Pulse Wave Velocity as a Marker of Vascular Dysfunction and Its Correlation with Cardiac Disease in Children with End-Stage Renal Disease (ESRD)

Figure 1. Schematical representation of the references used in the calculation of PWV (X—aortic valve level; Y—ascending aorta, 2 cm above the valve; Z—diaphragm level; L1 = distance from X to Y (2 cm), L2 = distance from X to Z (from the aortic valve to the diaphragm) = 1.7 cm + 0.1 × height (cm). PWV (ascending aorta) = L1/ΔT1, PWV (descending aorta) = L2/ΔT2.

Figure 2. Measurement of ΔT1 (T1-T0 = 85 − 81 = 4 msec) in the ascending aorta (echocardiography—apical window 5C) (A,B).

Figure 3. Measurement of ΔT2 (T2-T1 = 116 − 95 = 21 ms) in the descending aorta—echocardiography 5C apical window (A) and subcostal view (B).

Figure 4. (A) Measurement of the LV wall thickness by 2D echocardiography, parasternal long-axis view (14-year-old patient from the study sample); (B)—calculation of the LVMI for the same patient (LVMI = 170 g/m2—severe concentric LVH).

Figure 5. Violin plot of PWV values in the AscAo and DescAo, in groups with LVH with vascular stiffness (VS) and without vascular stiffness, by two-way ANOVA. p < 0.001, (***), p < 0.0001 (****).

Figure 6. Distribution of increased PWV depending on location in the aorta (vascular dysfunction group).

Figure 7. (A,B) Correlation between LVH type in patients without vascular impairment (A) and patients with vascular impairment (B).

Figure 8. (A,B) Severity of LVH in patients without vascular impairment (A) compared to patients with vascular impairment (B).