Showing papers by "Stéphane Laurent published in 2009"

Reappraisal of European guidelines on hypertension management: a European Society of Hypertension Task Force document.

Abstract: Abbreviations ACE: angiotensin-converting enzyme; BP: blood pressure; DBP: diastolic blood pressure; eGFR: estimated glomerular filtration rate; ESC: European Society of Cardiology; ESH: European Society of Hypertension; ET: endothelin; IMT: carotid intima-media thickness; JNC: Joint National Commit

Management of high blood pressure in children and adolescents: recommendations of the European Society of Hypertension

Abstract: Hypertension in children and adolescents has gained ground in cardiovascular medicine, thanks to the progress made in several areas of pathophysiological and clinical research. These guidelines represent a consensus among specialists involved in the detection and control of high blood pressure in children and adolescents. The guidelines synthesize a considerable amount of scientific data and clinical experience and represent best clinical wisdom upon which physicians, nurses and families should base their decisions. They call attention to the burden of hypertension in children and adolescents, and its contribution to the current epidemic of cardiovascular disease, these guidelines should encourage public policy makers, to develop a global effort to improve identification and treatment of high blood pressure among children and adolescents.

Vascular Aging A Tale of EVA and ADAM in Cardiovascular Risk Assessment and Prevention

Abstract: Cardiovascular disease (CVD) manifestations still pose a substantial threat to public health, as summarized in a recent report from the American Heart Association Statistics Committee for an update in 2009.1 Classic risk factors are of major importance to screen for, to evaluate, and to control with lifestyle advice or drug therapy. However, because the risk of CVD is still representing a challenge in spite of prevention and all treatment efforts, there is a need for new pathophysiological models for better understanding of cardiovascular risk and its treatment, based on new concepts. It has been shown that target organ damage (TOD) represents a mediating step between risk factors and CVD events. Examples of well-established TOD categories include left ventricular hypertrophy and albumin excretion. In addition, substantial evidence has accumulated to show that arterial stiffness and increased pulse wave velocity (PWV), as well as central aortic pulse pressure, are important independent predictors of CVD events.2 These are in fact not only examples of TOD but also of the underlying pathological process, because increased PWV might determine the degree of left ventricular hypertrophy through increased arterial pulse wave reflection, central pulse pressure, and postload.2 Because aging is a common denominator to many chronic disease manifestations, eg, CVD, type 2 diabetes mellitus, or cancer, we propose that early vascular aging (EVA) could be a useful concept to better guide clinical investigations in subjects at increased cardiovascular (CV) risk. This could be the case in individuals with marginal elevation of classic risk factors or with a strong family history of early CVD manifestations. There might also be a special link between adverse growth patterns in fetal or early postnatal life (the “mismatch” growth hypothesis) and the EVA syndrome, as summarized recently.3 Vascular aging in general, and EVA more specifically, can be …

Large and Small Artery Cross-Talk and Recent Morbidity-Mortality Trials in Hypertension

Abstract: The results of recent large clinical trials in hypertension invite re-evaluation of the mechanisms of action of antihypertensive drugs on large and small arteries in the context of their effects on cardiovascular outcomes. By increasing our understanding of the relationship between large and small artery damage, target organ damage, and clinical end points, the trials provide us with new insights into the management of hypertension. This short review aims at analyzing the following: (1) whether β-blockers may exert deleterious effects on cardiovascular CV prevention through the reduction in heart rate (HR) or the lack of arterial remodeling; (2) whether long-term arterial remodeling can explain the “legacy” effect of multifactorial treatment in patients with hypertension and type 2 diabetes mellitus (T2D); and (3) to which level diastolic BP (DBP) can be safely lowered in elderly patients with isolated systolic hypertension (ISH). Because these issues have the concept of large/small artery cross-talk in common, we analyzed it first. The damaging effect of local pulse pressure (PP) has been well demonstrated on large arteries and, to a lesser extent, on small arteries. Elevated PP can stimulate hypertrophy, remodeling (increased media:lumen ratio), or rarefaction in the microcirculation, leading to increased resistance to mean flow. Recent studies showed a close relationship between microvascular damage in the heart, brain, retina, and kidney and either PP or arterial stiffness. Indeed, significant relationships have been demonstrated between brachial PP and glomerular filtration rate,1,2 microalbuminuria,2 or white matter lesions3; between arterial stiffness and glomerular filtration rate,4,5 urinary albumin,5 retinal arteriolar narrowing,6,7 white matter lesions,3 or cognitive function8; and between carotid stiffness and glomerular filtration rate.4,5 Although not all of these relationships are independent of confounding factors,3 there is a large amount of evidence for linking the pulsatility …

Mechanisms of hypertension in the cardiometabolic syndrome.

