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OBJECTIVES: Overwhelming clinical evidence exists on disturbed vascular and endothelial function in the pathophysiology of preeclampsia (PE). In a non-pregnant (NP) population, L-FMC (low-flow mediated constriction) provides insight in the 'resting' endothelial capacity in contrast to the gold standard of flow mediated dilatation (FMD), reflecting endothelial nitric oxide bioavailability.STUDY DESIGN: Longitudinal follow-up of 100 healthy pregnant (HP) women, 33 PE women and 16 NP controls with non-invasive vascular assessments. HP women were evaluated at 12 and 35 weeks of gestation and at 6 months postpartum. PE patients were assessed at diagnosis (mean 30 weeks) and 6 months postpartum.MAIN OUTCOME MEASURES: Endothelial function (L-FMC, FMD, peripheral arterial tonometry (PAT)) and arterial stiffness (pulse wave velocity (PWV) and analysis (PWA)) were measured at the different visits and compared between groups.RESULTS: Overall endothelial dysfunction is present in PE (FMD HP 9.09 ± 4.20 vs PE 5.21 ± 4.47, p = 0.0004; L-FMC HP -1.90 ± 2.66 vs PE -0.40 ± 2.09, p = 0.03). L-FMC gradually elevates during the course of a HP (1st trim -0.31 ± 1.75 vs 3rd trim -1.97 ± 3.02, p 0.05).CONCLUSION: PE is characterized by dysfunction of both resting and recruitable endothelial capacity. This study offers new insights in different aspects of endothelial function in pregnancy, since L-FMC reflects an adaptation in HP that is absent in PE.

International audience; Obstructive sleep apnoea (OSA) is independently associated with various cardiovascular diseases, including myocardial infarction and stroke. OSA may promote atherosclerosis risk factors such as hypertension, diabetes and dyslipidaemia, and may have direct proatherogenic effects on the vascular wall. A growing number of studies have recently focused on the role of microparticles (MPs) in the atherogenic process. MPs are small plasma membrane vesicles that can be released by a variety of vascular or blood cells, and contain both membrane and cytosolic elements. Case–control studies have shown that platelet-, endothelium- and leukocyte-derived MP levels are increased in OSA. Experimental evidence has demonstrated that MPs from OSA patients induce endothelial dysfunction, inflammation and vascular hyperreactivity when injected into mice. In this review, we provide an overview of the main characteristics of MPs, their expression in OSA and their potential role in the atherogenic process associated with OSA.

BACKGROUND Childhood obesity is associated with premature cardiovascular complications. However, little is known about the effect of a family-based behavioural intervention on the relationship between arterial function, blood pressure and biomarkers in pre-pubertal children with obesity. DESIGN This was a single centre randomized controlled trial (RCT) including 74 children randomized to a 6-month behavioural intervention to treat obesity. In 48 children (13 controls and 35 interventions), we assessed: serum level of cytokine (CCL2), adiponectin, and neutrophil product (MMP-8), as well as carotid intima-media thickness, flow-mediated dilation (FMD), nitroglycerin-mediated dilation; arterial stiffness (incremental elastic modulus, Einc), pulse wave velocity (PWV), resting and 24-hour blood pressure (BP). RESULTS At baseline, resting systolic BP was positively associated with MMP-8 levels which was significantly higher in children with hypertension (P = 0.033). Biochemical markers were not related to endothelial function at baseline, but they globally increased after 6 months in the intervention group. The significant increase of CCL2 levels in the intervention group was associated with a decrease in diastolic BP. Furthermore, adiponectin change was positively related to a change in FMD and negatively to change in Einc and PWV. CONCLUSIONS The usefulness of serum biomarkers for the detection of cardiovascular diseases is not well established in children. In our population, MMP-8 concentration was higher in hypertensive children. Furthermore, behavioural interventions resulted in a paradoxical increase in some biomarkers in children, with potentially beneficial effects detected with CCL2 changes. Caution should be taken when using nonspecific serum biomarkers for the clinical monitoring of children with obesity.

International audience; Sleep disorders are associated with inflammation and sympathetic activation, which are suspected to induce endothelial dysfunction, a key factor in the increased risk of cardiovascular disease. Less is known about the early effects of acute sleep deprivation on vascular function. We evaluated microvascular reactivity and biological markers of endothelial activation during continuous 40 h of total sleep deprivation (TSD) in 12 healthy men (29 +/- 3 yr). The days before [day 1 (D1)] and during TSD (D3), at 1200 and 1800, endothelium-dependent and -independent cutaneous vascular conductance was assessed by iontophoresis of acetylcholine and sodium nitroprusside, respectively, coupled to laser-Doppler flowmetry. At 0900, 1200, 1500, and 1800, heart rate (HR) and instantaneous blood pressure (BP) were recorded in the supine position. At D1, D3, and the day after one night of sleep recovery (D4), markers of vascular endothelial cell activation, including soluble intercellular adhesion molecule-1, vascular cell adhesion molecule-1, E-selectin, and interleukin-6 were measured from blood samples at 0800. Compared with D1, plasma levels of E-selectin were raised at D3, whereas intercellular adhesion molecule-1 and interleukin-6 were raised at D4 (P < 0.05). The endothelium-dependent and -independent CVC were significantly decreased after 29 h of TSD (P < 0.05). By contrast, HR, systolic BP, and the normalized low-frequency component of HR variability (0.04-0.15 Hz), a marker of the sympathetic activity, increased significantly within 32 h of TSD (P < 0.05). In conclusion, acute exposure to 40 h of TSD appears to cause vascular dysfunction before the increase in sympathetic activity and systolic BP.

