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To determine the predictive factors of mortality after hospitalization for acute heart failure (AHF) in an internal medicine department. Retrospective observational analysis conducted on 164 patients hospitalized for AHF in 2016-2017. Demographic, clinical and biological characteristics were assessed during hospitalization. The primary endpoint was the occurrence of all-cause death. Multivariate analysis was performed using the Cox model adjusted for age and renal function. The study population was mostly female (n = 106, 64.6%), elderly (82.9 years ± 10.0), with a preserved LVEF (86%). Mean Charlson comorbidity index was 6.5 ± 2.5. After a median follow-up of 17.5 months (IQR 6-38), 109 patients (65%) had died with a median time to death of 14 months (IQR 3-29). In univariate analysis, patients who died were significantly older, had lower BMI and renal function, and higher CCI and NT-proBNP levels (median of 4944 ng/l [2370-14403] versus 1740 ng/l [1119-3503], p < 0.001). In multivariate analysis, risk factors for death were lower BMI (HR 0.69, CI [0.53-0.90], p = 0.005), lower albuminemia (HR 0.77 [0.63-0.94], p = 0.009), higher ferritinemia (HR 1.38 [1.08-1.76], p = 0.010), higher uricemia (HR 1.28 [1.02-1.59], p = 0.030), higher NT-proBNP (HR 2.46 [1.65-3.67], p < 0.001) and longer hospital stay (HR 1.25 [1.05-1.49] p = 0.013). In elderly multimorbid patients, AHF prognosis appears to be influenced by nutritional criteria, including lower BMI, hypoalbuminemia, and hyperuricemia (independently of renal function). These results underline the importance of nutritional status, especially as therapeutic options are available. This consideration paves the way for further research in this field., (© 2022. The Author(s), under exclusive licence to Società Italiana di Medicina Interna (SIMI).)

Purpose: Obesity is associated with increased cardiovascular risk. Bariatric surgery (BS) improves the clinical and metabolic profile. Retinal caliber changes could precede cardiovascular events. Different studies have shown an improvement in retinal caliber after BS. The aim of this study was to examine retinal caliber and other cardiovascular target organ damage before and after BS., Materials and Methods: Monocentric, prospective cohort study at the Montpellier University Hospital. Biologic features, vessel stiffness, echocardiograph variables, and retinal caliber at baseline and 6 and 12 months were assessed in consecutive patients with class 2 or 3 obesity undergoing BS. A mixed linear model adjusted for age and sex was used., Results: We included 88 patients (75 women). The mean (SD) age was 43 years (11) and mean (SD) baseline weight 117 (21) Kg. Mean changes in the first year after BS were - 5.1 µm in central retinal vein equivalent (CRVE) (p < 0.0001), + 0.02 in arteriole-to-venule ratio (AVR) (p < 0.0001), - 1.4 mmol/L in glycemia (p < 0.0001), - 1.0 mg/L in natural logarithm of C-reactive protein (p < 0.0001), and - 54.0 g in left ventricular mass (p = 0.0005). We observed no significant improvement in arterial stiffness markers. Predictors of improvement in CRVE were high baseline weight (p = 0.030), male sex (p = 0.025), and no diabetes history (p Dynamic links between variations = 0.047)., Conclusion: The retinal microvascular phenotype improved during the first year after bariatric surgery, with decreased CRVE and increased AVR. Factors associated with retinal microvascular plasticity were male sex, high baseline weight, and absence of diabetes. Longitudinal assessment of retinal vascular calibers may offer new insights into the pathophysiology of subclinical vascular processes., (© 2022. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)

Objectives: EULAR recently proposed to screen multimorbidities in chronic inflammatory rheumatic diseases. The aims of the study were to define the most common multimorbidities in chronic inflammatory rheumatic diseases, compare the screening approach performed in the clinic with the recent EULAR recommendations, validate the points to consider for the systematic standardized multimorbidity screening proposed by EULAR and assess feasibility of such a screening in a daily clinic., Methods: Data were collected prospectively during a 1-day multimorbidity clinic. Diabetes, hypertension, CVD damage, chronic respiratory diseases, osteoporosis and preventive measures were assessed. The comparison with EULAR points to consider was performed retrospectively., Results: We included 200 consecutive patients (157 with rheumatoid arthritis, 37 spondyloarthritis, and 6 connective tissue diseases or vasculitis). The most common multimorbidities already diagnosed in our patients were hypertension (26%) and diabetes (7.5%). Screening showed that 61.5% (CI95%: 54.6%-67.9%) patients presented at least one undiagnosed or uncontrolled diseases: diabetes (6%), hypertension (20.6%), dyslipidemia (16.1%) valvulopathies (16.8%), peripheral artery disease (4.5%); carotid stenosis (6.5%) and aortic aneurysm (5.5%). Overall, 39.9% patients had incomplete cancer screening and 52.8% incomplete vaccine schedule. Undiagnosed pulmonary obstruction and risk of sleep apnea were suspected in 15.5% and 40.1% patients, respectively., Conclusion: This study underlines the relevance of a systematic screening of multimorbidities in chronic inflammatory rheumatic diseases and its feasibility in a 1-day clinic. Spirometry and sleep apnea screening should be added to EULAR points to consider. The long-term impact of such screening needs to be evaluated., (Copyright © 2018 Société française de rhumatologie. Published by Elsevier Masson SAS. All rights reserved.)

Objective: It was shown that sodium can promote auto-immunity through the activation of the Th17 pathway. We aimed to compare sodium intake in patients with rheumatoid arthritis (RA) vs. matched controls., Methods: This case-control study included 24 patients with RA at diagnosis and 24 controls matched by age, gender and body mass index. Sodium intake was evaluated by 24-hr urinary sodium excretion., Results: Sodium excretion was greater for patients with early RA (2,849±1,350 vs. 2,182±751.7mg/day, p = 0.039) than controls. This difference remained significant after adjustment for smoking and the use of anti-hypertensive and nonsteroidal anti-inflammatory drugs (p = 0.043). Patients with radiographic erosion at the time of diagnosis had a higher sodium excretion than those without (p = 0.028)., Conclusion: Patients with early RA showed increased sodium excretion which may have contributed to autoimmunity.

End-systolic left ventricular (LV) elastance ( E es ) 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 E es 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 E es 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 (V 0 ). 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 ( r 2  = 0.92, P < 0.005) and good limits of agreement were found between the invasive calculation of E es and our new proposed ejection P-V curve method. In hypertensive patients, an increase in arterial elastance ( E a ) was compensated by a parallel increase in E es without change in E a / E es In addition, the clinical reproducibility of our method was similar to that of another noninvasive method. In conclusion, E es and V 0 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. NEW & NOTEWORTHY The use of real-time three-dimensional echocardiography-derived left ventricular volumes in conjunction with carotid tonometry was found to be reproducible and sensitive enough to detect expected differences in left ventricular elastance in arterial hypertension. Because of its noninvasive nature, this methodology may have clinical implications in various disease states., (Copyright © 2017 the American Physiological Society.)

