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Background and objective: The development of arterial stiffness (AS) in obesity is a multifactorial and complex process. The pleomorphic actions of adipokines and their local activity in perivascular adipose tissue (PVAT) are potential modulators of AS appearance and progression. We aimed to assess the correlations between two adipokines (chemerin, adiponectin), PVAT morphological changes (adipocyte size, blood vessel wall thickness) and AS parameters in the special subgroup of patients with morbid obesity. Material and methods: We enrolled 25 patients with morbid obesity and 25 non-obese patients, who were age- and gender-matched, untreated for cardiovascular risk factors, and admitted to hospital for laparoscopic surgical procedures (bariatric surgery for morbid obesity and non-inflammatory benign pathology surgery for non-obese patients). Before the surgical procedures, we evaluated demographic and anthropometric data and biochemical parameters including the studied adipokines. Arterial stiffness was evaluated using a Medexpert ArteriographTM TL2 device. In both groups, adipocyte size and vascular wall thickness as well as local adiponectin activity were analyzed in PVAT from intraoperative biopsies. Results: In our study, adiponectin (p = 0.0003), chemerin (p = 0.0001) and their ratio (p = 0.005) had statistically significant higher mean values in patients with morbid obesity compared to normal-weight patients. In patients with morbid obesity there were significant correlations between chemerin and AS parameters such as aortic pulse wave velocity (p = 0.006) and subendocardial viability index (p = 0.009). In the same group adipocyte size was significantly correlated with another AS parameter, namely, aortic systolic blood pressure (p = 0.030). In normal-weight patients, blood vessel wall thickness positively correlated with AS parameters such as brachial (p = 0.023) and aortic augmentation index (p = 0.023). An important finding was the negative adipoR1 and adipoR2 immunoexpression in PVAT adipocytes of patients with morbid obesity. Additionally, we found significant correlations between blood vessel wall thickness and blood fasting glucose (p < 0.05) in both groups. Conclusions: Chemerin and adipocyte size could be predictive biomarkers for AS in patients with morbid obesity. Given the small number of patients included, our results need further validation.

Background and objective: Morbid obesity is accompanied by an increased cardiovascular (CV) risk, which justifies a multidisciplinary, integrative approach. Arterial stiffness has a well-defined additional role in refining individual CV risk. Given that echocardiography and carotid ultrasound are usual methods for CV risk characterization, we aimed to identify the imaging parameters with a predictive value for early-onset arterial stiffness. Material and methods: We conducted a study in which 50 patients (divided into two equal groups with morbid obesity and without obesity), age and gender matched, untreated for cardiovascular risk factors, were addressed to bariatric surgery or non-inflammatory benign pathology surgery. Before the surgical procedures, we evaluated demographics, anthropometric data and biochemical parameters including adipokines (chemerin, adiponectin). Arterial stiffness was evaluated using the Medexpert ArteriographTM TL2 device. Transthoracic echocardiography and carotid ultrasound were also performed. We also analyzed adipocyte size and vascular wall thickness in intraoperative biopsies. Results: Left ventricle (LV) mass index (p = 0.2851), LV ejection fraction (LVEF) (p = 0.0073), epicardial adipose tissue thickness (p = 0.0001) as echocardiographic parameters and carotid intima–media thickness (p = 0.0033), relative wall thickness (p = 0.0295), wall to lumen thickness ratio (p = 0.0930) and carotid cross-sectional area (p = 0.0042) as ultrasound parameters were significant measures in our groups and were assessed in relation to adipocyte size, blood vessel wall thickness and adipokines serum levels. Statistical analysis revealed directly proportional relationships between LV mass index (p = 0.008), carotid systolic thickness of the media (p = 0.009), diastolic thickness of the media (p = 0.007), cross-sectional area (p = 0.001) and blood vessel wall thickness. Carotid relative wall thickness positively correlates with adipocyte size (p = 0.023). In patients with morbid obesity, chemerin and adiponectin/chemerin ratio positively correlates with carotid intima–media thickness (p = 0.050), systolic thickness of the media (p = 0.015) and diastolic thickness of the media (p = 0.001). The multiple linear regression models revealed the role of epicardial adipose tissue thickness and carotid cross-sectional area in predicting adipocyte size which in turn is an independent factor for arterial stiffness parameters such as pulse wave velocity, subendocardial viability ratio and aortic augmentation index. Conclusions: Our results suggest that epicardial adipose tissue thickness, carotid intima–media thickness, relative wall thickness and carotid cross-sectional area might be useful imaging parameters for early prediction of arterial stiffness in patients with morbid obesity.