Author
Stéphane Laurent
Other affiliations: University of Lausanne, Paris Descartes University, French Institute of Health and Medical Research
Bio: Stéphane Laurent is an academic researcher from University of Paris. The author has contributed to research in topics: Blood pressure & Arterial stiffness. The author has an hindex of 83, co-authored 424 publications receiving 75440 citations. Previous affiliations of Stéphane Laurent include University of Lausanne & Paris Descartes University.
Papers published on a yearly basis
Papers
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TL;DR: Antihypertensive treatments improve the arterial stiffness beyond their effect on blood pressure, a meta-analysis of 15 randomized, controlled, double-blind, parallel group trials performed between 1987 and 1994 shows.
Abstract: Background Arterial stiffness is an independent predictor of cardiovascular events and mortality in hypertensive patients. The influence of different antihypertensive drug classes on improving arterial stiffness beyond blood pressure reduction is not widely available. We aimed to determine whether the artery stiffness can be improved because of antihypertensive treatments independently of blood pressure lowering. Methods We conducted a meta-analysis of individual data from 15 randomized, controlled, double-blind, parallel group trials performed in our laboratory between 1987 and 1994. The primary endpoint was the changes of carotid-femoral pulse wave velocity (PWV) after treatment in 294 patients with mild-to-moderate essential hypertension untreated. Treatments tested were placebo (n = 88), angiotensin-converting enzyme inhibitors (ACEIs) (n = 75), calcium antagonists (n = 75), beta-blocker (n = 30), and diuretic (n = 26). Results In the short-term and long-term trials, PWV decreased significantly by -0.75 and -1.3 m/s in the active treatment group compared with by +0.17 and -0.44 m/s in the placebo group, respectively. Active treatment was independently related to the changes in PWV and explained 5 and 4% of the variance in the short-term and long-term trials, respectively. In the short-term trials, ACEIs were more effective than calcium antagonists and placebo on improving arterial stiffness. In the long-term trials, ACEI, calcium antagonists, beta-blocker, and diuretic reduced significantly PWV compared to placebo. Conclusion Our study shows that antihypertensive treatments improve the arterial stiffness beyond their effect on blood pressure.
208 citations
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TL;DR: The purpose of this article is to review some clinical and fundamental evidence that hypertension-induced arterial wall hypertrophy at the site of large and medium-sized arteries is not necessarily associated with a decreased arterial distensibility and increased elastic modulus, and to demonstrate the opposing effects of aging and hypertension- inducedhypertrophy on the arterial mechanics in vivo.
Abstract: The purpose of this article is to review some clinical and fundamental evidence that hypertension-induced arterial wall hypertrophy at the site of large and medium-sized arteries is not necessarily associated with a decreased arterial distensibility and increased elastic modulus, and to demonstrate the opposing effects of aging and hypertension-induced hypertrophy on the arterial mechanics in vivo. in the studies reported here, the elastic properties of large and medium-sized arteries were noninvasively assessed from the simultaneous measurement of internal diameter and blood pressure inside the systolic-diastolic range. The distensibility of a medium-sized artery, the radial artery, in untreated essential hypertensive patients was not significantly different from that of normotensive control subjects when the two groups were compared at their respective mean arterial pressures. Despite increased wall thickness, the stiffness of the radial artery wall material, assessed by the incremental modulus of elasticity (Young's modulus), was not increased in hypertensive patients. At the site of a larger, more elastic artery, such as the common carotid artery, distensibility of hypertensive patients was significantly lower than that of normotensive subjects when the two groups were compared at their respective mean arterial pressures, but distensibility at 100 mm Hg was not significantly different between the two groups. Aging may alter distensibility independently of blood pressure, because carotid distensibility at 100 mm Hg was negatively correlated with age. In spontaneously hypertensive rats the elastic modulus of the common carotid artery wall material was not significantly different from that of Wistar-Kyoto rats at a given circumferential stress.(ABSTRACT TRUNCATED AT 250 WORDS)
204 citations
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TL;DR: Differences in central systolic BP and rough AIx remained significant after adjustment to the changes in heart rate and the amlodipine-valsartan combination decreased central (systolic and pulse) pressure and AIx more than the am lodipines-atenolol combination.