Objective: The aim of this study was to assess the relationship between retinal vascular caliber and target organ damage in HT patients., Methods: Data were collected on cardiac, renal, vascular, and retinal variables in 88 consecutive never-treated HT subjects. Retinal vascular calibers were measured from fundus photographs by using a semi-automated computer-assisted program and summarized as CRAE and CRVE., Results: Mean CRAE and CRVE were significantly lower in patients with left ventricular hypertrophy (left ventricular mass ≥110 g/m² for women, 125 g/m² for men) than in those with normal left ventricular (CRAE: 129.4±3.7 vs 138.2±2.3 μm; P=.04; CRVE: 195.6±4.4 vs 209.8±2.7 μm; P=.008). CRAE and CRVE were negatively correlated with urinary albumin excretion (β±SE=-15.4±3.2, P<.0001 and β±SE=-11.9±4.4, P=.001, respectively) but were not correlated with estimated glomerular filtration rate (P=.21 and P=.75, respectively), carotid-to-femoral pulse wave velocity (P=.24 and P=.14), or carotid augmentation index (P=.43 and P=.16)., Conclusion: In never-treated HT patients, reduced CRAE and CRVE were associated with cardiac and renal preclinical damage, ie, left ventricular hypertrophy and albuminuria, but not estimated glomerular filtration rate or vascular stiffness., (© 2016 John Wiley & Sons Ltd.)

After kidney donation, the remaining kidney tends to hyperfiltrate, thus limiting the initial loss of renal function. The potential determinants of this adaptive glomerular hyperfiltration (GHF) and specifically the influence of arterial function are poorly known. In 45 normotensive healthy kidney donors [51 ± 10 yr (mean ± SD), 39 females], glomerular filtration rate (GFR) was measured as the clearance of continuously infused (99m)Tc-DTPA and timed urine collections at baseline, i.e., before donation, and 1 yr after donation. GHF was computed as postdonation GFR minus half of baseline GFR. Arterial function was assessed as baseline carotid-femoral pulse wave velocity (PWV) and carotid augmentation index (AIx). After kidney donation, no significant change in blood pressure (BP) was observed, but two subjects developed hypertension. GFR decreased from 107 ± 19 to 73 ± 15 ml·min(-1)·1.73 m(-2), and mean GHF was 20 ± 10 ml·min(-1)·1.73 m(-2). In univariate analysis, GHF was inversely correlated to age (r(2) = 0.24, P = 0.01), baseline PWV (r(2) = 0.23, P = 0.001), and Aix (r(2) = 0.11, P = 0.031). Nevertheless, GHF was not correlated to baseline peripheral or central BP. In multivariate analysis, baseline PWV, but not AIx, remained inversely correlated to GHF, independently of age, baseline mean BP, and GFR (model r(2) = 0.34, P < 0.001). In healthy subjects selected for renal donation, increased arterial stiffness is associated with decreased postdonation compensatory hyperfiltration., (Copyright © 2015 the American Physiological Society.)

Background: We hypothesized that dietary sodium may modulate the effect of systolic blood pressure and other nonhemodynamic factors, such as high uric acid and renal dysfunction, on changes in the left ventricular mass after renal transplantation. The objective of the present 3-year follow-up longitudinal study was to assess the concomitant influence of these factors on changes in the left ventricular mass after renal transplantation., Methods: Twenty-four-hour urinary sodium excretion, glomerular filtration rate (isotopic clearance), and left ventricular mass (echocardiography) assessment were done in 165 renal transplant patients during the first year and after a follow-up of 3 years after renal transplantation., Results: At follow-up, therapy of hypertension was associated with normalization of blood pressure in 64% and a decrease in the prevalence of left ventricular hypertrophy from 66% to 56%. At baseline and follow-up, systolic blood pressure, sodium intake, and serum uric acid emerged as independent and significant determinants of the final left ventricular mass index. When the population was divided according to sex-specific tertiles of the final 24-hr urinary sodium excretion, the relationship between change in serum uric acid during follow-up, final left ventricular mass index, and final glomerular filtration rate was significant only on the highest tertile of 24-hr urinary sodium excretion., Conclusion: The decrease in the prevalence of left ventricular hypertrophy after renal transplantation is blunted by high sodium intake. Persistence of the left ventricular hypertrophy may result from the combined adverse influences of excessive dietary sodium intake and increased serum uric acid during follow-up despite pharmacological control of blood pressure.

Because the functional interaction between the LV and arterial systems, termed ventricular-arterial coupling, is recognized as a key determinant of LV performance, the objective of the present study was to assess the impact of uncomplicated HT without LVH on LV performance using simultaneously echocardiography and carotid tonometry. LV maximal power (PmaxVG), cardiac power output (CPO), LV efficiency (CPO/PmaxVG), input aortic and output LV elastance (Ea and Ees) were assessed in 20 normotensive control subjects (NT) and 10 patients with untreated HT. PmaxVG was calculated according to the integral of the product of LV wall stress with strain rate (as an index of gradient velocity). Cyclic variation of wall thickness and SR were measured by speckel-tracking. Ea and Ees were derived and modelized from the pressure-volume curve. No difference in age, BMI and sex ratio was observed between NT and HT. Systolic BP (160±18 vs. 119±10mmHg), LV mass (99±15 vs. 76±12g/m(2)), PWV (9.7±2 vs. 6.9±1m/s) were significantly higher (P<0.01) in HT when compared to NT. In HT increased of CPO and Ea was compensated by an increase of LV (15±4 vs. 12±3%, P<0.02) and Ees (5.5±2 vs. 4.5±1.5mmHg/mL), which are significantly elevated in HT (P<0.05). No difference was observed in Ea/Ees between NT and HT. In conclusion at the early phase of HT, in patients without LVH, LV performance and ventricular-arterial coupling were adapted to post-load elevation. This adaptation may be the result of an increased of LV contractility., (Copyright © 2014 Elsevier Masson SAS. All rights reserved.)

Purpose: To assess the relation between retinal vascular caliber and renal function., Patients and Methods: Eighty apparently healthy subjects screened for cardiovascular risk factors (mean age 47 years, 51% female, 36% hypertensive, without diabetes or renal dysfunction) were recruited. Retinal vascular calibers were measured from fundus photographs and expressed as central retinal artery and venular equivalent. Renal function was assessed by measurement of glomerular filtration rate (urinary clearance of 99mTc-DTPA) and urinary albumin/creatinine ratio., Results: Mean glomerular filtration rate was 117 ml/min/1.73m(2). Overall, central retinal artery and venular equivalent were positively correlated with glomerular filtration rate (r = +0.31, p = 0.005 and r = +0.30, p = 0.006, respectively). In addition, central retinal artery equivalent was negatively correlated with urinary albumin/creatinine ratio (r = -0.34, p = 0.002). No significant relationship was found between central retinal venular equivalent and urinary albumin/creatinine ratio (r = +0.12, p = 0.32). The observed relations between retinal vascular calibers and renal function parameters remained significant after adjusting for potential confounding factors., Conclusion: In apparently healthy subjects with normal renal function, retinal arteriolar and venular calibers were negatively correlated with kidney function, suggesting common determinants of these preclinical target organ damages., (© 2013 The Authors. Acta Ophthalmologica © 2013 Acta Ophthalmologica Scandinavica Foundation. Published by Blackwell Publishing Ltd.)

