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. 2020 Nov;13(11):2357-2367.
doi: 10.1016/j.jcmg.2020.04.021. Epub 2020 Jul 15.

Defining Myocardial Abnormalities Across the Stages of Chronic Kidney Disease: A Cardiac Magnetic Resonance Imaging Study

Manvir K Hayer  1 , Ashwin Radhakrishnan  2 , Anna M Price  1 , Boyang Liu  2 , Shanat Baig  2 , Christopher J Weston  3 , Luca Biasiolli  4 , Charles J Ferro  1 , Jonathan N Townend  2 , Richard P Steeds  2 , Nicola C Edwards  5 ; Birmingham Cardio-Renal Group
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Defining Myocardial Abnormalities Across the Stages of Chronic Kidney Disease: A Cardiac Magnetic Resonance Imaging Study

Manvir K Hayer et al. JACC Cardiovasc Imaging. 2020 Nov.

Abstract

Objectives: A proof of concept cross-sectional study investigating changes in myocardial abnormalities across stages of chronic kidney disease (CKD). Characterizing noninvasive markers of myocardial fibrosis on cardiac magnetic resonance, echocardiography, and correlating with biomarkers of fibrosis, myocardial injury, and functional correlates including exercise tolerance.

Background: CKD is associated with an increased risk of cardiovascular death. Much of the excess mortality is attributed to uremic cardiomyopathy, defined by increased left ventricular hypertrophy, myocardial dysfunction, and fibrosis. The prevalence of these abnormalities across stages of CKD and their impact on cardiovascular performance is unknown.

Methods: A total of 134 nondiabetic, pre-dialysis subjects with CKD stages 2 to 5 without myocardial ischemia underwent cardiac magnetic resonance (1.5-T) including; T1 mapping (biomarker of diffuse fibrosis), T2 mapping (edema), late gadolinium enhancement, and assessment of aortic distensibility. Serum biomarkers including collagen turnover (P1NP, P3NP), troponin T, and N-terminal pro-B-type natriuretic peptide were measured. Cardiovascular performance was quantified by bicycle cardiopulmonary exercise testing and echocardiography.

Results: Native myocardial T1 times increased incrementally from stage 2 to 5 (966 ± 21 ms vs. 994 ± 33 ms; p < 0.001), independent of hypertension and aortic distensibility. Left atrial volume, E/e', N-terminal pro-B-type natriuretic peptide, P1NP, and P3NP increased with CKD stage (p < 0.05), while effort tolerance (% predicted VO2Peak, %VO2VT) decreased (p < 0.001). In multivariable linear regression models, estimated glomerular filtration rate was the strongest predictor of native myocardial T1 time (p < 0.001). Native myocardial T1 time, left atrial dilatation, and high-sensitivity troponin T were independent predictors of % predicted VO2Peak (p < 0.001).

Conclusions: Imaging and serum biomarkers of myocardial fibrosis increase with advancing CKD independent of effects of left ventricular afterload and might be a key intermediary in the development of uremic cardiomyopathy. Further studies are needed to determine whether these changes lead to the increased rates of heart failure and death in CKD. (Left Ventricular Fibrosis in Chronic Kidney Disease [FibroCKD]; NCT03176862).

Keywords: T(1) mapping; myocardial fibrosis; uremic cardiomyopathy.

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Conflict of interest statement

Author Relationship With Industry This study is supported by the British Heart Foundation (PG/15/117/31961). Dr. Weston is funded by the National Institute for Health Research (NIHR) Birmingham Biomedical Research Centre at the University Hospitals Birmingham NHS Foundation Trust and the University of Birmingham. All other authors have reported that they have no relationships relevant to the contents of this paper. This paper presents independent research supported by the NIHR Birmingham Biomedical Research Centre at the University Hospitals Birmingham NHS Foundation Trust and the University of Birmingham. The views expressed are those of the author(s) and not necessarily those of the NHS, the NIHR, or the Department of Health and Social Care.

Figures

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Graphical abstract
Central Illustration
Central Illustration
A Conceptual Overview of Myocardial Abnormalities Across the Spectrum of Chronic Kidney Disease Native myocardial T1 times increased with worsening stage of chronic kidney disease (CKD) and were accompanied by a rise in serum biomarkers of fibrosis and heart failure. Left ventricular (LV) mass only increased in severe CKD.
Figure 1
Figure 1
Trend in Myocardial Native T1 Times, LV Mass, Exercise and Echo-Based Global Longitudinal Strain Across the Stages of CKD The p values are derived from the Jonckheere Terpstra test for trend. The maximum height of the whisker is 1.5 times the interquartile range. CKD = chronic kidney disease; LV = left ventricular.
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