Abstract
In patients with chronic kidney disease (CKD), reverse left ventricular (LV) remodelling, including reduction in LV mass, can be observed following long-term haemodialysis (HD) and has been attributed to regression of LV hypertrophy. However, LV mass can vary in response to changes in myocyte volume, edema, or fibrosis. The aims of this study were to investigate the acute changes in structural (myocardial mass and biventricular volumes) and tissue characterization parameters (native T1 and T2) following HD using cardiovascular magnetic resonance (CMR). Twenty-five stable HD patients underwent non-contrast CMR including volumetric assessment and native T1 and T2 mapping immediately pre- and post-HD. The mean time between the first and second scan was 9.1 ± 1.1 hours and mean time from completion of dialysis to the second scan was 3.5 ± 1.3 hours. Post-HD, there was reduction in LV mass (pre-dialysis 98.9 ± 36.9 g/m2 vs post-dialysis 93.3 ± 35.8 g/m2, p = 0.003), which correlated with change in body weight (r = 0.717, p < 0.001). Both native T1 and T2 reduced significantly following HD (Native T1: pre-dialysis 1085 ± 43 ms, post-dialysis 1072 ± 43 ms; T2: pre-dialysis 53.3 ± 3.0 ms, post-dialysis 51.8 ± 3.1 ms, both p < 0.05). These changes presumably reflect acute reduction in myocardial water content rather than regression of LV hypertrophy. CMR with multiparametric mapping is a promising tool to assess the cardiac changes associated with HD.
Highlights
Patients with end-stage renal failure (ESRF) have increased risk of cardiovascular morbidity and mortality, and around 50% of all deaths in patients on haemodialysis (HD) are due to cardiovascular disease[1]
It has been suggested that increased afterload and preload in patients with chronic kidney disease (CKD) results in myocardial fibrosis and myocyte cell hypertrophy, and that regression in Left ventricular hypertrophy (LVH) following chronic HD is due to reduction in both fibrosis and myocyte cell volume[8]
Cardiovascular magnetic resonance (CMR) with late gadolinium enhancement is uniquely informative for the detection and quantification of myocardial fibrosis in a variety of conditions but the use of gadolinium contrast in patients with ESRF is constrained by concerns about the risk of nephrogenic systemic fibrosis[12]
Summary
Patients with end-stage renal failure (ESRF) have increased risk of cardiovascular morbidity and mortality, and around 50% of all deaths in patients on haemodialysis (HD) are due to cardiovascular disease[1]. It has been suggested that increased afterload and preload in patients with chronic kidney disease (CKD) results in myocardial fibrosis and myocyte cell hypertrophy, and that regression in LVH following chronic HD is due to reduction in both fibrosis and myocyte cell volume[8]. Cardiovascular magnetic resonance (CMR) is established as the gold standard for quantification of ventricular volumes, mass and function[11] but it can provide unique information on tissue composition. CMR with late gadolinium enhancement is uniquely informative for the detection and quantification of myocardial fibrosis in a variety of conditions but the use of gadolinium contrast in patients with ESRF is constrained by concerns about the risk of nephrogenic systemic fibrosis[12]. The aims of this study were (1) To assess the changes in myocardial volumes and mass pre- and post-HD and (2) To assess the changes in native T1 and myocardial T2 pre- and post-HD
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