Background: Cardiovascular mortality is increased in patients with rheumatoid arthritis (RA). RA is associated with an increased left ventricular mass index (LVMI), a strong marker of cardiovascular mortality, and vessel abnormalities. Experimental studies have suggested that tumour necrosis factor α (TNFα) may induce LV hypertrophy., Objective: To study the effect of medium-term (3- and 6-months) treatment with the TNFα inhibitor etanercept (ETN) and synthetic disease-modifying antirheumatic drugs (sDMARDs) on LV morphological features and arterial stiffness in patients with RA., Methods: Consecutive female patients with active RA requiring treatment with ETN (n=28) or sDMARDs (n=20) were included. Clinical and biological monitoring, echocardiography and pulse wave velocity (PWV) assessment were performed at inclusion and at 3 and 6 months after the start of treatment. Paired t tests and multivariate linear regression analysis were used., Results: Mean LVMI tended to be higher at baseline in the ETN group than in the sDMARD group (96.5±19.8 vs 84.3±26.8 g/m2; p=0.11 for the ETN and sDMARD groups, respectively). In patients with ETN treatment, mean LVMI was significantly decreased at 3 and 6 months (-6.3±7.6 and -14.2±9.3 g/m2; p<0.001), with no change from baseline for patients with sDMARD treatment (-2.2±10.9 and -2.7±10.2 g/m2, respectively). Blood pressure (BP) and aortic PWV were not changed by either treatment., Conclusions: ETN induced a significant decrease in LVMI with medium-term treatment with no change in BP or PWV. TNFα may be an important factor of LV hypertrophy, which may explain the benefit of TNF inhibitors on cardiovascular morbidity and mortality in RA. These results need to be confirmed by larger studies and with other TNF inhibitors.

Background/aim: In chronic renal failure the increase in cardiovascular risk is in part related to the high prevalence of left ventricular hypertrophy. The aim of the present monocentric retrospective study was to evaluate the influence of the presence of parenchymal kidney disease on left ventricular geometry in normotensive (arterial pressure <140/90 mm Hg) patients (KD+, n = 50, mean age 39 ± 19 years) with mild to moderate renal failure (stage 2-3 chronic kidney disease)., Methods: Left ventricular geometry was estimated by echocardiography and compared to a group of healthy subjects with similarly reduced renal function as a consequence of renal donation (KD-, n = 63, mean age 52 ± 12 years)., Results: Subjects with and without kidney disease had similar blood pressure, body mass index and isotopic glomerular filtration rate. Left ventricular mass (LVM) indexed to body surface area was greater in KD+ as compared to KD- subjects and the difference was more pronounced in women than in men. The increase in LVM in KD+ patients was associated with lower albuminemia and hematocrit, and a higher plasma renin activity and aldosterone as compared to KD- subjects. In multivariate analysis, kidney disease emerged as an important determinant of LVM index independently of age, gender and blood pressure., Conclusion: This observation suggests that the presence of kidney disease has an independent amplifying effect on LVM which could be related to volume overload and/or prohypertrophic factors such as aldosterone., (Copyright © 2013 S. Karger AG, Basel.)

Background: To determine whether inhibitors of the renin-angiotensin system (RAS) reduce the incidence of renal dysfunction when compared to other antihypertensive treatments in patients with essential hypertension and no pre-existent renal disease., Methods: The search strategy used the Cochrane Library, Medline, previous meta-analyses, and journal reviews. The selection criteria included randomized, controlled trials of antihypertensive drugs that compared a RAS inhibitor with another treatment in essential hypertension. Studies that specifically enrolled only patients with diabetes or renal disease were not included. The quality assessment and data extraction of studies were performed by two independent reviewers. Effects on dichotomous renal outcome (serum creatinine (SCreat) higher than a prespecified value, doubling of SCreat or end-stage renal disease) and secondary continuous marker of renal outcome (change in SCreat) were calculated using Peto's method., Results: 33,240 patients met the inclusion criteria for studies with a dichotomous outcome and 10,634 patients for studies with a continuous outcome. The mean follow-up was 42 ± 13 months. Patients randomized to RAS inhibitors did not show a significant reduction in the risk of developing renal dysfunction as compared to other antihypertensive strategies (odds ratio = 1.05; 95% confidence interval (CI) 0.89-1.25; P = 0.54). There was no significant difference in change of SCreat between groups (mean difference = 0.0005 mg/dl; 95% CI -0.0068 to 0.0077 mg/dl; P = 0.91)., Conclusion: In patients with essential hypertension and no pre-existent renal disease, prevention of renal dysfunction is not significantly different with RAS inhibitors when compared to other antihypertensive agents.

Objective: L-Thyroxine-suppressive therapy benefits high-risk differentiated thyroid cancer patients by decreasing recurrence rates and cancer-related mortality. However, fully suppressed serum thyroid-stimulating hormone (TSH) implies a state of subclinical hyperthyroidism (SCH) with associated adverse cardiac effects. Because left ventricular (LV) diastolic dysfunction may be the first manifestation of more severe LV failure, and to balance the risks from thyroid cancer recurrence with risks of cardiac failure, the purpose of this study was to analyse new parameters of LV function in asymptomatic patients with exogenous SCH., Design: Case-control study with 24 patients on TSH-suppressive therapy of short duration (≤ 4 years) after thyroid ablative therapy for differentiated thyroid carcinoma and 20 age- and sex-matched subjects., Measurements: LV function [LV global strain and strain rate (SR) curves] was assessed by speckle tracking imaging echocardiography in each subject., Results: Patients and controls do not differ in body mass index, systolic blood pressure and heart rate. No significant differences were observed in LV morphology (LV mass and relative wall thickness), cardiac output and parameters of LV systolic function between patients on suppressive therapy and controls. When compared with controls, patients with exogenous SCH had a significantly impaired longitudinal protodiastolic strain, SR and strain diastolic index but preserved radial strain and SR function., Conclusions: In subjects with SCH at the early phase of TSH-suppressive therapy, evidence of isolated longitudinal LV diastolic dysfunction was observed, despite a normal LV morphology. Further prospective studies to clarify the prognosis of picking-up early diastolic dysfunction in asymptomatic patients are needed before serial measurements could be recommended., (© 2011 Blackwell Publishing Ltd.)

Objective: To determine the relationship between arterial function (stiffness and wave reflection) and glomerular hemodynamics., Methods: In 49 healthy normotensive individuals, glomerular filtration rate (GFR) and effective renal plasma flow (ERPF) were measured by urinary clearances of 99mTC-DTPA and 131I-hippuran, respectively. Filtration fraction was computed as GFR/ERPF. Arterial stiffness was estimated by carotid-femoral pulse wave velocity (PWV). Wave reflection was evaluated by carotid augmentation index (AIx), reflection magnitude and the round-trip travel time of the pressure wave., Results: PWV and round-trip travel time were not independently correlated with any renal hemodynamic parameter or urinary albumin-creatinine ratio (UACR). AIx and reflection magnitude were directly correlated with filtration fraction (r = 0.35 and 0.37, respectively) and UACR (r = 0.43 and 0.53, respectively). When the population was divided into quartiles of reflection magnitude, filtration fraction and UACR progressively increased from the lowest to the highest quartile and after adjustment for age, mean arterial pressure, heart rate but also sex for UACR (P linear trend = 0.031 and 0.001, respectively)., Conclusion: It is suggested that in normal individuals, the amplitude of wave reflection but not arterial stiffness is associated with signs evocative of increased glomerular pressure (filtration fraction and UACR), independently of systemic blood pressure.

