1.
Brachial Artery Flow-mediated Dilatation and Carotid Intima-Media Thickness in Children With Idiopathic Nephrotic Syndrome.
Youssef, DM, Gomaa, MA, El-Akhras, A, Tolba, SAR, Abd Allah, GM, Daoud, O, Saber, S
Iranian journal of kidney diseases. 2018;(6):331-340
Abstract
INTRODUCTION Disturbances of lipid metabolism has been reported in nephrotic syndrome (NS) and may predispose to atherosclerosis. This study aimed to investigate the correlation between cardiovascular risk factors and carotid intima-media thickness (CIMT) and brachial artery flow-mediated dilatation in patients with idiopathic NS. MATERIALS AND METHODS This case-control study included 31 patients with NS and 31 healthy individuals as the control group. All patients were subjected to full clinical examination; laboratory investigations in the form of lipid profile, kidney function tests, serum protein, serum albumin, C-reactive protein, and ferritin; carotid ultrasonography, and brachial artery flow-mediated dilatation. RESULTS Serum cholesterol, low-density lipoprotein cholesterol, and triglyceride levels was significantly higher in the case group than the control group. High-density lipoprotein cholesterol and albumin levels were significantly lower in the case group. The absolute change in brachial artery diameter was significantly lower in the case group than that of the control group. Proportionate change in brachial artery diameter was significantly lower in the case group than that of the control group. Common carotid artery CIMT in the case group was significantly higher than that of the controls. Lastly, there were significant increases in weight and body mass index in the relapse group than the remission group. CONCLUSIONS Patients with NS are more prone to atherosclerosis and vascular changes; CIMT was thicker in nephrotic children compared to the controls. The significantly abnormal values of flow-mediated dilatation in children with NS suggests an ongoing process of endothelial dysfunction.
2.
Circuit resistance training attenuates acute exertion-induced reductions in arterial function but not inflammation in obese women.
Franklin, NC, Robinson, AT, Bian, JT, Ali, MM, Norkeviciute, E, McGinty, P, Phillips, SA
Metabolic syndrome and related disorders. 2015;(5):227-34
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Abstract
BACKGROUND Cardiovascular disease (CVD) is a leading cause of preventable death among young women in the United States. Habitual resistance exercise training is known to have beneficial effects on endothelial function and CVD risk factors, including obesity; however, previous studies show that acute resistance exercise impairs endothelial function in obese adults who are sedentary, a response that may be linked to inflammation. We sought to determine if circuit-based resistance training (CRT) attenuates acute resistance exercise-induced reductions in endothelial function in a population of young, obese, sedentary women and whether or not inflammation plays a role in this response. METHODS Eighteen obese [body mass index (BMI) 30.0-40.0 kg · m(-2)] young premenopausal women were randomly assigned to either a CRT group or a no-exercise control group (CON). Conduit artery endothelial function was assessed using brachial artery flow-mediated dilation (FMD) determined by ultrasound before and after a single bout of strenuous weightlifting (SWL). In addition, circulating inflammatory mediators (tumor necrosis factor-α and C-reactive protein), blood pressure, fasting blood lipids, glucose, waist circumference, body composition, and aerobic capacity were assessed. RESULTS Among participants randomized to the CRT group, 8 weeks of training led to considerable increases in FMD after SWL (P=0.001) compared to the CON group. However, no significant differences between the groups were observed in circulating inflammatory mediators, blood pressure, fasting blood lipids, or other physical and physiological characteristics. CONCLUSIONS This study shows that CRT alleviates acute exertion-induced reductions in endothelial function among obese sedentary women in the absence of changes in inflammation.