Learning to run a power network with trust

Artificial agents are promising for realtime power system operations, particularly, to compute remedial actions for congestion management. Currently, these agents are limited to only autonomously run by themselves. However, autonomous agents will not be deployed any time soon. Operators will still be in charge of taking action in the future. Aiming at designing an assistant for operators, we here consider humans in the loop and propose an original formulation for this problem. We first advance an agent with the ability to send to the operator alarms ahead of time when the proposed actions are of low confidence. We further model the operator's available attention as a budget that decreases when alarms are sent. We present the design and results of our competition "Learning to run a power network with trust" in which we benchmark the ability of submitted agents to send relevant alarms while operating the network to their best

Dynamic expression of the pro-dopaminergic transcription factors Pax6 and Dlx2 during postnatal olfactory bulb neurogenesis

Olfactory bulb (OB) neurogenesis generates neurons that use GABA or dopamine as their neurotransmitters throughout life. Regionalized stem cell populations in the periventricular zone (PVZ) of the lateral ventricles (LVs) have been shown to be at the basis of neuronal diversity in the system. For example dopaminergic neurons arise predominantly from neural stem cells (NSCs) residing in the dorsal PVZ and depend on the expression of the transcription factors Pax6 and Dlx2 for their specification. In addition, Dlx2 is required for neurogenesis in general. Using targeted in vivo electroporation combined with immuno-fluorescence imaging and microarray analysis, we provide here detailed spatial and temporal expression data with cellular resolution in this system. We find that all along the neurogenic process Pax6 expression remains restricted to the dorsal PVZ, whereas nearly all neuroblasts express Dlx2, including those of the dorsal lineage, which are switched on for Dlx2 when they enter the rostral migratory stream (RMS). These data allow to explain and precise the functions of these two genes in postnatal OB neurogenesis

MiR-200 family controls late steps of postnatal forebrain neurogenesis via Zeb2 inhibition

During neurogenesis, generation, migration and integration of the correct numbers of each neuron sub-Type depends on complex molecular interactions in space and time. MicroRNAs represent a key control level allowing the flexibility and stability needed f

