Early effects of kidney transplantation on the heart - A cardiac magnetic resonance multi-parametric study

Research output: Contribution to journalArticlepeer-review

Standard

Early effects of kidney transplantation on the heart - A cardiac magnetic resonance multi-parametric study. / Hayer, Manvir K; Radhakrishnan, Ashwin; Price, Anna M; Baig, Shanat; Liu, Boyang; Ferro, Charles J; Captur, Gabriella; Townend, Jonathan N; Moon, James C; Edwards, Nicola C; Steeds, Richard P.

In: International Journal of Cardiology, Vol. 293, 15.10.2019, p. 272-277.

Research output: Contribution to journalArticlepeer-review

Harvard

APA

Vancouver

Author

Bibtex

@article{5f0e6cd32188434aad07c746deccd518,
title = "Early effects of kidney transplantation on the heart - A cardiac magnetic resonance multi-parametric study",
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.",
keywords = "myocardial fibrosis, uremic cardiomyopathy, kidney transplantation, multiparametric T1/T2 mapping, Myocardial fibrosis, Multiparametric T1/T2 mapping, Uremic cardiomyopathy, Kidney transplantation",
author = "Hayer, {Manvir K} and Ashwin Radhakrishnan and Price, {Anna M} and Shanat Baig and Boyang Liu and Ferro, {Charles J} and Gabriella Captur and Townend, {Jonathan N} and Moon, {James C} and Edwards, {Nicola C} and Steeds, {Richard P}",
year = "2019",
month = oct,
day = "15",
doi = "10.1016/j.ijcard.2019.06.007",
language = "English",
volume = "293",
pages = "272--277",
journal = "International Journal of Cardiology",
issn = "0167-5273",
publisher = "Elsevier",

}

RIS

TY - JOUR

T1 - Early effects of kidney transplantation on the heart - A cardiac magnetic resonance multi-parametric study

AU - Hayer, Manvir K

AU - Radhakrishnan, Ashwin

AU - Price, Anna M

AU - Baig, Shanat

AU - Liu, Boyang

AU - Ferro, Charles J

AU - Captur, Gabriella

AU - Townend, Jonathan N

AU - Moon, James C

AU - Edwards, Nicola C

AU - Steeds, Richard P

PY - 2019/10/15

Y1 - 2019/10/15

N2 - 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.

AB - 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.

KW - myocardial fibrosis

KW - uremic cardiomyopathy

KW - kidney transplantation

KW - multiparametric T1/T2 mapping

KW - Myocardial fibrosis

KW - Multiparametric T1/T2 mapping

KW - Uremic cardiomyopathy

KW - Kidney transplantation

UR - http://www.scopus.com/inward/record.url?scp=85068122635&partnerID=8YFLogxK

U2 - 10.1016/j.ijcard.2019.06.007

DO - 10.1016/j.ijcard.2019.06.007

M3 - Article

C2 - 31272740

VL - 293

SP - 272

EP - 277

JO - International Journal of Cardiology

JF - International Journal of Cardiology

SN - 0167-5273

ER -