“…21,22 In non-invasive ultrasound studies, a correlation was found between metabolic risk factors and arterial remodelling. [23][24][25] The relation between MS and arterial structure has been evaluated in adults, [26][27][28][29] but not in children. The present data are in line and complement a recent observation of an increased carotid stiffness in obese children with MS as compared to these without MS.…”
Preclinical vascular changes (increased stiffness and/or wall thickness) have been observed in children with known metabolic risk factors. Aim of the present study was to evaluate different carotid parameters, representative of vascular health, in children with and without metabolic syndrome (MS). We studied 38 children with MS (mean age 9.672.6 years; range 6-14 years) and 45 healthy age-matched subjects. Children who met three or more of the following criteria qualified as having the MS: fasting glucose 4110 mg dl À1 , fasting triglyceride concentration 4100 mg dl À1 , fasting high-density lipoprotein cholesterol concentration o50 mg dl À1 for females or o45 mg dl À1 for the males, waist circumference 475th percentile for age and gender and systolic or diastolic blood pressure 490th percentile for age, gender and height. Carotid B-mode ultrasound examinations were performed and intima-media thickness and diameters were measured in all subjects. Arterial geometry was further characterized by calculation of carotid cross-sectional area. Carotid intimamedia thickness and lumen diameters were increased in children with MS as compared to children without MS. Moreover, carotid cross-sectional area was significantly higher in the group of children with MS 9.8371.86 mm 2 [mean7s.d.] compared with the control group: 7.7771.72 mm 2 , Po0.001, even after adjustment for age, gender and height. Carotid hypertrophy is already detectable in children with MS. High-resolution B-mode ultrasound could provide a valuable tool for the cardiovascular risk stratification of children.
“…21,22 In non-invasive ultrasound studies, a correlation was found between metabolic risk factors and arterial remodelling. [23][24][25] The relation between MS and arterial structure has been evaluated in adults, [26][27][28][29] but not in children. The present data are in line and complement a recent observation of an increased carotid stiffness in obese children with MS as compared to these without MS.…”
Preclinical vascular changes (increased stiffness and/or wall thickness) have been observed in children with known metabolic risk factors. Aim of the present study was to evaluate different carotid parameters, representative of vascular health, in children with and without metabolic syndrome (MS). We studied 38 children with MS (mean age 9.672.6 years; range 6-14 years) and 45 healthy age-matched subjects. Children who met three or more of the following criteria qualified as having the MS: fasting glucose 4110 mg dl À1 , fasting triglyceride concentration 4100 mg dl À1 , fasting high-density lipoprotein cholesterol concentration o50 mg dl À1 for females or o45 mg dl À1 for the males, waist circumference 475th percentile for age and gender and systolic or diastolic blood pressure 490th percentile for age, gender and height. Carotid B-mode ultrasound examinations were performed and intima-media thickness and diameters were measured in all subjects. Arterial geometry was further characterized by calculation of carotid cross-sectional area. Carotid intimamedia thickness and lumen diameters were increased in children with MS as compared to children without MS. Moreover, carotid cross-sectional area was significantly higher in the group of children with MS 9.8371.86 mm 2 [mean7s.d.] compared with the control group: 7.7771.72 mm 2 , Po0.001, even after adjustment for age, gender and height. Carotid hypertrophy is already detectable in children with MS. High-resolution B-mode ultrasound could provide a valuable tool for the cardiovascular risk stratification of children.
