Introduction. Obesity is regarded as a risk factor contributing to the development of atherosclerosis. Cardio-Ankle Vascular Index (CAVI) quantifies arterial stiffness from the aortic arch to the distal arteries of the lower extremities potentially increased by atherosclerotic process and is therefore regarded as a measure of early atherosclerotic development. Surprisingly, most previous studies show a negative correlation between CAVI and the BMI (Body Mass Index). However, CAVI involves not only the structural changes in the vessel wall related to the ATS process, but also the functional stiffness – arterial vasomotor tone controlled by the sympathetic branch of autonomic nervous system. Vasodilation – a lower peripheral vascular resistance – observed in previous hemodynamic studies in obese subjects could explain the reduced CAVI in this patient population. The aim of our study was to compare CAVI values, peripheral vascular resistance (PVR) and sympathetic indices in obese adolescents and lean controls and to explain paradoxically decreased CAVI in obesity. Methods. We examined 30 obese (15f, age: 16.27 ± 2.8y, BMI: 33.03 ± 4.4kg.m-2) and 30 non-obese (15f, age: 16.31 ± 2.8y, BMI: 20.93 ± 2.3kg.m-2) gender and age matched adolescents. CAVI was measured using VaSera VS-1500 (Fukuda Denshi, Japan). At supine rest, we recorded continuously and non-invasively (300 beats long recordings) blood pressure by volume-clamp plethysmography (Finometer Pro, FMS, Netherlands) and impedance cardiography (ICG) measures (CardioScreen 2000, Medis GmbH, Germany). PVR was calculated as follows: PVR = 80*(median MBP/median CO); MBP – mean blood pressure from Finometer, CO – cardiac output from ICG. Sympathetic nervous system activity related indices included Velocity Index (VI) and Heather index (HI) from ICG reflecting myocardial contractility. The statistical analysis was performed using SYSTAT 13. Values are expressed as means ± SD and Kruskal-wallis test and Spearman correlation were used for the analysis. Results. As expected, significantly lower CAVI was found in obese group compared to control group (4.57 ± 0.87 vs. 5.19 ± 0.62, p = 0.001). PVR (850 ± 145 vs. 1112 ± 235 dyn.s/cm5, p < 0.001) and sympathetic nervous system activity indices VI (61.8 ± 17.5 vs. 88.7 ± 16.1 1/1000 s, p < 0.001) and HI (16.1 ± 5.2 vs. 21.4 6.5 ± Ω/s2, p = 0.002) were all significantly lower in obese group. In addition, we found positive correlation between CAVI and PVR (ρ = 0.386, p = 0.038) in the group of obese subjects. Conclusion. In accordance with recent studies, we observed lower CAVI in obese adolescents. This result could be at least partially attributed to the lower PVR observed in obese group related to lower sympathetic activity. Thus, lower CAVI values in obese patients may not mean the absence of atherosclerotic damage of the vessels and could lead to underestimation of the complications development in this high-risk patients.