Trials

OBJECTIVES: To assess the efficacy of several repurposed drugs to prevent hospitalisation or death in patients aged 65 or more with recent symptomatic SARS-CoV-2 infection (COVID-19) and no criteria for hospitalisation. TRIAL DESIGN: Phase III, multi-arm (5) and multi-stage (MAMS), randomized, open-label controlled superiority trial. Participants will be randomly allocated 1:1:1:1:1 to the following strategies: Arm 1: Control arm Arms 2 to 5: Experimental treatment arms Planned interim analyses will be conducted at regular intervals. Their results will be reviewed by an Independent Data and Safety Monitoring Board. Experimental arms may be terminated for futility, efficacy or toxicity before the end of the trial. New experimental arms may be added if new evidence suggests that other treatments should be tested. A feasibility and acceptability substudy as well as an immunological substudy will be conducted alongside the trial. PARTICIPANTS: Inclusion criteria are: 65-year-old or more; Positive test for SARS-CoV-2 on a nasopharyngeal swab; Symptoms onset within 3 days before diagnosis; No hospitalisation criteria; Signed informed consent; Health insurance. Exclusion criteria are: Inability to make an informed decision to participate (e.g.: dementia, guardianship); Rockwood Clinical Frailty Scale ≥7; Long QT syndrome; QTc interval > 500 ms; Heart rate 5.5 mmol/L or <3.5 mmol/L; Ongoing treatment with piperaquine, halofantrine, dasatinib, nilotinib, hydroxyzine, domperidone, citalopram, escitalopram, potent inhibitors or inducers of cytochrome P450 CYP3A4 isoenzyme, repaglinide, azathioprine, 6-mercaptopurine, theophylline, pyrazinamide, warfarin; Known hypersensitivity to any of the trial drugs or to chloroquine and other 4-aminoquinolines, amodiaquine, mefloquine, glafenine, floctafenine, antrafenine, ARB; Hepatic porphyria; Liver failure (Child-Pugh stage ≥B); Stage 4 or 5 chronic kidney disease (GFR <30 mL/min/1.73 m²); Dialysis; Hypersentivity to lactose; Lactase deficiency; Abnormalities in galactose metabolism; Malabsorption syndrome; Glucose-6-phosphate dehydrogenase deficiency; Symptomatic hyperuricemia; Ileus; Colitis; Enterocolitis; Chronic hepatitis B virus disease. The trial is being conducted in France in the Bordeaux, Corse, Dijon, Nancy, Paris and Toulouse areas as well as in the Grand Duchy of Luxembourg. Participants are recruited either at home, nursing homes, general practices, primary care centres or hospital outpatient consultations. INTERVENTION AND COMPARATOR: The four experimental treatments planned in protocol version 1.2 (April 8(th), 2020) are: (1) Hydroxychloroquine 200 mg, 2 tablets BID on day 0, 2 tablets QD from day 1 to 9; (2) Imatinib 400 mg, 1 tablet QD from day 0 to 9; (3) Favipiravir 200 mg, 12 tablets BID on day 0, 6 tablets BID from day 1 to 9; (4) Telmisartan 20 mg, 1 tablet QD from day 0 to 9. The comparator is a complex of vitamins and trace elements (AZINC Forme et Vitalité®), 1 capsule BID for 10 days, for which there is no reason to believe that they are active on the virus. In protocol version 1.2 (April 8th, 2020): People in the control arm will receive a combination of vitamins and trace elements; people in the experimental arms will receive hydroxychloroquine, or favipiravir, or imatinib, or telmisartan. MAIN OUTCOME: The primary outcome is the proportion of participants with an incidence of hospitalisation and/or death between inclusion and day 14 in each arm. RANDOMISATION: Participants are randomized in a 1:1:1:1:1 ratio to each arm using a web-based randomisation tool. Participants not treated with an ARB or ACEI prior to enrolment are randomized to receive the comparator or one of the four experimental drugs. Participants already treated with an ARB or ACEI are randomized to receive the comparator or one of the experimental drugs except telmisartan (i.e.: hydroxychloroquine, imatinib, or favipiravir). Randomisation is stratified on ACEI or ARBs treatment at inclusion and on the type of residence (personal home vs. nursing home). BLINDING (MASKING): This is an open-label trial. Participants, caregivers, investigators and statisticians are not blinded to group assignment. NUMBERS TO BE RANDOMISED (SAMPLE SIZE): A total of 1057 participants will be enrolled if all arms are maintained until the final analysis and no additional arm is added. Three successive futility interim analyses are planned, when the number of participants reaches 30, 60 and 102 in the control arm. Two efficacy analyses (interim n°3 and final) will be performed successively. TRIAL STATUS: This describes the Version 1.2 (April 8(th), 2020) of the COVERAGE protocol that was approved by the French regulatory authority and ethics committee. The trial was opened for enrolment on April 15(th), 2020 in the Nouvelle Aquitaine region (South-West France). Given the current decline of the COVID-19 pandemic in France and its unforeseeable dynamic in the coming months, new trial sites in 5 other French regions and in Luxembourg are currently being opened. A revised version of the protocol was submitted to the regulatory authority and ethics committee on June 15(th), 2020. It contains the following amendments: (i) Inclusion criteria: age ≥65 replaced by age ≥60; time since first symptoms <3 days replaced by time since first symptoms <5 days; (ii) Withdrawal of the hydroxychloroquine arm (due to external data); (iii) increase in the number of trial sites. TRIAL REGISTRATION: The trial was registered on Clinical Trials.gov on April 22(nd), 2020 (Identifier: NCT04356495): and on EudraCT on April 10(th), 2020 (Identifier: 2020-001435-27). FULL PROTOCOL: The full protocol is attached as an additional file, accessible from the Trials website (Additional file 1). In the interest of expediting dissemination of this material, the familiar formatting has been eliminated; this Letter serves as a summary of the key elements of the full protocol. The study protocol has been reported in accordance with the Standard Protocol Items: Recommendations for Clinical Interventional Trials (SPIRIT) guidelines (Additional file 2)

Effect of angiotensin-converting enzyme inhibitor and angiotensin receptor blocker initiation on organ support-free days in patients hospitalized with COVID-19

