I023 Modulation de la dysfonction endothelium dependente par la maladie artérielle liée aux pathologies associées chez l’hémodialysé

ObjectifsLa fonction endothéliale (vasodilatation flux dépendante, FMD) est réduite chez l’hémodialysé. Nous avons étudié le rôle des atteintes artérielles reflétant les pathologies cardiovasculaires associées, dans l’altération de la FMD en fonction de la contrainte de cisaillement mesurée localement.MéthodologieChez 35 patients avec insuffisance rénale dialysés (ESRD), 16 avec un antécédent de maladie cardio-vasculaire (CV+), 19 indemnes (CV-) et chez 22 contrôles appariés, nous avons évalué la géométrie de l’artère humérale (diamètre : D et épaisseur : IMT, Wall Track System) et ses changements (FMD) en réponse aux modifications du taux de cisaillement et de la contrainte de cisaillement (SS), calculée avec mesure de viscosité sanguine (viscosimètre Brookfield), pendant une hyperhémie induite par chauffage de la main dans un bain thermostaté (paliers de 35 à 44°C). Les comparaisons multiples ont été faites par ANOVA et analyses post Hoc par test de Bonferonni.RésultatsESRD CV+ étaient plus agés avec pressions systolique et pulsée, D, IMT et module élastique plus élevés alors que SS étaient significativement réduit en baseline versus les deux autres groupes. Avec chauffage, les ESRD CV- et contrôles avaient une augmentation similaire de la pente D vs SS pour les températures faibles mais la pente devenait significativement plus faible pour ESRD à 44°. Les ESRD CV+ ont présenté une altération de la relation D vs SS pour toute la gamme de température. La réponse à la TNT était réduite pour ESRD CV+ versus les deux autres groupes.ConclusionLes altérations artérielles des ESRD avec pathologies cardio-vasculaires associées sont structurales, mais également fonctionnelles. Par contre en absence de maladie vasculaire les ESRD ont un comportement non différent des contrôles pour des stimulations non maximales mais ont une réduction de la réserve de dilatation altérée lors de stimulations soutenues et maximales

Arterial Stiffness in the Heart Disease of CKD

CKD frequently leads to chronic cardiac dysfunction. This complex relationship has been termed as cardiorenal syndrome type 4 or cardio-renal link. Despite numerous studies and reviews focused on the pathophysiology and therapy of this syndrome, the role of arterial stiffness has been frequently overlooked. In this regard, several pathogenic factors, including uremic toxins (, uric acid, phosphates, endothelin-1, advanced glycation end-products, and asymmetric dimethylarginine), can be involved. Their effect on the arterial wall, direct or mediated by chronic inflammation and oxidative stress, results in arterial stiffening and decreased vascular compliance. The increase in aortic stiffness results in increased cardiac workload and reduced coronary artery perfusion pressure that, in turn, may lead to microvascular cardiac ischemia. Conversely, reduced arterial stiffness has been associated with increased survival. Several approaches can be considered to reduce vascular stiffness and improve vascular function in patients with CKD. This review primarily discusses current understanding of the mechanisms concerning uremic toxins, arterial stiffening, and impaired cardiac function, and the therapeutic options to reduce arterial stiffness in patients with CKD

Pulse wave velocity differs between ulcerative colitis and chronic kidney disease

Background: We hypothesized that a reversal of the physiological stiffness gradient, previously reported in end-stage renal disease, begins in the early stages of chronic kidney disease (CKD) and that chronic inflammation produces a different arterial phenotype in patients with ulcerative colitis (UC). Objectives: To assess the extent of arterial stiffening in the central (carotid-femoral pulse wave velocity, cf.-PWV) and peripheral arteries (carotid-radial pulse wave velocity, cr-PWV) and to explore the determinants of the stiffness gradient in UC and in CKD. Methods: We enrolled 45 patients with UC, 45 patients with stage 3-4 CKD and 45 matched controls. Results: Despite the comparable cf.-PWV, the cr-PWV was higher in patients with UC than in those with CKD (median: 8.7 vs. 7.5. m/s; p <. 0.001) and, consequently, the PWV ratio was lower (median: 0.97 vs. 1.12; p <. 0.001). In patients with CKD a stiffness mismatch was reported starting from stage 3B. The PWV ratio was associated with age and C-reactive protein (beta: 0.08 z-score, 95%CI 0.02-0.14; p = 0.01) or active disease (beta: 0.43 z-score, 95%CI 0.003-0.857; p = 0.048) in patients with UC and with age and glomerular filtration rate (beta: -0.56 z-score, 95%CI -1.05 to -0.07; p = 0.02) in patients with CKD. Conclusions: The arterial phenotype differed between UC and CKD. The reversal of the arterial stiffness gradient is evident in CKD patients starting from stage 3B but not in patients with UC and comparable cf.-PWV. In patients with UC, the stiffness of both elastic and muscular arteries is increased as a consequence of inflammation