In essential hypertension, the regression of left ventricular hypertrophy is an important goal of treatment. In addition to treatment-associated changes in blood pressure (BP), the roles of other determinants of left ventricular hypertrophy regression, including dietary sodium intake, deserve investigation. In the present study, the change in echographic left ventricular mass index (LVMI) was assessed in 182 patients with never-treated essential hypertension at baseline and after 3 years of treatment by angiotensin converting enzyme inhibitors or angiotensin II receptor antagonists given at recommended doses and associated with other antihypertensive agents. Treatment was associated with satisfactory control of BP (<140/90 mm Hg) in 64% of patients, and left ventricular hypertrophy prevalence decreased from 56% to 39%. Twenty-four-hour urinary sodium was positively related to LVMI at baseline and at the end of the study, independently of age, sex, and systolic BP. Supine plasma aldosterone concentration was correlated with LVMI only at baseline but not in multivariate analysis. In response to treatment, the percentage of change in LVMI was positively correlated with the absolute changes in systolic BP, urinary sodium, and plasma aldosterone concentration, independently of baseline LVMI. The population was divided into 3 tertiles according to final values of gender-specific urinary sodium. When, within each urinary sodium tertile, patients were divided into those with plasma aldosterone concentration below and above the median (11.6 ng/dL), LVMI progressively increased across sodium tertiles only in patients with high plasma aldosterone concentration. Systolic BP was similar across all of the groups. In conclusion, aldosterone requires the presence of high dietary salt for the expression of its unfavorable effect on the heart.

After the demonstration of a positive correlation between sodium intake and arterial pressure in large population studies, the effect of short-term reduction in sodium intake demonstrated the efficacy of this nonpharmacologic therapy. In addition, a positive relation between urinary sodium (the most reliable estimate of salt intake) and left ventricular hypertrophy was found; and in recent years it was shown that cardiovascular morbidity clearly progressed with increasing sodium intake, despite one contradictory study. The role of non-pressure-related effects of dietary sodium is discussed in order to bring more arguments for a large-scale attempt to reduce sodium intake by 30% to 50%.

Background: In large epidemiological studies and using serum creatinine or estimates of glomerular filtration rate (GFR), blood pressure has emerged as a predominant determinant of the age-associated decline in renal function., Methods: The present longitudinal study (median follow-up period of 5.8 years) was conducted in 132 never-treated patients with essential hypertension at baseline. The effect of treatment on the GFR and effective renal plasma flow, estimated by urinary clearances of isotopic markers, was assessed., Results: Satisfactory control of hypertension (<140/90 mmHg) was achieved in 57% of the population. During follow-up, the yearly change in the GFR was -1.72+/-0.21 ml/min per year (mean+/-SEM). In univariate regression analysis, the change in the GFR was correlated with baseline pulse pressure (r=-0.27, P=0.002), whereas no influence of systolic, diastolic or mean blood pressures, as well as baseline albuminuria or left ventricular mass index, was found. Multivariate logistic regression analysis showed that only baseline pulse pressure conveyed a significant odds ratio of accelerated decline of GFR (>median of 1.5 ml/min per year), independently of age, baseline GFR, mean blood pressure and other known cardiovascular risk factors. No influence of the type of antihypertensive treatment (64% of the population had received angiotensin-converting enzyme inhibitor) was detected., Conclusion: Pulse pressure (a marker of arterial stiffening) is suggested as an independent determinant of the treatment-associated decline in renal function in essential hypertension. No influence of target organ damage (albuminuria of left ventricular hypertrophy) was detected.

Background: The Cockcroft-Gault (CG) and simplified Modification of Diet in Renal Disease (MDRD) formulas are the most widely used estimates of renal function. The influence of age and body mass index (BMI) on the performance of these equations was analyzed in 850 subjects with serum creatinine levels less than 1.5 mg/dL (<133 micromol/L)., Methods: Glomerular filtration rate (GFR) was measured as urinary clearance of continuously infused technetium Tc 99m-labeled diethylene triaminopentaacetic acid. Performance was assessed as bias, precision, and accuracy., Results: In the total population, the CG and MDRD calculations based on enzymatic measurement of serum creatinine (which is constantly less than that obtained by using the alkaline picrate [Jaffé] method) significantly underestimated GFR by 4.9 and 12.4 mL/min/1.73 m2 (0.08 and 0.21 mL/s/1.73 m2), respectively. In patients 65 years and older, underestimation by means of the CG formula was enhanced, whereas that by means of the MDRD formula was blunted, compared with the group younger than 65 years (-11.3 versus -3.7 mL/min/1.73 m2 [-0.19 versus -0.06 mL/s/1.73 m2] for CG and -3.7 versus -14.0 mL/min/1.73 m2 [-0.06 versus -0.23 mL/s/1.73 m2] for MDRD). GFR was underestimated to a large extent by means of the MDRD equation irrespective of BMI. Conversely, the underestimation by means of the CG formula found in lean people (-13.0 mL/min/1.73 m2 [-0.22 mL/s/1.73 m2]) was blunted in overweight people (BMI, 25 to 30 kg/m2) and reversed to overestimation (+10.1 mL/min/1.73 m2 [+0.17 mL/s/1.73 m2]) in obese subjects (BMI > 30 kg/m2)., Conclusion: As suggested by estimations obtained using enzymatic serum creatinine measurement, the MDRD equation may be the estimation of choice in elderly patients, whereas the CG estimate is preferable in subjects younger than 65 years. Nevertheless, when obesity is present, no reliable estimation can be obtained by using the CG or MDRD formula.

Background: In the present longitudinal study, we attempted to identify the determinants of cardiorenal damage progression in normotensive subjects (<140/90 mm Hg) and patients with never-treated essential hypertension., Methods: Renal hemodynamics and function and cardiac morphology were evaluated by isotopic techniques and echocardiography at baseline and after a median follow-up period of 5.2 years (range 3 to 13) in 30 normotensive and 33 hypertensive subjects., Results: The results are mean +/- SD. Among normotensive subjects at baseline, 50% became hypertensive during follow-up. In the whole population, multivariate analysis showed that age was the main determinant of the progression of systolic blood pressure. The yearly change in glomerular filtration rate (GFR) was exaggerated in hypertensive when compared to normotensive subjects at baseline (-1.22 +/- 2.71 vs. 0.12 +/- 2.08 mL/min/year, respectively) (P= 0.033). In the whole population, only baseline systolic blood pressure remained correlated to the change in GFR, independently of GFR at baseline (model r(2)= 0.44) (P < 0.0001). The observed increase in albuminuria was correlated with change in blood pressure only in hypertensive subjects at baseline. Left ventricular mass (LVM) progression was significant only in men and its determinants were basal plasma aldosterone, serum uric acid, and triglyceride and change in systolic blood pressure (r(2)= 0.71) (P < 0.0001)., Conclusion: In a population of untreated subjects, baseline blood pressure as well as progression of blood pressure during follow-up are the main determinants of the decline in GFR, progression of albuminuria, and LVM.

Experimental and clinical data suggest that primary aldosteronism (PA) may be associated with cardiovascular hypertrophy and fibrosis, in part independent of the BP level. Whether PA may also result in specific deleterious effects on the kidneys was less studied. In 25 patients with tumoral PA, renal studies (urinary excretion of proteins, GFR, and effective renal plasma flow [ERPF], as clearances of technetium-labeled diethylene triaminopentaacetic acid and 131I-ortho iodohippurate, respectively) were performed both before and 6 mo after surgical cure. A control group consisting of patients with essential hypertension (EH) was studied before and after 6 mo of antihypertensive therapy. At baseline, PA and EH patients were similar with respect to demographic data, duration and level of hypertension, and GFR and ERPF. Urinary excretion of albumin and beta2 microglobulin were higher in PA than EH (88 +/- 26 versus 39 +/- 12 and 0.91 +/- 0.23 versus 0.26 +/- 0.19 mg/24 h, respectively; both P < 0.05). Adrenalectomy was followed by a decrease in arterial BP (by 28 +/- 3/13 +/- 2 mmHg), urinary excretion of albumin and beta2 microglobulin (by 48 +/- 19 and 0.53 +/- 0.21 mg/24 h, respectively), and GFR and ERPF (by 15 +/- 3 and 54 +/- 15 ml/min per 1.73 m(2), respectively). In EH, a similar decrease in pressure was associated with a decrease in albuminuria but no change in GFR or ERPF. In 17 of the 25 PA patients who received a 6-mo treatment of spironolactone, both GFR and ERPF decreased in parallel with BP, similar to what was observed after surgery. These data suggest that PA was associated with relative hyperfiltration, unmasked after suppression of aldosterone excess.