IMPORTANCE Overactivation of the renin-angiotensin system (RAS) may contribute to poor clinical outcomes in patients with COVID-19. Objective To determine whether angiotensin-converting enzyme (ACE) inhibitor or angiotensin receptor blocker (ARB) initiation improves outcomes in patients hospitalized for COVID-19. DESIGN, SETTING, AND PARTICIPANTS In an ongoing, adaptive platform randomized clinical trial, 721 critically ill and 58 non–critically ill hospitalized adults were randomized to receive an RAS inhibitor or control between March 16, 2021, and February 25, 2022, at 69 sites in 7 countries (final follow-up on June 1, 2022). INTERVENTIONS Patients were randomized to receive open-label initiation of an ACE inhibitor (n = 257), ARB (n = 248), ARB in combination with DMX-200 (a chemokine receptor-2 inhibitor; n = 10), or no RAS inhibitor (control; n = 264) for up to 10 days. MAIN OUTCOMES AND MEASURES The primary outcome was organ support–free days, a composite of hospital survival and days alive without cardiovascular or respiratory organ support through 21 days. The primary analysis was a bayesian cumulative logistic model. Odds ratios (ORs) greater than 1 represent improved outcomes. RESULTS On February 25, 2022, enrollment was discontinued due to safety concerns. Among 679 critically ill patients with available primary outcome data, the median age was 56 years and 239 participants (35.2%) were women. Median (IQR) organ support–free days among critically ill patients was 10 (–1 to 16) in the ACE inhibitor group (n = 231), 8 (–1 to 17) in the ARB group (n = 217), and 12 (0 to 17) in the control group (n = 231) (median adjusted odds ratios of 0.77 [95% bayesian credible interval, 0.58-1.06] for improvement for ACE inhibitor and 0.76 [95% credible interval, 0.56-1.05] for ARB compared with control). The posterior probabilities that ACE inhibitors and ARBs worsened organ support–free days compared with control were 94.9% and 95.4%, respectively. Hospital survival occurred in 166 of 231 critically ill participants (71.9%) in the ACE inhibitor group, 152 of 217 (70.0%) in the ARB group, and 182 of 231 (78.8%) in the control group (posterior probabilities that ACE inhibitor and ARB worsened hospital survival compared with control were 95.3% and 98.1%, respectively). CONCLUSIONS AND RELEVANCE In this trial, among critically ill adults with COVID-19, initiation of an ACE inhibitor or ARB did not improve, and likely worsened, clinical outcomes. TRIAL REGISTRATION ClinicalTrials.gov Identifier: NCT0273570

Determinants and consequences of orthostatic hypotension in general and hypertensive population

