#5621 BENEFICIAL EFFECTS OF CHRONIC INTRADIALYTIC EXERCISE TRAINING ON HEMODIALYSIS-INDUCED-MYOCARDIAL STUNNING

Abstract

Abstract Background and Aims Hemodialysis (HD) induces left ventricular (LV) segmental regional wall motion abnormalities (RWMAs) due to hypoperfusion, leading to acute LV transient dysfunction, well known as myocardial stunning. Repeated episodes of HD-related myocardial stunning contribute directly to the development of heart failure and increased mortality in patients receiving HD (Burton et al., 2009). Exercise training exert pleiotropic favorable effects on the cardiovascular system. No study has however investigated its impact on the kinetics of regional myocardial function during HD. This study aims to evaluate the effect of intradialytic exercise (IDE) on RWMAs compared with standard care. Method This was a prospective, open-label, two-center trial (clinicaltrials.gov NCT04697459) with two parallel groups: 31 patients (ENT) undergoing a 4-month IDE program (30min of cycling + 30min of resistance training starting 30 min after HD onset) and 21 patients continuing usual care (CTRL). Untrained adults, aged 20-79 years, undertaking maintenance HD for >3 months were eligible to participate. Exclusion criteria were poor echogenicity, contraindication to exercise, orthopedic complications, severe heart (ischemic, valvular, ...), vascular or respiratory diseases, ejection fraction <45% and body mass index >35. Longitudinal strain (LS) using speckle-tracking echocardiography were measured during a standard HD session, just before HD onset (HDT0) and at peak stress of HD (30 min before HD-ending, HDPeak). The same procedure was used before and after 4-months of IDE or usual care. LS from a 18 LV segment model were used to assess the presence of HD-induced RWMAs, defined as a ≥20% reduction in LS at peak stress compared to baseline. A generalized linear mixed model (Poisson model) was used to analyze the effect of IDE on RWMAs. Results After 4 months of IDE, we observed a significant reduction of RWMAs at HDPeak (mean before: 6.03±3.19 vs after: 4.55±2.26; point estimate: -1.48, 95% confident interval CI: -0.39/-2.57, p = 0.03), whereas its occurrence remained unchanged in CTRL (mean before: 6.14±3.51 vs after: 6.09±3.16; point estimate: -0.05; 95% CI: 1.45/-1.54, p = 0.96). There was also evidence that IDE program significantly attenuated the decline of global LS observed during HD (before: 2.11±2.39% vs after: 1.10±1.95%; point estimate: -1.01%; 95% CI: -1.86/-0.13, p = 0.02) compared to the similar impairment in CTRL (before: 1.60±2.30% vs after: 1.79±2.08%; point estimate: +0.18%; 95% CI: +1.20/-0.85 p = 0.72). Conclusion There is clear evidence that chronic IDE is cardioprotective. Identifying the underlying mechanisms responsible for exercise-induced cardioprotection was beyond the scope of our study, but we can reasonably assume that structural and/or functional changes in the coronary arteries, especially in microcirculatory territories (i.e. increased collateral circulation due to angiogenesis/arteriogenesis, improved endothelial function, reduced blood viscosity) and/or intrinsic changes in the cardiac myocyte (reduced fibrosis, enhanced calcium handling/sensitivity, altered mitochondrial turnover and phenotype), related among others to reduced oxidative stress and/or inflammation, might play a role (Powers et al 2014). Whether our results translate to longer-term reduction in clinical outcomes and cardiovascular mortality in end-stage renal disease patients require further studies.