2.1.1. Left Ventricular Cardiomyopathy

LV hypertrophy is the most frequent cardiac finding in dialysis patients, and it is almost universal [8]. The prevalence of LVH is estimated to be between 16% and 31% in individuals with GFR >30 mL/min; it rises to 60%–75% before renal replacement therapy initiation and increases up to 90% after the dialysis initiation [10]. It is related to chronic volume and pressure overload, neurohormonal activation, and uremic toxin accumulation [11]. The pathophysiological factors involved in LVH of CKD patients are (1) related to afterload, (2) related to preload, and (3) not related to afterload or preload [5,12–14]. The ones in the first group give a picture of an increase in systemic arterial resistance, elevated arterial blood pressure, and reduced large-vessel compliance [11–14] partially correlated to aortic 'calcification', which is specific in CKD patients. LV hypertrophy is a compensatory response that acts to maintain wall stress in the course of long-term loading conditions, where all these factors lead to myocardial cell thickening and concentric LV remodeling. Among the preload-related factors, the role of intravascular volume expansion (salt and fluid retention), secondary anemia, and the presence of arteriovenous fistulas which result in myocardial cell lengthening and eccentric or asymmetric LV remodeling need to be underlined. Both afterload and preload-related factors act with additive and/or synergistic effects. It is suggested that fluid overload and increased arterial stiffness play a role in LVH even before the start of dialysis therapy [15]. Arteriosclerosis, being a hallmark of arterial remodeling in ESRD, is characterized by diffuse calcification in combination with dilatation, and an increased wall thickness of the medial layer of the aorta and its main branches which drives increased arterial stiffness [11,16,17]. Here, LVH happens regardless of the effective control of hypertension. Blood pressure independent LVH also occurs in diabetics with known diabetic nephropathy [18].

Hypertrophied hearts have reduced coronary blood flow reserve and are at increased risk for myocardial ischemia [19]. The coexistence of left atrial enlargement is common, and atrial fibrillation occurs frequently. Eventually, continuing LV load can promote structural changes in the LV, apoptosis of cardiomyocytes, and triggers metabolic pathways able to increase the extracellular matrix production up to fibrosis [9,10,20,21].