L’hypotension orthostatique correspond à une baisse de la pression artérielle lors du passage à la position debout. Ce paramètre est associé à un sur-risque d’accident vasculaire cérébral, d’infarctus du myocarde, d’insuffisance cardiaque et de mortalité totale. Il est de ce point de vu proche des marqueurs de variabilité tensionnelle conventionnels que sont la variabilité tensionnelle inter-visite, la variabilité de moyen terme mesurée en auto-mesure tensionnelle et la variabilité de court terme mesurée en holter tensionnel. Cependant, contrairement à ces marqueurs conventionnels, l’association avec la démence n’a pas été démontrée. D’autre part, les relations entre l’hypotension orthostatique et ces autres marqueurs de variabilités ne sont pas connus. Enfin, si le diagnostic de l’hypotension orthostatique est relativement simple, la généralisation du dépistage en consultation n’est pas réalisée faute de temps. Objectifs : Nous proposons dans ce travail de mesurer l’association entre la présence d’une hypotension orthostatique et la survenue d’une démence. Nous réaliserons une étude mécanistique des déterminants de l’hypotension orthostatique à travers ses relations avec deux paramètres particuliers qui sont la variabilité tensionnelle en auto-mesure et la rigidité artérielle. Enfin, nous proposerons une méthode diagnostic par l’usage de l’auto-mesure tensionnelle. Matériel et méthode : Ces travaux sont réalisés à partir de la cohorte des 3 Cités qui est une cohorte de population générale de sujets de plus de 65ans recrutés sur trois centres : Bordeaux, Dijon et Montpellier. Une première étude longitudinale étudiera l’association entre la présence d’une hypotension orthostatique à l’inclusion dans la cohorte et la survenue d’une démence dans le suivi à 12 ans à travers des analyses de survie. Une deuxième étude transversale, utilisera un échantillon des sujets de Dijon autour du suivi à 10 ans qui ont bénéficié à la fois d’un dépistage de l’hypotension orthostatique, de la mesure de la rigidité artérielle et de la réalisation d’une série d’auto-mesure tensionnelle. Enfin, le dernier travail proposera une étude de faisabilité en soins courant de dépistage de l’hypotension orthostatique à travers un protocole d’auto-mesure tensionnelle adapté. Résultats : 7425 sujets ont été suivis sur une période de 12ans. La prévalence de l’hypotension orthostatique était de 13%. Le nombre de cas incidents de démence était de 512 cas. Les analyses de survie ont montré que l’hypotension orthostatique était associée à un sur-risque de démence de l’ordre de 25% dans des modèles ajustés en particulier sur le niveau de pression artérielle. Dans le deuxième travail une analyse transversale chez 1150 sujets a montré que l’hypotension orthostatique était associée de manière indépendante à la fois à la variabilité tensionnelle en autom-esure et à la rigidité artérielle. La variabilité tensionnelle et la rigidité artérielle ne sont pas associés. Dans le troisième travail, plus de 500 séries d’auto-mesure tensionnelle furent réalisées avec mesure de la pression artérielle en position debout sans altérer la qualité de l’auto-mesure tensionnelle classique. Conclusion : L’hypotension orthostatique est un paramètre hémodynamique riche qui reflète à la fois un vieillissement vasculaire marquée et un défaut de régulation de la pression artérielle immédiate. Elle est associée de manière indépendante au risque de démence. Une amélioration du diagnostic est possible par l’auto-mesure tensionnelle qui permet de multiplier les mesures en position debout et qui améliore le taux de dépistage.Orthostatic hypotension is a blood pressure drop when moving to standing position. It is associated with an over-risk of stroke, myocardial infarction, heart failure and total mortality. From this point of view, it is close to the conventional markers of blood pressure variability which are the inter-visit blood pressure variability, the mid-term variability measured by home blood pressure and the short-term variability measured by an ambulatory blood pressure monitoring. However, unlike these conventional markers, the association with dementia has not been demonstrated. In addition, the relationships between orthostatic hypotension and these other markers of variability are not known. Finally, although the diagnosis of orthostatic hypotension is relatively simple, the generalization of screening in consultation is not achieved. Objectives: In this work, we propose to measure the association of the orthostatic hypotension and the occurrence of dementia. In addition, we will carry out a mechanistic study of the determinants of orthostatic hypotension through its relations with two particular parameters : mid term variability and arterial stiffness. Finally, we will propose a diagnostic method using home blood pressure measurement. Material and methods: This work is based on the "3 Cities" cohort which is a general population cohort of subjects over 65 years old recruited from three centres: Bordeaux, Dijon and Montpellier. We will first study the association between orthostatic hypotension at baseline cohort and the occurrence of dementia in the 12-year follow-up through survival analyses. A second cross-sectional study will use a sample of Dijon subjects around the 10-year follow-up who were screened for orthostatic hypotension, pulse wave velocity measurement and performed a series of home blood pressure measurement. Finally, the last work will propose a feasibility study on the routine care of screening for orthostatic hypotension using an adapted blood pressure self-measurement protocol. Results: 7425 subjects were followed over a 12-year period. The prevalence of orthostatic hypotension was 13%. The number of incident cases of dementia was 512. Survival analyses showed that orthostatic hypotension was associated with an over-risk of dementia in the order of 25% adjusted with blood pressure level. In the second work, a cross-sectional analysis in 1000 subjects showed that orthostatic hypotension was independently associated with both mid-term blood pressure variability and arterial stiffness. Pressure variability and arterial stiffness were not associated. In the third work, we performed 500 series of home blood pressure with a BP measurement in the standing position without altering the quality of the classical report. Conclusion: Orthostatic hypotension is a rich hemodynamic parameter that reflects both a marked vascular ageing and a defect of immediate blood pressure regulation. It is independently associated with the risk of dementia. An improvement in diagnosis is possible through self-measurement of blood pressure, which allows more measurements to be taken in the standing position and improves the screening rate

Déterminants et conséquences de l'hypotension orthostatique en population générale et hypertendue