Abstract: Arterial hypertension is often part of a constellation of anthropometric and metabolic abnormalities that occur simultaneously to a higher degree than would be expected by chance alone, supporting the existence of a discrete disorder, the so-called metabolic syndrome. It is the result of interactions among a large number of interconnected mechanisms, which eventually lead to both an increase in cardiovascular and renal risk, and the development of diabetes. Mechanisms involved in the metabolic syndrome are obesity, insulin resistance, and a constellation of independent factors, which include molecules of hepatic, vascular, and immunologic origin with pro-inflammatory properties. At each of these key points are interactions of demographics, lifestyle, genetic factors, and environmental fetal programming. Superimposing upon these are infections or chronic exposure or both to certain drugs that can also make their contribution. Skeletal muscle and the liver, not adipose tissue, are the two key insulin-response tissues involved in maintaining glucose balance, although abnormal insulin action in the adipocytes also plays a role in development of the syndrome. Factors commonly associated with and partly dependent on obesity, insulin resistance, such as overactivity of the sympathetic, stimulation of the renin-angiotensin-aldosterone systems, abnormal renal sodium handling, endothelial dysfunction, and large vessels' alterations, may play a key role in the blood pressure elevation of the syndrome.

Distance measurements for the assessment of carotid to femoral pulse wave velocity

Abstract: Background Carotid–femoral pulse wave velocity can be determined using different distances – either direct carotid–femoral distance or subtracted [(sternal–femoral) − (carotid–sternal)] distance – resulting in pulse wave velocity differences of up to 30%. The present study aims to present and validate a population-based model for the conversion between distances. Method Three thousand one hundred and sixteen participants from the Asklepios study (n = 2510) and Hopital Europeen Georges Pompidou (n = 606) databases, in which all distance measurements were available, were randomly distributed in a model (n = 311) and validation (n = 2805) population. Model parameters for the conversion equations were selected and evaluated using multiple linear regression with stepwise selection of covariates (age, sex, weight, height, BMI and waist circumference). The proposed model was evaluated on the validation population. Results The difference between direct and subtracted distances was found to be partially dependent on body height, and its inclusion in the multivariate model improved model performance by over 20%. Other combinations of adjustments did not improve model prediction. Conversion equations derived in the model population were: Estimated Direct_distance = 0.45*Subtracted_distance + 0.21*height + 0.08 and Estimated Subtracted_distance = 1.04*Direct_distance − 0.11*height − 0.02, respectively. Applying these equations for estimation of direct and subtracted distances in the validation population yielded good correspondence to measured results (r2 = 0.73 and 0.57, respectively), with nonsignificant mean differences between estimated and measured values. Increasing the size of the model population did not significantly change the model validity. Conclusion In cases in which not all distance measurements are available for exact conversion, the presented equations can be used to convert between distance definitions.

Fixed-dose manidipine/delapril versus losartan/hydrochlorothiazide in hypertensive patients with type 2 diabetes and microalbuminuria.

Abstract: Patients with diabetes complicated by hypertension and microalbuminuria have elevated cardiovascular risk, and controlling blood pressure in these patients is an urgent clinical priority. The present study aimed to examine the effects of a fixed-dose combination of antihypertensives on blood pressure and microalbuminuria. Patients with type 2 diabetes, mild-to-moderate hypertension (diastolic blood pressure 85–105 mmHg, systolic blood pressure 130 mmHg), and microalbuminuria were randomized to 1 year of doubleblind treatment with fixed-dose manidipine/delapril (n=54) or losartan/hydrochlorothiazide (HCTZ) (n=56). Blood pressure was significantly reduced at 1 year in both groups (−22.2/−14.6 mmHg and −19.5/−14.3 mmHg, for systolic and diastolic blood pressure respectively, P<0.001 for each), with no significant between-group difference. Reductions in microalbuminuria occurred in both groups, with mean changes at 1 year of −3.9 mg/mmol creatinine (95% CI −5.3, −2.5) for manidipine/delapril (P<0.001 vs. baseline) and −2.7 mg/mmol creatinine (95% CI −4.0, −1.3) for losartan/HCTZ (P<0.001 vs. baseline and P=0.199 between groups). Glycemia over the 1-year study was largely unaffected; the blood glucose concentration was reduced from baseline with manidipine/delapril, although not statistically significant (mean change −0.2 mmol/L, P=0.064). Both treatments were well tolerated, with discontinuation for adverse events for one (1.9%) patient in the manidipine/delapril group and two (3.6%) in the losartan/HCTZ group. A fixed-dose manidipine/delapril combination represents a useful addition to the treatment options available to control hypertension complicated by diabetes and microalbuminuria.