“…ILVM has been attributed to an increase in body size, adverse metabolic profile or to the presence of myocardial fibrosis as a consequence of different stimuli such as hyperactivation of the reninangiotensin-aldosterone system, growth factors, inflammation or chronic myocardial ischemia [16,18]. We reported that among dialysis patients, those undergoing HD displayed an increased prevalence of ILVM and this finding was strongly associated with lower myocardial function as well as reduced afterload-independent LV systolic chamber function [19]. Indeed LV dysfunction, identified by stress-corrected midwall shortening, was largely increased in HD patients compared to PD group and healthy controls.…”