Silicon photonics-based laser Doppler vibrometer array for carotid-femoral pulse wave velocity (PWV) measurement

Pulse wave velocity (PWV) is a reference measure for aortic stiffness, itself an important biomarker of cardiovascular risk. To enable low-cost and easy-to-use PWV measurement devices that can be used in routine clinical practice, we have designed several handheld PWV sensors using miniaturized laser Doppler vibrometer (LDV) arrays in a silicon photonics platform. The LDV-based PWV sensor design and the signal processing protocol to obtain pulse transit time (PTT) and carotid-femoral PWV in a feasibility study in humans, are described in this paper. Compared with a commercial reference PWV measurement system, measuring arterial pressure waveforms by applanation tonometry, LDV-based displacement signals resulted in more complex signals. However, we have shown that it is possible to identify reliable fiducial points for PTT calculation using the maximum of the 2nd derivative algorithm in LDV-based signals, comparable to those obtained by the reference technique, applanation tonometry. (C) 2020 Optical Society of America under the terms of the OSA Open Access Publishing Agreemen

Oral Condition and Incident Coronary Heart Disease: A Clustering Analysis

Poor oral health has been linked to coronary heart disease (CHD). Clustering clinical oral conditions routinely recorded in adults may identify their CHD risk profile. Participants from the Paris Prospective Study 3 received, between 2008 and 2012, a baseline routine full-mouth clinical examination and an extensive physical examination and were thereafter followed up every 2 y until September 2020. Three axes defined oral health conditions: 1) healthy, missing, filled, and decayed teeth; 2) masticatory capacity denoted by functional masticatory units; and 3) gingival inflammation and dental plaque. Hierarchical cluster analysis was performed with multivariate Cox proportional hazards regression models and adjusted for age, sex, smoking, body mass index, education, deprivation (EPICES score; Evaluation of Deprivation and Inequalities in Health Examination Centres), hypertension, type 2 diabetes, LDL and HDL serum cholesterol (low- and high-density lipoprotein), triglycerides, lipid-lowering medications, NT-proBNP and IL-6 serum level. A sample of 5,294 participants (age, 50 to 75 y; 37.10% women) were included in the study. Cluster analysis identified 3,688 (69.66%) participants with optimal oral health and preserved masticatory capacity (cluster 1), 1,356 (25.61%) with moderate oral health and moderately impaired masticatory capacity (cluster 2), and 250 (4.72%) with poor oral health and severely impaired masticatory capacity (cluster 3). After a median follow-up of 8.32 y (interquartile range, 8.00 to 10.05), 128 nonfatal incident CHD events occurred. As compared with cluster 1, the risk of CHD progressively increased from cluster 2 (hazard ratio, 1.45; 95% CI, 0.98 to 2.15) to cluster 3 (hazard ratio, 2.47; 95% CI, 1.34 to 4.57; P < 0.05 for trend). To conclude, middle-aged individuals with poor oral health and severely impaired masticatory capacity have more than twice the risk of incident CHD than those with optimal oral health and preserved masticatory capacity (ClinicalTrials.gov NCT00741728)

Association of hearing impairment with incident depressive symptoms: a community-based prospective study

Objective: The aim was to investigate the potential association between hearing impairment and incident depressive symptoms.Methods: Using a prospective community-based cohort study in France (the Paris Prospective Study III), participants aged 50-75 years were recruited between 2008 and 2012 and thereafter followed up every 2 years up to 2018. Hearing impairment, measured at study recruitment by audiometry testing, was defined as a pure tone average >25 decibels in the better ear. Incident depressive symptoms, measured using the validated 13-item Questionnaire of Depression 2nd version, was assessed during follow-up. Multivariate generalized estimating equations were used to compute odds ratio (OR) and 95% confidence intervals (CI).Results: Among 7591 participants free of depressive symptoms at baseline (mean age 59.8 years, 63% of men), 14.3% had hearing impairment. Over 6 years of follow-up, 479 subjects (6.3%) had incident depressive symptoms. The OR for incident depressive symptoms was 1.36 for subjects with baseline hearing impairment (95% CI, 1.06-1.73). A pooled analysis of 4 published prospective studies yielded a multivariable relative risk of baseline hearing impairment for incident depressive symptoms of 1.29 (95% CI, 1.09-1.53).Conclusions: In this community-based prospective cohort study of participants aged 50 to 75 years, baseline hearing impairment was associated with a 36% increased odds of incident depressive symptoms

Self-reported body silhouette trajectories across the lifespan and excessive daytime sleepiness in adulthood: a retrospective analysis. The Paris Prospective Study III.