In the past decade, pulse pressure has emerged as a strong predictor of cardiovascular morbidity and mortality. During aging, elevation of pulse pressure is a consequence of stiffening of the arterial wall. The relationship between pulse pressure and the renal aging process was studied in a cohort of 212 patients with never-treated isolated systolic hypertension. Glomerular filtration rate and effective renal plasma flow were measured using constant infusion of technetium 99m (99mTc)-DTPA and 131I-ortho-iodohippurate, respectively, and timed urine collections. The relationship between pulse pressure and renal function was studied using a linear regression model in the total population and in 40 to 49, 50 to 59, and 60 years and older age categories. In the whole population, there was an inverse relationship between pulse pressure and glomerular filtration rate; however, this relation did not persist after adjustment for age. In fact, the inverse relationship between pulse pressure and glomerular filtration rate was only present in patients 60 years of age or older. This relationship in elderly patients remained after adjustment for age, gender, MAP, and cardiovascular risk factors (P=0.006). It is suggested that pulse pressure, a marker of arterial stiffening, may have a detrimental influence on the age-related decline in glomerular filtration rate, after 60 years of age in patients with never-treated isolated systolic hypertension.

Background: Pulse pressure (PP), a marker of cyclic strain on the arterial wall, is a significant predictor of cardiovascular (CV) risk, particularly regarding the incidence of coronary arterial stenosis. Genes related to haemostatic and/or fibrinolytic factors are consistently influenced in vitro by mechanical strain., Objective: The goal of the present study was to determine, in the three genotypes of the plasminogen activator inhibitor (PAI)-1 gene polymorphism, the gender-adjusted difference in the relationships between age and PP in subjects with never treated essential hypertension., Results: In the studied population, the genotype deletion (D)/D at position -675 of the PAI-1 insertion (I)/D gene polymorphism was associated with a significant increase in the adjusted slope of the curve relating age to PP by comparison with the two other genotypes. No comparable difference in age-related changes in systolic, diastolic or mean blood pressure was found., Conclusion: In subjects with essential hypertension, the PAI-1 I/D gene polymorphism modulates the age-mediated increase of PP, suggesting new insights on the complex interactions between genes, mechanical factors and CV risk.

The activation of the renin-angiotensin system is associated with vascular and cardiac hypertrophy. But there are few data on the renal and cardiac consequences of the hypersecretion of aldosterone. In the experimental setting, hyperaldosteronism leads to an excess of fibrous interstitial tissue and cardiac hypertrophy. In man, these consequences are those of hyperaldosteronism. The aim of this study was to assess the cardiac consequences of hyperaldosteronism in a series of 31 patients with a documented Conn adenoma, in comparison with a matched population of 31 patients with primary hypertension. For the same level of blood pressure, cardiac hypertrophy is more prominent in hyperaldosteronism and there is a positive correlation between the level of plasma aldosterone and left ventricular wall thickness. Left ventricular hypertrophy is of the concentric type. In addition, an increase in myocardial fibrosis (that can now be quantified by echocardiography) is observed, with a positive correlation between plasma aldosterone and reflected ultrasound which might correspond to increased myocardial collagen. These anatomic modifications of myocardial structure result in diastolic dysfunction. Overall, Conn adenoma is associated in accelerated disease, which is partly independent of the level of blood pressure.

Objectives: To assess the influence of sodium intake on the two components of arterial blood pressure [mean blood pressure (MBP) and pulse pressure] and left ventricular mass (LVM) in normotensive subjects and never-treated hypertensive patients., Methods: Blood pressure, LVM (M-mode echocardiography) and sodium excretion as an index of dietary sodium were measured in 459 males and 396 females, aged 14-93 years, with elevated (63% of population) or normal blood pressure., Results: Because pulse pressure decreased with age up to approximately 40 years of age, and increased thereafter, analysis was undertaken separately in 438 young (age < or = 40 years) and 417 middle-aged to elderly subjects. Before age 40 years, only pulse pressure was independently and positively influenced by urinary sodium excretion. After age 40 years, MBP and LVM index but not pulse pressure were positively influenced by urinary sodium excretion. When men and women were analysed separately according to tertiles of urinary sodium excretion, pulse pressure adjusted for MBP and age increased from the first to the third tertile of urinary sodium excretion in males (P < 0.03), but not in females., Conclusions: The influence of sodium intake on pulse pressure was found in the younger subjects of both males and females and only in men older than 40 years.

Blood pressure is a marker of elevated risk for cardiovascular disease, even within the normotensive range. The present study evaluates cardiorenal modifications observed in normotensive (<140/90 mm Hg) subjects. Using World Health Organization-International Society of Hypertension definitions, 265 normotensive subjects were categorized as having optimal (n=73), normal (n=84), and high-normal (n=108) blood pressure. Renal hemodynamics and function and cardiac morphology were evaluated by isotopic clearance techniques and ultrasonography, respectively. Urinary albumin excretion was measured in 24-hour urine collections. Body mass index and 24-hour urinary sodium (estimate of sodium intake), as well as left ventricular mass index, relative wall thickness, and glomerular filtration rate and filtration fraction, progressively increased in the optimal to high-normal groups. In contrast, effective renal plasma flow remained constant. Albuminuria was similar in all groups. Of interest, the proportion of subjects with concentric pattern of cardiac geometry (relative wall thickness > or =0.44) increased from 7% in optimal to 13% and 20% in normal and high-normal groups, respectively (P<0.05). Within this normotensive range of blood pressure, left ventricular mass index and relative wall thickness but not albuminuria were linearly correlated to systolic blood pressure; however, no correlation with diastolic blood pressure was found. In conclusion, changes in cardiac geometry and renal hemodynamics (increase in glomerular filtration rate and filtration fraction, an approximate index of glomerular pressure) that could predispose to cardiovascular morbidity and renal risk are already present in normotensive subjects with blood pressure higher than 120/80 mm Hg.

Background: The present study was designed to assess whether the angiotensin-converting enzyme (ACE) gene I/D polymorphism influence the ACE inhibitors effect on the regression of left ventricular hypertrophy., Methods: Sixty hypertensive subjects never treated by antihypertensive drugs, aged 46 +/- 11 years, were included in the study. Follow-up with ACE inhibitor treatment was 60 +/- 26 months. Genotypes for ACE I/D polymorphism (DD, ID or II) were determined by PCR. The left ventricular mass index (LVMI) was assessed by two-dimensional directed M-mode echocardiography., Results: ACE genotype distribution was in agreement with the Hardy-Weinberg equilibrium: 21 patients had the DD genotype, 29 were ID, and 10 were II. At baseline, age, systolic arterial pressure and LVMI didn't differ on the basis of genotype. Body mass index was significantly higher in II than in ID and DD groups. Regression of LVMI with ACE inhibitor treatment was similar in the 3 genotypes (-8.9%, -0.6%, -12.1% in DD, ID and II groups respectively). In addition, decrease of systolic arterial pressure was identical in 3 groups., Conclusion: ACE gene I/D polymorphism seems not to influence regression of left ventricular hypertrophy by ACE inhibitors in essential hypertension.