Orthostatic hypotension is a blood pressure drop when moving to standing position. It is associated with an over-risk of stroke, myocardial infarction, heart failure and total mortality. From this point of view, it is close to the conventional markers of blood pressure variability which are the inter-visit blood pressure variability, the mid-term variability measured by home blood pressure and the short-term variability measured by an ambulatory blood pressure monitoring. However, unlike these conventional markers, the association with dementia has not been demonstrated. In addition, the relationships between orthostatic hypotension and these other markers of variability are not known. Finally, although the diagnosis of orthostatic hypotension is relatively simple, the generalization of screening in consultation is not achieved. Objectives: In this work, we propose to measure the association of the orthostatic hypotension and the occurrence of dementia. In addition, we will carry out a mechanistic study of the determinants of orthostatic hypotension through its relations with two particular parameters : mid term variability and arterial stiffness. Finally, we will propose a diagnostic method using home blood pressure measurement. Material and methods: This work is based on the "3 Cities" cohort which is a general population cohort of subjects over 65 years old recruited from three centres: Bordeaux, Dijon and Montpellier. We will first study the association between orthostatic hypotension at baseline cohort and the occurrence of dementia in the 12-year follow-up through survival analyses. A second cross-sectional study will use a sample of Dijon subjects around the 10-year follow-up who were screened for orthostatic hypotension, pulse wave velocity measurement and performed a series of home blood pressure measurement. Finally, the last work will propose a feasibility study on the routine care of screening for orthostatic hypotension using an adapted blood pressure self-measurement protocol. Results: 7425 subjects were followed over a 12-year period. The prevalence of orthostatic hypotension was 13%. The number of incident cases of dementia was 512. Survival analyses showed that orthostatic hypotension was associated with an over-risk of dementia in the order of 25% adjusted with blood pressure level. In the second work, a cross-sectional analysis in 1000 subjects showed that orthostatic hypotension was independently associated with both mid-term blood pressure variability and arterial stiffness. Pressure variability and arterial stiffness were not associated. In the third work, we performed 500 series of home blood pressure with a BP measurement in the standing position without altering the quality of the classical report. Conclusion: Orthostatic hypotension is a rich hemodynamic parameter that reflects both a marked vascular ageing and a defect of immediate blood pressure regulation. It is independently associated with the risk of dementia. An improvement in diagnosis is possible through self-measurement of blood pressure, which allows more measurements to be taken in the standing position and improves the screening rate.L’hypotension orthostatique correspond à une baisse de la pression artérielle lors du passage à la position debout. Ce paramètre est associé à un sur-risque d’accident vasculaire cérébral, d’infarctus du myocarde, d’insuffisance cardiaque et de mortalité totale. Il est de ce point de vu proche des marqueurs de variabilité tensionnelle conventionnels que sont la variabilité tensionnelle inter-visite, la variabilité de moyen terme mesurée en auto-mesure tensionnelle et la variabilité de court terme mesurée en holter tensionnel. Cependant, contrairement à ces marqueurs conventionnels, l’association avec la démence n’a pas été démontrée. D’autre part, les relations entre l’hypotension orthostatique et ces autres marqueurs de variabilités ne sont pas connus. Enfin, si le diagnostic de l’hypotension orthostatique est relativement simple, la généralisation du dépistage en consultation n’est pas réalisée faute de temps. Objectifs : Nous proposons dans ce travail de mesurer l’association entre la présence d’une hypotension orthostatique et la survenue d’une démence. Nous réaliserons une étude mécanistique des déterminants de l’hypotension orthostatique à travers ses relations avec deux paramètres particuliers qui sont la variabilité tensionnelle en auto-mesure et la rigidité artérielle. Enfin, nous proposerons une méthode diagnostic par l’usage de l’auto-mesure tensionnelle. Matériel et méthode : Ces travaux sont réalisés à partir de la cohorte des 3 Cités qui est une cohorte de population générale de sujets de plus de 65ans recrutés sur trois centres : Bordeaux, Dijon et Montpellier. Une première étude longitudinale étudiera l’association entre la présence d’une hypotension orthostatique à l’inclusion dans la cohorte et la survenue d’une démence dans le suivi à 12 ans à travers des analyses de survie. Une deuxième étude transversale, utilisera un échantillon des sujets de Dijon autour du suivi à 10 ans qui ont bénéficié à la fois d’un dépistage de l’hypotension orthostatique, de la mesure de la rigidité artérielle et de la réalisation d’une série d’auto-mesure tensionnelle. Enfin, le dernier travail proposera une étude de faisabilité en soins courant de dépistage de l’hypotension orthostatique à travers un protocole d’auto-mesure tensionnelle adapté. Résultats : 7425 sujets ont été suivis sur une période de 12ans. La prévalence de l’hypotension orthostatique était de 13%. Le nombre de cas incidents de démence était de 512 cas. Les analyses de survie ont montré que l’hypotension orthostatique était associée à un sur-risque de démence de l’ordre de 25% dans des modèles ajustés en particulier sur le niveau de pression artérielle. Dans le deuxième travail une analyse transversale chez 1150 sujets a montré que l’hypotension orthostatique était associée de manière indépendante à la fois à la variabilité tensionnelle en autom-esure et à la rigidité artérielle. La variabilité tensionnelle et la rigidité artérielle ne sont pas associés. Dans le troisième travail, plus de 500 séries d’auto-mesure tensionnelle furent réalisées avec mesure de la pression artérielle en position debout sans altérer la qualité de l’auto-mesure tensionnelle classique. Conclusion : L’hypotension orthostatique est un paramètre hémodynamique riche qui reflète à la fois un vieillissement vasculaire marquée et un défaut de régulation de la pression artérielle immédiate. Elle est associée de manière indépendante au risque de démence. Une amélioration du diagnostic est possible par l’auto-mesure tensionnelle qui permet de multiplier les mesures en position debout et qui améliore le taux de dépistage

