**3.1 Left ventricular hypertrophy**

Left ventricular hypertrophy is a well-known potent predictor of CV mortality in patients on renal replacement therapy (Ma et al., 1992). This may result either from pressure overload, causing increased tensile stress, or from volume overload, causing increased shear stres (Tomson, 2000). Recently published results demonstrated that even with good control of hypertension and anaemia, conventional hemodialysis is associated with significant left ventricular hypertrophy. And high prevalence of CV disease was positively associated with left ventricular hypertrophy in hemodialysis population.

In the study assessing the predictive markers of CV risk in asymptomatic hemodialysis patients, in total, 113 hemodialysis patients were included. Demographic, anthropometric, clinical, and laboratory data were collected. Silent myocardial damage was defined by elevated cardiac troponin I values above cutoff values. Cardiac troponin I concentrations were below cutoff value in 103 (91.2%) patients (group 1), whereas 10 (8.8%) patients (group 2) had elevated concentrations. Group 1 patients had higher levels of hemoglobin and highdensity lipoprotein cholesterol and lower C-reactive protein and tumor necrosis factor-alpha levels, as well as less incidence of left ventricular hypertrophy, when compared to group 2 patients. Diabetes mellitus, left ventricular hypertrophy, uncontrolled blood pressure, normalized protein equivalent of total nitrogen appearence, hemoglobin and tumor necrosis factor-alpha were found to be independently associated with silent myocardial damage (Afsar et al., 2009).

In hemodialysis patients without comorbidities, mean carotid intima-media thickness, which reflects generalized atherosclerosis and CV risk, was significantly greater in patients with left ventricular hypertrophy, than it was in patients without left ventricular hypertrophy. Mean carotid intima-media thickness in subjects in the heathy control group was significantly lower than it was in hemodialysis patients both with and without left ventricular hypertrophy. The mean serum cardiac troponin I level in the control group was significantly lower than it was in patients both with and without left ventricular hypertrophy. The mean serum cardiac troponin I level was significantly higher in patients with left ventricular hypertrophy than it was in those without left ventricular hypertrophy (Zumrutdal et al., 2005). The relationship between carotid artery intima-media thickness, serum cardiac troponin I levels and left ventricular hypertrophy may demonstrate that subclinical atherosclerotic changes and/or adaptation may occur along with cardiac alterations. So it may be reasonable to apply early strategies for prevention and treatment of left ventricular hypertrophy in hemodialysis patients before clinically evident CV disease.
