Abstract
Increased native myocardial T1 times in chronic kidney disease (CKD) may be due to diffuse interstitial myocardial fibrosis (DIF) or due to interstitial edema/inflammation. Concerns relating to nephrogenic systemic fibrosis with gadolinium-based contrast agents (GBCA) limit their use in end-stage kidney disease (ESKD) to measure extracellular volume (ECV) and characterise myocardial fibrosis. This study aimed to examine stability of myocardial T1 and T2 times before, and within 2 months after kidney transplantation; a time frame when volume status normalises but myocardial remodelling is unlikely to have occurred, and to compare these with ECV using GBCA after transplantation. Twenty-four patients with ESKD underwent serial cardiovascular magnetic resonance imaging, including T1 and T2 mapping. GBCA was administered on follow-up provided eGFR was >30 ml/min/1.73 m2. Eighteen age- and sex-matched controls were studied at one timepoint. ECV (ECV 28 ± 2% vs. 24 ± 2%, p = 0.001) and T2 times were higher in ESKD compared to controls. After transplantation, septal T1 times increased (MOLLI 985 ms ± 25 vs. 1002 ms ± 30, p = 0.014; ShMOLLI 974 ms ± 39 vs. 992 ms ± 33, p = 0.113), LV volumes reduced (LVEDvol indexed 79 ± 24 vs. 63 ± 20 ml/m2, p = 0.005) but LV mass was unchanged (LV mass index 89 g/m2 ± 38 to 83 g/m2 ± 23, p = 0.141). T2 times did not change after transplantation. Both ECV and myocardial T1 times are elevated in ESKD, supporting the theory that elevated T1 times are due to DIF, although a contribution from myocardial edema cannot be fully excluded. The lack of any fall in T1 or T2 times after transplantation suggests that myocardial T1 times are a stable measure of DIF in CKD.
Highlights
Cardiovascular (CV) disease is the leading cause of mortality in patients with chronic kidney disease (CKD)
Eleven patients were on hemodialysis prior to transplantation, three were on peritoneal dialysis, and ten underwent pre-emptive kidney transplantation
There was no difference in LV volumes at baseline between the CKD cohort and healthy controls, but LV mass was higher in end-stage kidney disease (ESKD)
Summary
Cardiovascular (CV) disease is the leading cause of mortality in patients with chronic kidney disease (CKD). Most of the excess CV mortality in patients with end-stage kidney disease (ESKD) arises from heart failure, arrhythmia and sudden cardiac death rather than atherothrombotic events such as myocardial infarction; these events are thought to be attributable to uremic cardiomyopathy (UC) [1]. Histological and imaging studies have shown that this specific heart muscle disease is characterised by left ventricular hypertrophy (LVH). ☆ Clinical trials registration - URL: https://clinicaltrials.gov. ⁎ Corresponding author at: 1st Floor Nuffield House, Department of Cardiology, Mendelsohn Way, Queen Elizabeth Hospital Birmingham, B15 2TH, United Kingdom of Great Britain and Northern Ireland
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