Estimation de la pression centrale par le QKD, validations par mesures invasives

Depuis une vingtaine d'années, il existe une révolution dans le domaine de l'hypertension artérielle. En effet il est maintenant acquis que la PAS et la PP sont les principaux facteurs pronostics de survenue d'accidents cardiovasculaires, plus puissant que l'historique PAD. L'étude de la rigidité artérielle a permis de démontrer qu'elle était un témoin central du vieillissement physiologique ou pathologique du réseau artériel. La PP est un marqueur de rigidité artérielle. Nous savons aujourd'hui que la rigidité artérielle atteint préférentiellement les sites centraux et que l'incidence du niveau de pression artérielle dans les sites centraux est fondamental pour la perfusion coronaire, le travail myocardique et la perfusion cérébrale. Plusieurs métodes non invasives de mesure de la pression centrale existent : méthode de calibration de Kelly et Fitchett ou le Sphygmocor® d'O'Rourke, toutes deux basées sur la tonométrie d'applanation. Pour autant ces méthodes, bien qu'ayant permis d'avancer dans les mécanismes de compréhension de l'HTA, comportent des limites qui restreignent leur usage en pratique courante. La pression centrale est liée au niveau de rigidité artérielle, de débit cardiaque et des résistances périphériques. A partir de ces données il semble possible de calculer la pression centrale. Nous avons choisi comme marqueur de rigidité artérielle le QKD dont l'intérêt principal est le caractère automatique de sa mesure au cours d'une mesure ambulatoire de la PA avec le diasys (Novacor, France). Au cours de coronarographies chez 65 patients (âge moyen 64 ans), la pression périphérique humérale moyenne, le QKD, la FC étaient mesurés de manière simultanée à la pression centrale invasive. 136 mesures de pressions ont ainsi été réalisées permettant à partir d'un modèle de régression linéaire multiple de proposer une équation de calcul de la pression centrale. L'équation suitante : PASc = 33,223 + 1,348 x PAMh - 0,405 x FC + 0,335 x âge - 0,105 x QKD, permet d'estimer 80 % de la variance de la PAS centrale invasive. Conclusion : Ce travail est très encourageant quant aux possibilités de calcul de la pression centrale de manière non invasive et permet d'espérer à terme son inclusion dans la mesure ambulatoire de la PA.For about twenty years there exists a revolution in the domain of hypertension. It is now certain that the Systolic BP and the Pulse Pressure are the principal prognostic factors in occuring cardiovascular events, more efficient than previous DBP. The sUtdy of arterial stiffness allows us to show the physiological and pathological aging process. The pulse pressure is a marker of arterial stiffness. Today we know that arterial stiffness mostly affects the ascending aorta. There, the level of central blood pressure determines the coronary perfusion, the cerebral perfusion and the heart's work. So the monitoring of the central SBP is a major stake for the follow up of our patients. Several techniques of non invasive central blood pressure measurement still exist like the calibration technique from Kelly & Fitchett or the Sphygmocor® from O'Rourke. But these two techniques have some limits which reduce their impact in daily clinical practice. The central SBP is linked to the arterial stiffness, the resistances and the cardiac output. With these elements it seems reasonable to estimate the the true level of the central SBP. We choose to do so with the QKD as a validated marker of arterial stiffness because it can be measured automatically during ambulatory BP monitoring with the Diasys Integra® (Novacor, France). During cardiac catheterization of 65 subjects (mean age 64,5 years), direct central SBP were measured and at the same time non invasive humeral IBP recorded with the QKD and the heart rate. 136 recording were done to allow us to propose by multiple linear equation model an estimation of the central SBP taking into account 80 % of its variance. Our equation is : cSBP = 33,223 + 1,348 x MBP-0,405 x HR + 0,335 x age - 0,105 x QKD. Conclusion : this work gives some very stimulating results to continue the development of these new method of non invasive central SBP estimation.BORDEAUX2-BU Santé (330632101) / SudocSudocFranceF