Qualité du greffon et risque cardiovasculaire en transplantation rénale (influence de la présence d'athérome chez le donneur)

MONTPELLIER-BU Médecine UPM (341722108) / SudocPARIS-BIUM (751062103) / SudocMONTPELLIER-BU Médecine (341722104) / SudocSudocFranceF

Apport sodé et influence des inhibiteurs de l'enzyme de conversion sur la régression de l'hypertrophie ventriculaire gauche chez l'hypertendu traité

MONTPELLIER-BU Médecine UPM (341722108) / SudocPARIS-BIUM (751062103) / SudocMONTPELLIER-BU Médecine (341722104) / SudocSudocFranceF

Valeur prédictive de l'hypertrophie ventriculaire gauche sur la morbi-mortalité cardio-vasculaire chez le transplanté rénal

MONTPELLIER-BU Médecine UPM (341722108) / SudocPARIS-BIUM (751062103) / SudocMONTPELLIER-BU Médecine (341722104) / SudocSudocFranceF

Existe-t-il un lien entre l'atteinte cardiaque, rénale et vasculaire chez le sujet hypertendu ?

MONTPELLIER-BU Médecine UPM (341722108) / SudocMONTPELLIER-BU Médecine (341722104) / SudocPARIS-BIUM (751062103) / SudocSudocFranceF

Cardiac and renal damage in the elderly hypertensive

In the elderly patient with essential hypertension of long duration or de novo systolic hypertension, the prevalence of co-morbid conditions, be they apparent or not, the burden of associated diseases and the alteration in nutritional status and lifestyle, result in specific problems with regards to hypertension-related target organ damage. Accumulating data suggest that left ventricular (LV) remodelling is a common finding in the nor-motensive elderly, and that LV hypertrophy (LVH) will herald the development of heart failure in a fraction of patients with either systolic/diastolic or isolated systolic hypertension. Increased arterial stiffness, as well as impaired myocardial relaxation, reduced early diastolic filling and decreased ?-adrenergic responsiveness, contribute to the large prevalence of abnormalities in LV function in the elderly hypertensive. The response to exercise is clearly attenuated, and coronary heart disease, although highly prevalent, may be misdiagnosed because symptoms are altered. The elderly hypertensive is exquisitely sensitive to both volume depletion and excessive sodium intake, due to a marked sodium sensitivity of blood pressure (BP). A decline in renal blood flow and glomerular filtration rate (GFR) is a common finding in the elderly. Although structural alterations attributed to age and hypertension may differ, hypertension is often looked upon as an accelerated form of ageing with regards to the heart and the kidney. Lifestyle modifications and initial monotherapy with a low-dose diuretic are warranted in the elderly hypertensive with no co-morbidity; a variety of specific approaches are considered when associated clinical conditions are present. Blockers of the renin-angiotensin system (RAS) may be the preferred first-line agents in many patients with cardiac or renal damage

Non invasive evaluation of end systolic left ventricular elastance according to pressure-volume curve modeling during ejection in arterial hypertension

International audienceObjective: End systolic left ventricular (LV) elastance (Ees) has been previouslycalculated and validated invasively using LV pressure-volume (P-V) loop. Noninvasive studies have been proposed, but clinical application remains complex.The aim of the present study was to 1) estimate Ees according to modeling ofLV P-V curve during ejection (“Ejection PV Curve’’ method) and validate ourmethod with existing published LV P-V loop data; 2) test clinical applicability todetect non invasively a difference in Ees between normotensive and hypertensivesubjects.Design and method: Based on P-V curve and a linear relationship between LV elastanceand time during ejection, we used a non linear least square method to fi t the systolicpressure curve. We then computed slope and intercept of time varying elastance,and calculated Ees as LV elastance at the end of ejection. As a validation, 22 P-V loopsobtained from previous invasive studies were digitized and analyzed with our method.To test clinical applicability, P-V curve was obtained from 33 hypertensive and 32normotensive subjects, using carotid tonometry and real time 3D echocardiography.Results: A good univariate relationship (r2 = 0.92, p < 0.005) and a good limit ofagreement were found between previous invasive calculation of Ees and our newproposed “Ejection P-V Curve’’ method. In addition, the clinical reproductibilityof our method was similar to that of another non invasive method proposed byChen et al. In hypertensive patients, the increase in arterial elastance (Ea) wascompensated by an increase in Ees without change in Ea/Ees (see Figure).Conclusions: Ees can be estimated non invasively from modeling of P-V curve duringejection. This approach was found to be reproducible and sensitive enough to detect anexpected difference in LV contractility in hypertensive patients. Due to its non invasivenature, this methodology may have clinical implications in various disease states

Non invasive evaluation of left ventricular elastance according to pressure-volume curves modeling in arterial hypertension

International audienceEnd-systolic left ventricular (LV) elastance (Ees) has been previously calculated and validated invasively using LV pressure-volume (P-V) loops. Noninvasive methods have been proposed, but clinical application remains complex. The aims of the present study were to 1) estimate Ees according to modeling of the LV P-V curve during ejection (“ejection P-V curve” method) and validate our method with existing published LV P-V loop data and 2) test the clinical applicability of noninvasively detecting a difference in Ees between normotensive and hypertensive subjects. On the basis of the ejection P-V curve and a linear relationship between elastance and time during ejection, we used a nonlinear least-squares method to fit the pressure waveform. We then computed the slope and intercept of time-varying elastance as well as the volume intercept (V0). As a validation, 22 P-V loops obtained from previous invasive studies were digitized and analyzed using the ejection P-V curve method. To test clinical applicability, ejection P-V curves were obtained from 33 hypertensive subjects and 32 normotensive subjects with carotid tonometry and real-time three-dimensional echocardiography during the same procedure. A good univariate relationship (r2 = 0.92, P < 0.005) and good limits of agreement were found between the invasive calculation of Ees and our new proposed ejection P-V curve method. In hypertensive patients, an increase in arterial elastance (Ea) was compensated by a parallel increase in Ees without change in Ea/Ees. In addition, the clinical reproducibility of our method was similar to that of another noninvasive method. In conclusion, Ees and V0 can be estimated noninvasively from modeling of the P-V curve during ejection. This approach was found to be reproducible and sensitive enough to detect an expected increase in LV contractility in hypertensive patients. Because of its noninvasive nature, this methodology may have clinical implications in various disease states

Retinal vascular caliber associated with cardiac and renal target organ damage in never-treated hypertensive patients

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Application of the 2015/2016 EULAR recommendations for cardiovascular risk in daily practice: data from an observational study

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