Objective. Physical activity (PhA) has proven to be a protective factor for normal erectile function. The aim of this study was to evaluate the effects of a standard protocol of aerobic PhA on quality of erectile dysfunction (ED) in patients with arterial ED. Materials and methods. Fifty patients (48–62 years) were selected and underwent to standard protocol of aerobic PhA: 150 min of moderate intensity aerobic activity per week (group A). Twenty patients, matched aged, with vascular ED who did not accept to undergo the standard PhA’s protocol, represented the control group. All patients were evaluated, by IIEF-5 questionnaire administration, penile eco color doppler and flow-cytometric analysis for detection of serum concentrations of original immunophenotype endothelial progenitor cells (EPCs) ¼ CD45neg/CD34pos/CD144pos and endothelial microparticles (EMPs) ¼ CD45neg/CD34neg/CD144pos. Results. After 3 months, group A showed IIEF 5 score and peak systolic velocity significantly higher (p5 0.05) compared to controls, and significantly lower values (p5 0.05) of acceleration time, in addition serum concentrations of EPCs and EMPs were significantly lower (p5 0.05) in group A compared to controls. Conclusions. PhA improves quality of arterial ED, without other pharmacological approach, probably by reduced endothelial apoptosis. This study characterises the study of endothelial dysfunction by new cell circulating markers.

Introduction The lack of phosphodiesterase type 5 inhibitor effects in patients with erectile dysfunction (ED) of arterial origin may be caused by an endothelial dysfunction that causes a series of biochemical alterations leading to a reduced nitric oxide (NO) bioavailability and increased oxidative stress. Aim The aim of this study was to evaluate the effects of the treatment with endothelial antioxidant compounds (EAC) on the erectile response to sildenafil in patients with arterial ED already treated with sildenafil (100 mg twice a week for 8 weeks). Mean Outcome Measures A patient was considered responsive when the 5-item International Index of Erectile Function questionnaire score increased by >5 points. Methods Fifty-three patients with arterial ED, hypertension, and diabetes mellitus were randomly given, for 8 weeks, EAC (1 dose/day) and, after a wash out of 8 weeks, sildenafil (100 mg) plus EAC. The patients were divided into the following four groups: A (N=12): patients with ED alone; B (N=14): patients with ED plus atheromasic plaques and/or increased intima-media thickness of common carotid arteries; C (N=14): patients with ED plus lower limb artery abnormalities; and D (N=13): patients with ED plus carotid and lower limb artery abnormalities. Results The administration of EAC plus sildenafil resulted in a significantly higher number of responsive patients (N=36, 68%) compared with sildenafil alone (N=24, 45%) or EAC alone (N=17, 32%). The percentage of patients who successfully responded to the combined treatment increased in the various groups. It was 83%, 64%, 71%, and 54%, respectively, for groups A, B, C, and D. Furthermore, patients treated with EAC and sildenafil reached a successful response in a shorter length of time (3 weeks) compared with patients responsive to sildenafil (5.2 weeks) or EAC (5.7 weeks) alone. Conclusion EAC administration to patients with arterial ED improved the success rate to sildenafil. These data suggest that, in such patients, a combined treatment may be considered to increase bioavailable NO and to neutralize radical oxygen species, which in turn inactive NO.

Adriana Aparecida Siviero-Miachon1, Angela Maria Spinola-Castro1, Gil Guerra-Junior21Division of Pediatric Endocrinology, Department of Pediatrics, Federal University of Sao Paulo – UNIFESP/EPM, Brazil; 2Division of Pediatric Endocrinology, Department of Pediatrics, State University of Campinas – FCM/UNICAMP, BrazilAbstract: Along with the growing epidemic of obesity, the risk of atherosclerosis, cardiovascular disease morbidity, and mortality are increasing markedly. Several risk factors for cardiovascular disease, such as visceral obesity, glucose intolerance, arterial hypertension, and dyslipidemia commonly cluster together as a condition currently known as metabolic syndrome. Thus far, insulin resistance, and endothelial dysfunction are the primary events of the metabolic syndrome. Several groups have recommended clinical criteria for the diagnosis of metabolic syndrome in adults. Nonetheless, in what concerns children and adolescents, there are no unified definitions, and modified adult criteria have been suggested by many authors, despite major problems. Some pediatric disease states are at risk for premature cardiovascular disease, with clinical coronary events occurring very early in adult life. Survivors of specific pediatric cancer groups, particularly acute lymphocytic leukemia, central nervous system tumors, sarcomas, lymphomas, testicular cancer, and following bone marrow transplantation, may develop metabolic syndrome traits due to: hormonal deficiencies (growth hormone deficiency, thyroid dysfunction, and gonadal failure), drug or radiotherapy damage, endothelial impairment, physical inactivity, adipose tissue dysfunction, and/or drug-induced magnesium deficiency. In conclusion, some primary and secondary prevention remarks are proposed in order to reduce premature cardiovascular disease risk in this particular group of patients.Keywords: metabolic syndrome X, cardiovascular diseases, insulin resistance, obesity, growth hormone/deficiency, endothelium, vascular/physiopathology