In the general population, renal function linearly declines with age; hypertension may accelerate this decline. Because concentric left ventricular (LV) hypertrophy is a strong marker of the severity of hypertension, the influence of LV geometry on the age-associated decline in renal function was assessed in 195 normotensive subjects and 645 patients with never-treated essential hypertension with an average duration of 30 mo. According to LV mass and relative wall thickness, hypertensive patients were divided into normal LV (NL, 48%), concentric remodeling (CR, 19%), and concentric (CH, 22%) and eccentric (EH, 11%) hypertrophy. GFR and effective renal plasma flow (ERPF) were estimated by isotopic clearance technique. GFR and ERPF were inversely correlated with age in normotensive and hypertensive subjects, and no marked influence of the BP level or the presence of LV hypertrophy was detected. However, the slope of the regression line of GFR versus age was accentuated (P < 0.01) in patients with CH or CR (slope values of -0.95 +/- 0.11, -0.86 +/- 0.14 ml/min per yr, respectively) when compared with patients with EH or NL (slope values of -0.58 +/- 0.16 and -0.58 +/- 0.08 ml/min per yr, respectively). No such results were obtained when creatinine clearance was considered. Urinary albumin excretion was higher in patients with concentric or eccentric LV hypertrophy than in patients with concentric LV remodeling or normal LV. These results demonstrate that in never-treated essential hypertension, the age-associated decline in GFR is markedly influenced by the concentric pattern of LV response to hypertension rather than the level of BP and/or the presence of LV hypertrophy.

In addition to its widely contested influence on arterial pressure, dietary sodium may exert some nonpressure-related effects on left ventricular mass in humans. In the present study, we hypothesized that sodium intake (estimated by two consecutive measurements of 24-h urinary sodium excretion) may amplify the effect of arterial pressure on target organ damage (ie, left ventricular mass and microalbuminuria) in a large group of normotensive subjects and patients with never-treated uncomplicated essential hypertension. Left ventricular mass (M-mode echocardiography) and urinary albumin excretion were assessed in 839 subjects (471 men and 368 women) aged 15 to 70 years, with elevated (60%) or normal arterial pressure. In the entire population, multivariate analysis indicated that the relationship between urinary sodium excretion and left ventricular mass index (beta = 0.02, P < .01) as well as urinary albumin excretion (beta = 0.001, P < .0001) was independent from sex, age, body mass index, and systolic arterial pressure. When subjects were divided into quintiles according to urinary sodium excretion, left ventricular mass index and urinary albumin excretion increased significantly from the lowest to the highest quintile in both genders, despite similar values of systolic arterial pressure. The slope of the regression line linking systolic arterial pressure to left ventricular mass index (in men) and urinary albumin excretion (in the entire population) obtained within each quintile of urinary sodium excretion, progressively and linearly increased from the lowest to the highest quintile. These results suggest that sodium intake may amplify the effect of arterial pressure on both the left ventricle and the kidney, and thus suggest that dietary sodium may be an independent factor of cardiovascular risk.

Background: Renal function is thought to decrease with age in the general population, but the determinants of this age-associated evolution are poorly understood. Hypertension and diabetes mellitus, two leading causes of chronic renal failure in the elderly, may accelerate this decline., Patients and Methods: Urinary clearances of [99mTc]diethylene triaminopentaacetic acid (DTPA) (glomerular filtration rate) and [131I]hippuran (effective renal plasma flow) were assessed in 227 never-treated essential hypertensives aged 20-69 years. Based on the oral glucose tolerance test, the study population consisted of 4% patients with previously unknown diabetes mellitus, 24% with impaired glucose tolerance and 72% with normal glucose tolerance., Results: When the population of 218 non-diabetic subjects was considered, glomerular filtration rate was inversely correlated with age and arterial blood pressure, and positively correlated with effective renal plasma flow, filtration fraction and fasting plasma glucose. In multivariate analysis, age and blood pressure were independent determinants of renal plasma flow, whereas renal plasma flow, age and fasting plasma glucose were independent determinants of glomerular filtration rate. The slope of the regression line relating glomerular filtration rate to age was steeper in patients with impaired glucose tolerance than in those with normal glucose tolerance (-1.52 +/- 0.28 versus -0.65 +/- 0.12, P < 0.01)., Conclusions: These results suggest that impaired glucose tolerance, which is seldom searched for in patients with essential hypertension, may be an important determinant of the age-associated decline in renal function.

Chronic pressure and volume overload result in morphologically and functionally distinct forms of myocardial hypertrophy. In essential hypertension, the respective effect of these factors on the morphology of the left ventricle remains unknown. In the present study, we hypothesised that activity of the renin angiotensin system (assessed by plasma renin activity) may be associated to the variability of the left ventricular adaptation to essential hypertension. To assess this relation, we categorised by echocardiography 333 never-treated hypertensive patients, according to values of left ventricular mass and relative wall thickness. Higher systolic and pulse arterial pressure was strongly associated with concentric left ventricular hypertrophy (27% of hypertensives). When compared to the normal left ventricle group, patients with eccentric left ventricular hypertrophy (15% of hypertensives) had a high cardiac index (5 +/- 1 vs 4 +/- 0.8 L/min/m2; P = 0.0001), a lower basal plasma renin activity (0.81 +/- 0.63 vs 1.45 +/- 1.3 ng/ml/h; P = 0.02) and similar mean values of left ventricular performance and glomerular filtration rate. A tendency for depressed myocardial contractility assessed by the midwall shortening/end-systolic stress was associated with concentric left ventricular remodelling and hypertrophy when compared to hypertensive with a normal left ventricle. In conclusion, at the early phase of essential hypertension, in patients without renal dysfunction, each anatomic pattern of cardiac adaptation to hypertension was associated with a distinct profile of haemodynamics, myocardial function and activity of the renin-angiotensin system. Journal of Human Hypertension (2000) 14, 181-188.

Purpose: Proteinuria is usually considered a manifestation of glomerular disease. We sought to describe the characteristics of patients with nephrotic-range proteinuria resulting from renovascular disease and to compare them with those of patients who had glomerulonephritis., Subjects and Methods: We identified 14 patients with nephrotic-range proteinuria and renovascular disease and compared them with 14 patients who had nephrotic-range proteinuria and biopsy-proven glomerulonephritis, matched for sex, age, and glomerular filtration rate., Results: Patients with renovascular disease were more likely to have known atherosclerotic vascular disease [13 of 14 (93%) vs 3 of 14 (21%), P < 0.0001) and were usually smokers [12 of 14 (85%) vs 3 of 14 (21%), P < 0.0001]. They also had a greater mean (+/- SD) difference between the lengths of their kidneys (29 +/- 10 vs 5 +/- 5 mm, P < 0.001); greater systolic blood pressure (203 +/- 22 vs 174 +/- 25 mm Hg, P < 0.005), plasma renin activity (17 +/- 19 vs 2 +/- 2 ng/mL/h, P = 0.005), and plasma aldosterone concentration (40 +/- 23 vs 11 +/- 10 ng/dL, P = 0.0001); and lower serum potassium levels (3.3 +/- 0.5 vs 3.8 +/- 0.5, P <0.05). Effective renal plasma flow was lower (139 +/- 68 vs 307 +/- 185 mL/min/1.73 m3) and filtration fraction was markedly greater (0.28 +/- 0.04 vs 0.15 +/- 0.07, P = 0.0001) in the patients with renovascular disease. After the oral administration of captopril, blood pressure, effective renal plasma flow, and glomerular filtration rate decreased only among patients with renovascular disease. Of the 14 patients with renovascular disease, 13 had evidence of renal artery thrombosis seen at angiography; 2 patients required dialysis, and 3 others died during follow-up., Conclusion: Our findings suggest that the patients with nephrotic-range proteinuria resulting from renovascular disease have distinct characteristics and a poor prognosis.