Excessive daytime sleepiness (EDS) is a common sleep complaint in the population and is increasingly recognised as deleterious for health. Simple and sensitive tools allowing identifying individuals at greater risk of EDS would be of public health importance. Hence, we determined trajectories of body silhouette from early childhood to adulthood and evaluated their association with EDS in adulthood. A retrospective analysis in a prospective community-based study. 6820 men and women self-reported their silhouette at ages 8, 15, 25, 35 and 45 using the body silhouettes proposed by Stunkard &lt;i&gt;et al&lt;/i&gt; . EDS was defined by an Epworth Sleepiness Scale score ≥11. Presence of EDS in adulthood. The study population comprised 6820 participants (mean age 59.8 years, 61.1% men). Five distinct body silhouettes trajectories over the lifespan were identified: 31.9% 'lean stable', 11.1% 'lean increase', 16.1% 'lean-marked increase', 32.5% 'moderate stable' and 8.4% 'heavy stable'. Subjects with a 'heavy-stable' trajectory (OR 1.24, 95% CI 0.94 to 1.62) and those with a 'lean-marked increase' trajectory (OR 1.46, 95% CI 1.18 to 1.81) were more likely to have EDS when compared with the 'lean-stable' group after adjusting for confounding. Further adjustment for birth weight strengthened the magnitude of the ORs. Increasing body silhouette and to a lesser extent constantly high body silhouette trajectory from childhood to adulthood are associated with increased likelihood of EDS, independently of major confounding variables. NCT00741728; Pre-results

Body silhouette trajectories across the lifespan and vascular aging: The Paris Prospective Study 3

Vascular aging is a major contributor to cardiovascular disease and can be quantified by higher carotid stiffness, intima-media thickness and diameter, and hypertension. Weight gain across the lifetime may be an important, modifiable determinant of vascular aging. We therefore aimed to assess lifetime body silhouette trajectories (a marker of weight change across the lifespan) in relation to vascular aging in late adulthood. We used cross-sectional data from a community-based cohort study (n=8243; age, 59.4; 38.7% women). A linear mixed model was used to assess trajectories of recalled body silhouettes from age 8 to 45 years. We assessed carotid artery properties (ultrasonography), resting hypertension (blood pressure ≥140/90 mm Hg or use of antihypertensives), and exaggerated exercise blood pressure, a marker of masked hypertension (systolic blood pressure ≥150 mm Hg during submaximal exercise) at study recruitment when the participants were 50 to 75 years of age. We identified 5 distinct body silhouette trajectories: lean stable (32.0%), lean increase (11.1%), moderate stable (32.5%), lean-marked increase (16.3%), and heavy stable (8.1%). Compared with individuals in the lean-stable trajectory, those in the moderate-stable, lean-marked increase, and heavy-stable trajectories had higher carotid stiffness, intima-media thickness and diameter (odds ratios between 1.23 and 2.10 for highest quartile versus lowest quartile of manifestations of vascular aging; PP<0.05). Vascular aging was most prominent among individuals who were lean in early life but markedly gained weight during young adulthood and among those who were heavy in early life and maintained weight

Carotid artery stiffness and incident depressive symptoms: The Paris Prospective Study III

Background: Arterial stiffness may contribute to late-life depression via cerebral microvascular damage, but evidence is scarce. No longitudinal study has evaluated the association between arterial stiffness and risk of depressive symptoms. Therefore, we investigated the association between carotid artery stiffness and incident depressive symptoms in a large community-based cohort study.Methods: This longitudinal study included 7013 participants (mean age 59.7 ± 6.3 years; 35.8% women) free of depressive symptoms at baseline. Carotid artery stiffness (high-resolution echo tracking) was determined at baseline. Presence of depressive symptoms was determined at baseline and at 4 and 6 years of follow-up, and was defined as a score ≥7 on the validated Questionnaire of Depression, Second Version, Abridged and/or new use of antidepressant medication. Logistic regression and generalized estimating equations were used.Results: In total, 6.9% (n = 484) of the participants had incident depressive symptoms. Individuals in the lowest tertile of carotid distensibility coefficient (indicating greater carotid artery stiffness) compared with those in the highest tertile had a higher risk of incident depressive symptoms (odds ratio: 1.43; 95% confidence interval: 1.10-1.87), after adjustment for age, sex, living alone, education, lifestyle, cardiovascular risk factors, and baseline Questionnaire of Depression, Second Version, Abridged scores. Results were qualitatively similar when we used carotid Young's elastic modulus as a measure of carotid stiffness instead of carotid distensibility coefficient, and when we used generalized estimating equations instead of logistic regression.Conclusions: Greater carotid stiffness is associated with a higher incidence of depressive symptoms. This supports the hypothesis that carotid stiffness may contribute to the development of late-life depression