“…In contrast, no significant changes were observed in CA branches of similar order from OZRs, demonstrating a preserved vascular structure. Vascular remodeling has recently been reported in asymptomatic middle-aged women with metabolic syndrome, where carotid artery measurements by noninvasive B-mode ultrasound technique showed a preserved luminal diameter and blood flow in response to arterial wall thickening (24). On the other hand, skeletal muscle resistance arterioles of OZRs have consistently been demonstrated to remodel, resulting in a reduced passive diameter and distensibility but also thinner walls, indicative of atrophic vascular remodeling (11,45).…”
Erectile dysfunction frequently coexists with coronary artery disease and has been proposed as a potential marker for silent coronary artery disease in type 2 diabetes. In the present study, we comparatively assessed the structural and functional changes of both penile arteries (PAs) and coronary arteries (CAs) from a prediabetic animal model. PAs and CAs from 17-to 18-wk-old obese Zucker rats (OZRs) and from their control counterparts [lean Zucker rats (LZRs)] were mounted in microvascular myographs to evaluate vascular function, and stained arteries were subjected to morphometric analysis. Endothelial nitric oxide (NO) synthase (eNOS) protein expression was also assessed. The internal diameter was reduced and the wall-to-lumen ratio was increased in PAs from OZRs, but structure was preserved in CAs. ACh-elicited relaxations were severely impaired in PAs but not in CAs from OZRs, although eNOS expression was unaltered. Contractions to norepinephrine and 5-HT were significantly enhanced in both PAs and CAs, respectively, from OZRs. Blockade of NOS abolished endothelium-dependent relaxations in PAs and CAs and potentiated norepinephrine and 5-HT contractions in arteries from LZRs but not from OZRs. The vasodilator response to the phosphodiesterase 5 inhibitor sildenafil was reduced in both PAs and CAs from OZRs. Pretreatment with SOD reduced the enhanced vasoconstriction in both PAs and CAs from OZRs but did not restore ACh-induced relaxations in PAs. In conclusion, the present results demonstrate vascular inward remodeling in PAs and a differential impairment of endothelial relaxant responses in PAs and CAs from insulin-resistant OZRs. Enhanced superoxide production and reduced basal NO activity seem to underlie the augmented vasoconstriction in both PAs and CAs. The severity of the structural and functional abnormalities in PAs might anticipate the vascular dysfunction of the more preserved coronary vascular bed. vascular remodeling; endothelial dysfunction; coronary artery; penile artery; erectile dysfunction ERECTILE DYSFUNCTION (ED) is currently considered an early clinical manifestation of a more generalized vascular disease due to its high prevalence in patients with cardiovascular risk factors including diabetes, hypertension, hyperlipidemia, and tobacco abuse (32,46). ED is a common complication and an important cause of decreased quality of life in men with diabetes, and its prevalence is three times higher in type 1 and type 2 diabetic patients than in the general population (18,48).Growing epidemiological evidence associates the subsequent risk of ED with the presence of risk factors for coronary artery disease (CAD) such as obesity, hypertension, and dyslipidemia (32, 34). On the other hand, the rate of ED in patients with CAD is as high as 42-57%, and the incidence of ED in diabetic patients with silent ischemia is 34.8% versus 4.7% in those without silent ischemia (16,32,34). This has recently led to the suggestion that ED could be a potential marker for silent CAD in type 2 diabetes mellitus patie...
“…[3][4][5][6][7] Despite recent evidence of a major impact on cardiovascular risk, [8][9][10] there is debate in the scientific community about whether identification of the metabolic syndrome improves prediction of cardiovascular events compared to use of single risk factors. [11][12][13][14] Paralleling this debate, however, there is emerging evidence that the metabolic syndrome is associated with preclinical cardiovascular disease [15][16][17][18][19][20] and higher rates of cardiovascular events, [8][9][10] suggesting that the metabolic syndrome may have more adverse cardiovascular effects than predicted by its individual components.…”
The relation of metabolic syndrome (MetS) with cardiovascular outcome may be less evident when preclinical cardiovascular disease is present. We explored, in a post hoc analysis, whether MetS predicts cardiovascular events in hypertensive patients with electrocardiographic left ventricular hypertrophy (ECG-LVH) in the Losartan Intervention For Endpoint (LIFE) reduction in hypertension study. MetS was defined by X2 risk factors plus hypertension: body mass index X30 kg/m 2 , high-density lipoprotein (HDL)-cholesterol o1.0/1.3 mmol/l (o40/ 50 mg/dl) (men/women), glucose X6.1 mmol/l (X110 mg/ dl) fasting or X7.8 mmol/l (X140 mg/dl) nonfasting or diabetes. Cardiovascular death and the primary composite end point (CEP) of cardiovascular death, stroke and myocardial infarction were examined. In MetS (1591 (19.3%) of 8243 eligible patients), low HDL-cholesterol (72%), obesity (77%) and impaired glucose (73%) were similarly prevalent, with higher blood pressure, serum creatinine and Cornell product, but lower Sokolow-Lyon voltage (all Po0.001). After adjusting for baseline covariates, hazard ratios for CEPs and cardiovascular death (4.871.1 years follow-up) were 1.47 (95% confidence interval (CI), 1.27-1.71)-and 1.73 (95% CI, 1.38-2.17)-fold higher with MetS (both Po0.0001), and were only marginally reduced when further adjusted for diabetes, obesity, low HDL-cholesterol, non-HDL-cholesterol, pulse pressure and in-treatment systolic blood pressure and heart rate. Thus, MetS is associated with increased cardiovascular events in hypertensive patients with ECG-LVH, independently of single cardiovascular risk factors.
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