Modifications of left ventricular morphology observed during ageing are very similar to those encountered during hypertension, as if hypertensive patients present premature ageing of their cardiovascular system. Hypertension in the elderly amplifies the concentric remodelling and alteration of diastolic function observed in normotensive subjects during ageing. The main determinant of these modifications of morphology and cardiac function is the increased rigidity of large arterial trunks with age. Treatment of hypertension therefore represents one of the essential ways to control this pathological ageing.

Background: This study investigated the influence of hormone replacement therapy on the variability of the cardiac hypertrophic response to hypertension in postmenopausal women., Methods: 25 menopausal essential hypertensive women (mean age 54 +/- 0.8 years, range 45 to 70) treated with estrogen (without progestin) for at least 1 year were studied and compared with 25 menopausal age-matched women (55 +/- 1 years old, range 46 to 70) not taking such therapy. No women had ever received antihypertensive therapy. Left ventricular mass corrected by height2.7 and relative wall thickness were assessed by M mode echocardiography., Results: Age, blood pressure, body mass index, 24 h urinary sodium excretion and plasma renin activity were in the 2 groups with and without hormone replacement therapy. Left ventricular mass corrected by height2.7 was significantly higher in the group with without estrogen replacement therapy when compared to menopausal women with estrogen replacement (55 +/- 3 vs 45 +/- 4 g/m2.7 p < 0.02). In addition the slope of the regression line between LV mass and systolic BP was significantly higher (p < 0.01) in the group of women without hormonal therapy r = 0.50 p < 0.001., Conclusion: These results suggest that estrogen therapy of menopause attenuate the cardiac hypertrophic response to hypertension.

Urinary excretion of albumin exceeds normal values in 10 to 25% of patients with essential hypertension. The level of albuminuria is highly correlated with arterial pressure, and more closely with ambulatory arterial pressure. The interaction between albuminuria and arterial pressure is enhanced by overweight, smoking, protein intake, insulin resistance, lipid abnormalities, and possibly genotypes of the components of the renin-angiotensin system. The renal mechanisms of microalbuminuria are not well elucidated. Notably, an increase in filtration fraction suggestive of intraglomerular hypertension was observed in patients with hyperfiltration. Microalbuminuria may be a marker of diffuse vascular abnormalities predisposing to cardiovascular disease and/or hypertensive renal disease heralding future renal failure, but its predictive value needs to be tested in more long-term follow-up studies. Antihypertensive treatment has a varied influence on albuminuria; angiotensin-converting enzyme inhibitors may correct this abnormality (at least partially) better than other agents.

Purpose: Ambulatory blood pressure monitoring allows characterization of the circadian variations in blood pressure., Methods: In order to investigate the diagnostic value of circadian variations in blood pressure in the elderly, 11 patients with autonomic failure and 11 control subjects paired on age, blood pressure level and daily life activity range were studied., Results: Periodic postural disorders, positive response to passive tilt-test and alpha denervation supersensitivity to noradrenaline were found in all patients with autonomic failure. In control subjects, blood pressure levels assessed by ambulatory monitoring were lower at night. Conversely, circadian variations in blood pressure were higher at night and lower in the morning in patients with autonomic failure. The nadir of blood pressure measurement was related with the reported time of peak incidence of orthostatic symptoms., Conclusion: Ambulatory 24-hour blood pressure monitoring may therefore be of value in the diagnosis and management of patients with autonomic failure.

-The determinants of the increase in arterial blood pressure associated with the use of estrogen-progestogen oral contraceptives (OC) remain poorly known. The purpose of this study was to assess the renal characteristics and the role of the renin-angiotensin system in women with OC-associated hypertension. Urinary clearances of technetium-labeled diethylene triaminopentaacetic acid (glomerular filtration rate) and 131I-ortho iodohippurate (effective renal plasma flow) were estimated before and after acute administration of captopril in 38 women who became hypertensive while taking OC, 38 non-OC users with essential hypertension matched for age, body mass index, and level of blood pressure, and 38 normotensive women (19 with and 19 without OC). Plasma renin activity was higher in OC hypertensives when compared with those with essential hypertension, but captopril-induced changes in blood pressure and renal hemodynamics and function were similar in both groups. In addition, 24-hours urinary albumin excretion was increased in OC users when compared with nonusers with similar arterial blood pressure. In 13 hypertensive women followed up for 6 months after OC withdrawal, a decrease in plasma renin activity, blood pressure, and glomerular filtration rate but no significant change in urinary albumin excretion and captopril-induced changes in blood pressure and renal hemodynamics were observed. These results indicate that the use of OC is associated with an increased albuminuria and no evidence of a prominent role for the renin-angiotensin system in the maintenance of high blood pressure and renal hemodynamics when compared with non-OC users with essential hypertension.

Objective: This study was aimed at determining factors acting on the regression of left ventricular hypertrophy due to essential hypertension., Methods: It was a non-randomized, echocardiographic study of 60 previously untreated hypertensive subjects (20 to 75 years of age)., Results: Following a 5-year therapy, the decrease in the left ventricular mass was 14%. Normalization of blood pressure and reversal of left ventricular hypertrophy were obtained in 50% and 58% of patients, respectively. Patients of the non-responder group (non-response being defined as a less than 10% decrease in the left ventricular mass) were older and had a longer history of high blood pressure. A positive correlation was observed between age and decrease in the left ventricular mass, the latter being less marked in older patients. Antihypertensive drugs classes had no influence on reversal of left ventricular hypertrophy., Conclusion: Ageing may be a factor of resistance to the decrease in left ventricular mass with therapy. These results suggest that early screening and management of hypertension are essential.

In previous studies, we demonstrated that in ANG II-treated rats, prevention of cardiac hypertrophy (CH) by enalapril was blunted by bradykinin (BK) blockade by Hoe140. The putative role of BK was assessed by chronic exogenous BK infusion and in 46 male Sprague-Dawley rats infused with ANG II. ANG II (200 ng/kg/min) alone and associated with BK at low (BKlow, 15 ng/kg/day), mid (BKmid, 100 ng/kg/day) and high doses (BKhigh, 100 ng/kg/min) were delivered by Alzet osmotic pumps for 10 days and compared to control animals (Veh). Values of systolic arterial pressure (SAP, mmHg) in conscious rats and heart weight (HW, mg/g bw) at the end of the study are reported below. Results were submitted to ANOVA and are expressed as mean +/- SEM.

