi-parametric cardiac magnetic resonance study.

Objectives: To map time-dependent cardiac structural and functional change patterns after renal transplantation (KT) using cardiac magnetic resonance (CMR). Methods: Fifty-three patients with pre-KT and post-KT CMR exams were retrospectively analyzed. Patients were divided into three groups according to the time of post-KT CMR: group 1 (3 months post-KT, n = 16), group 2 (6 months post-KT, n = 21), and group 3 (over 9 months post-KT, n = 16). Twenty-one age- and sex-matched healthy controls (HC) were recruited for the study. CMR-derived left ventricular (LV) volumes, LV mass index (LVMi), LV ejection fraction (LVEF), global radial strain (GRS), global circumferential strain (GCS), global longitudinal strain (GLS), and native T1 value were compared. The association between the changes of CMR parameters was assessed. Results: LVMi post-KT decreased in groups 2 (p < 0.001) and 3 (p = 0.004) but both groups had higher LVMi values compared to HC (both p < 0.001). GLS post-KT was decreased in group 1 (p = 0.021), but slightly increased in group 2 (p = 0.728) and group 3 (p = 0.100) without significant difference. GLS post-KT in group 3 was not different from HC (p = 0.104). LVEF, GRS, and GCS post-KT in groups 2 and 3 significantly increased and showed no significant difference from HC. The post-KT native T1 value in all three groups significantly decreased; however, no group showed any significant difference from HC. The change of LVEF was associated with the change of GCS, GRS, and GLS. Conclusions: Although GRS, GCS, GLS, and native T1 values reversed to normal level, LVMi remained impaired in median 14 months after KT. Key Points: • Kidney transplantation has favorable effects on cardiac structure and function. • In a median 14 months of follow-up after KT, left ventricle strain and native T1 value reversed to normal level while LV mass index (LVMi) did not. Left ventricular hypertrophy may help to explain why KT recipients are still at increased cardiovascular risk. • The reason for the decrease of native T1 value after KT may be more than myocardial fibrosis and needs to be further studied. [ABSTRACT FROM AUTHOR]