Imaging of Myocardial Fibrosis in Patients with End-Stage Renal Disease: Current Limitations and Future Possibilities.

M P M Graham-Brown,D J Stensel,J O Burton,D S March,J Mcadam,A S Patel,A.-M Marsh,G P Mccann

doi:10.1155/2017/5453606

Abstract

Cardiovascular disease in patients with end-stage renal disease (ESRD) is driven by a different set of processes than in the general population. These processes lead to pathological changes in cardiac structure and function that include the development of left ventricular hypertrophy and left ventricular dilatation and the development of myocardial fibrosis. Reduction in left ventricular hypertrophy has been the established goal of many interventional trials in patients with chronic kidney disease, but a recent systematic review has questioned whether reduction of left ventricular hypertrophy improves cardiovascular mortality as previously thought. The development of novel imaging biomarkers that link to cardiovascular outcomes and that are specific to the disease processes in ESRD is therefore required. Postmortem studies of patients with ESRD on hemodialysis have shown that the extent of myocardial fibrosis is strongly linked to cardiovascular death and accurate imaging of myocardial fibrosis would be an attractive target as an imaging biomarker. In this article we will discuss the current imaging methods available to measure myocardial fibrosis in patients with ESRD, the reliability of the techniques, specific challenges and important limitations in patients with ESRD, and how to further develop the techniques we have so they are sufficiently robust for use in future clinical trials.

Highlights

Patients with end-stage renal disease (ESRD) are at significantly increased risk of cardiovascular death compared to age-matched peers [1]
The pathophysiological processes that drive cardiovascular disease (CVD) in patients with ESRD are different to those that drive classical atherosclerotic CVD and include chronic inflammation, increased arterial stiffness, autonomic instability, and sympathetic overactivity. These factors lead to the development of changes in cardiac structure and function including left ventricular hypertrophy (LVH), left ventricular (LV) dilatation, diffuse myocardial fibrosis (DMF), and replacement fibrosis [5]
Peak global radial and circumferential strain was reduced and correlated with interstitial fibrosis (PCC of 0.701 and 0.678, resp.) on histological examination In ESRD patients, mean (±standard deviation) global longitudinal peak systolic was significantly reduced in comparison to healthy subjects

Summary

Introduction

Patients with end-stage renal disease (ESRD) are at significantly increased risk of cardiovascular death compared to age-matched peers [1]. The US Renal Data System reports that “cardiac death, cause unknown” and arrhythmia account for 25% of all deaths amongst hemodialysis (HD) patients, at an event rate of 90–200/1000 patient years [2] These excessive rates of cardiovascular disease (CVD) are unexplained by traditional risk factors [3] and strategies to improve CVD related outcomes, such as coronary artery revascularization, do not improve outcomes for patients on HD [4]. The pathophysiological processes that drive CVD in patients with ESRD are different to those that drive classical atherosclerotic CVD and include chronic inflammation, increased arterial stiffness, autonomic instability, and sympathetic overactivity These factors lead to the development of changes in cardiac structure and function including left ventricular hypertrophy (LVH), left ventricular (LV) dilatation, diffuse myocardial fibrosis (DMF), and replacement fibrosis (myocardial scarring) [5]. Levels of MF were more severe in patients on dialysis, progressed over time to replacement

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