Systolic blood pressure and body mass index (BMI) are the main determinants of the left ventricular mass (LVM). The mechanism of this cardiac hypertrophy in the obese individual is multifactorial and involves hemodynamic as well as metabolic factors. The association of LVM with the morphologic features of the individual are well known. The aim of this study was to assess the influence of the morphologic and metabolic features of obese women on LVM. 2D echocardiography evaluation of LVM was done in 24 normotensive, normoglycemic obese women (BMI [27.5-52.2 Kg/m2). Lean and fat body mass were determined by bio-impedancemetry, insulin sensitivity (Si) by the minimal model (Bergman), and basal metabolism by using indirect calorimetry. There was a positive correlation between LVM and BMI (r = 0.61; p = 0.001), waist to hip ratio (r = 0.45; p = 0.03), basal metabolism (r = 0.61, p = 0.001), lean (r = 0.74, p = 0.0002) and fat (r = 0.49; p = 0.01) body mass. Fasting glycemia was positively correlated with LVM (r = 0.62; p = 0.001), but not Si. LVM was also positively correlated to the triglyceride level. No relations were found with systolic or diastolic blood pressure. Multivariate regression analysis was performed to determine the relative contribution of lean body mass (the morphologic variable with the best association to LVM in univariate analysis), blood glucose, waist to hip ratio, age and triglycerides. The multiple r for the model was 0.87 (p < 0.001). Lean body mass and blood glucose were found to be the only significant and independent predictors of LVM (p = 0.001 and p = 0.03 respectively). We conclude that: 1) lean body mass is an important determinant of LVM in obese normotensive individuals. Hence, in obese women, correcting LVM for lean body mass might be more accurate than correcting it for body surface area or height. 2) There is no relationship between LVM and insulin sensitivity. The link between blood glucose and LVM needs to be studied further.

Similar to endothelial modulation of vascular tone, nitric oxide (NO) released from the coronary and endocardial endothelium may modulated LV performance with an improvement of LV diastolic distensibility. The aim of the present study was to assess a potential relationship between endothelial function and LV performance in essential hypertension. Thirty-nine normotensive subjects (NT) and 46 never treated hypertensive patients (HT) were grouped according to the renal vasodilatatory response to infusion of L-arginine (30 g within 60 min). HT patients responders to L-arginine (n = 19) were defined by an increased > or = 5% of renal plasma flow (RPF) estimated by the clearance of I-Hippuran. LV mass index and afterload-corrected fractional shortening were determined by echocardiography. Mitral peak early (E) and late (A) diastolic flow velocity were assessed by Doppler. Results of ANOVA were (means +/- SD): [table: see text] In HT patients E/A was positively correlated with %RPF (r = 0.27; p < 0.01) and negatively correlated with age (r = -0.52 p < 0.01) and systolic BP (r = -0.36 p < 0.01). In multiple regression analysis the relation between E/A and %RPF was dependent of age. This results confirm that aging and hypertension are the main determinants of the alteration of LV diastolic function. The link between these factors may be the endothelium which abnormal regulatory function secondary to aging and HT may be associated to an impairment of NO dependent LV relaxation.

Background: Atheromatous renovascular disease is increasingly recognized as a cause of renal failure; however, the benefit of intervention on renal function outcome cannot be clearly anticipated., Objective: To identify reliable predictor(s) of renal functional outcome after revascularization in patients with atheromatous renovascular disease., Design: The effect of percutaneous transluminal renal angioplasty (n = 5) or surgery (n = 18) on glomerular filtration rate ([99mTc]-diethylene triaminopenta-acetic acid clearance) and renal haemodynamics was prospectively assessed in 23 patients with atheromatous renovascular disease (unilateral occlusion in five, unilateral stenosis in four, stenosis of a single kidney in five, unilateral occlusion associated with contralateral stenosis in six, bilateral stenosis in three). Renal function was altered in 18 patients., Results: At early follow-up study (5 +/- 1 months) after intervention, glomerular filtration rate improved (i.e. increased by more than 15%) in six patients, deteriorated in five and remained unchanged in 12 patients. The change in glomerular filtration rate associated with intervention was inversely correlated with the pre-intervention level of urinary albumin excretion and positively with the change in effective renal plasma flow after intervention. Stepwise regression analysis showed that pre-intervention urinary albumin excretion was the only predictor of the glomerular filtration rate response to intervention. At late follow-up study (32 +/- 6 months, n = 13), glomerular filtration rate was stable compared with early follow-up determination in non-proteinuric patients whereas it had deteriorated further in proteinuric patients., Conclusion: In patients with atheromatous renovascular disease, albuminuria may be considered as a marker of pre-existing intra-renal vascular and glomerular damage and a reliable predictor of renal functional outcome after intervention.

The existence of a direct relationship between body mass and arterial pressure is well recognized; however, the effect of obesity on known target organs of hypertension is not clearly understood. We undertook the present studies to assess the influence of obesity on renal function and urinary albumin excretion in 40 normotensive subjects and 80 nevertreated hypertensive patients matched for age, sex, arterial pressure level, and known duration of hypertension in whom an oral glucose tolerance test was within normal limits. Glomerular filtration rate and effective renal plasma flow (expressed as absolute values or values normalized for height) were increased in overweight compared with lean subjects whether normotensive or hypertensive. Glomerular filtration rate was positively correlated with protein intake (as assessed from urinary excretion of urea) and fasting serum insulin level. Urinary excretion of albumin but not IgG and beta 2 microglobulin was higher in hypertensive patients compared with normotensive subjects. The overweight condition clearly enhanced the influence of arterial pressure on albuminuria; in fact, a steeper regression line between albumin excretion rate and arterial pressure was found in overweight compared with lean subjects. These results indicate that the overweight condition is associated with renal hyperfiltration and hyperperfusion, irrespective of the presence of hypertension, and that obesity magnifies the effect of hypertension on albuminuria, thus raising the possibility of an increased susceptibility of obese hypertensive patients to the development of renal damage.

The level of arterial pressure is not the sole determinant of cardiac and vascular adaptation to hypertension. In order to identify other factors (such as preload) we categorized by echocardiography, 55 never treated hypertensive patients and 39 age and gender-matched normal subjects, according to values of relative wall thickness and left ventricular mass index. Normal left ventricular anatomy was found in 63% hypertensives, whereas among hypertensives 7% had "concentric left ventricular remodeling", 16% concentric left ventricular hypertrophy and 14% had eccentric left ventricular hypertrophy. Systolic left atrial area (LA) was obtained from the four-chamber views. Mitral peak early diastolic (E) and late diastolic (A) flow velocity was assessed by Doppler. Because clinical characteristics such age and sex differed among the 5 groups only results of ANCOVA were reported (means +/- SD). [table: see text] We conclude that eccentric left ventricular hypertrophy may be associated with a parallel increase of left atrial area. Thus the association of an increase of cardiac volume in hypertensive patients with normal diastolic function suggest that volume overload may modulate the effect of arterial pressure on cardiac morphology.

Dietary sodium is an environmental factor capable of amplifying or limiting the consequences of hypertension on the heart. In a given population of hypertensive subjects, recent clinical trials have shown a positive relationship between sodium intake and the degree of left ventricular hypertrophy, independently of the value of blood pressure and body weight. In addition, dietary sodium could play a role in modulating the myocardial response to a decrease in blood pressure by antihypertensive therapy. The logical consequence of these observations is to try and prove the possible advantages of restricting dietary sodium in reducing the blood pressure and reversing left ventricular hypertrophy. With this in mind, the evaluation of dietary sodium excretion is certainly an element to take into account in the initial evaluation and also the follow-up of hypertensive subjects and of the effects of antihypertensive therapy.