Abstract: The beta-blocker atenolol is less effective than angiotensin-receptor blockers and calcium-channel blockers for reducing central blood pressure (BP). The trial was designed to determine whether the advantages of angiotensin-receptor blockers over atenolol remained significant when both were combined with the calcium-channel blocker amlodipine. A prospective, randomized, blinded endpoint (PROBE design) parallel group, multicenter trial including 393 patients with essential hypertension resistant to 4 weeks of 5 mg of amlodipine was set out. Central systolic BP, augmentation index (AIx; either rough or adjusted on heart rate), and carotid-to-femoral pulse wave velocity were measured with applanation tonometry (SphygmoCor) at inclusion and after 8 and 24 weeks of active treatment with an amlodipine-valsartan combination (5/80 mg and then 10/160 mg) or an amlodipine-atenolol combination (5/50 mg and then 10/100 mg). From baseline to week 24, central systolic BP decreased significantly more in the amlodipine-valsartan group (-13.70+/-1.15 mm Hg; P<0.0001) than in the amlodipine-atenolol group (-9.70+/-1.10 mm Hg; P<0.0001; difference: -4.00 mm Hg [95% CI: -7.10 to -0.90]; P=0.013), despite similar changes in brachial systolic BP. The difference in rough AIx reduction was -6.5% (95% CI: -8.3 to -4.7; P<0.0001) in favor of amlodipine-valsartan. AIx adjusted on heart rate was significantly reduced in favor of amlodipine-valsartan (-2.8% [95% CI: -4.92 to -0.68]; P<0.01). Heart rate decreased significantly more with amlodipine-atenolol (difference: -11 bpm [95% CI: -14 to -8 bpm]; P<0.001). Pulse wave velocity decreased by 0.95 m/s in both groups with no significant difference. Differences in central systolic BP and rough AIx remained significant after adjustment to the changes in heart rate. The amlodipine-valsartan combination decreased central (systolic and pulse) pressure and AIx more than the amlodipine-atenolol combination.
200 citations
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TL;DR: The results suggest that the structural adaptations of the arterial wall to a chronic increase in blood flow normalize wall shear stress and overcome stretch-induced changes in the particular circumstance of arteriovenous fistula.
Abstract: Chronic changes in large artery blood flow rates induce corresponding adjustments in arterial diameter, but little is known about structural adaptations of the vessel wall in humans. We used a high-resolution echo-tracking system to measure radial artery internal diameter, wall thickness, and mean blood flow on both arms of 11 patients with end-stage renal disease. Measurements were performed on the wrist side of the arteriovenous fistula. The contralateral radial artery was investigated as control. Wall cross-sectional area, circumferential wall stress, and mean wall shear stress were calculated. Results indicate a sixfold increase in blood flow on the side of the arteriovenous fistula compared with the control side, with a 1.4-fold increase in internal diameter. The diameter enlargement was sufficient to normalize wall shear stress. Changes in diameter were not associated with arterial wall hypertrophy because wall cross-sectional area was not increased and rather suggest a "remodeling" of the arterial wall. For the same level of blood pressure, circumferential wall stress was increased on the side of the arteriovenous fistula. These results suggest that the structural adaptations of the arterial wall to a chronic increase in blood flow normalize wall shear stress and overcome stretch-induced changes in the particular circumstance of arteriovenous fistula.
198 citations
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TL;DR: This short review aims at analyzing whether β-blockers may exert deleterious effects on cardiovascular CV prevention through the reduction in heart rate (HR) or the lack of arterial remodeling, and whether long-term arterIAL remodeling can explain the “legacy” effect of multifactorial treatment in patients with hypertension and type 2 diabetes mellitus (T2D).
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 …
195 citations
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28,685 citations
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TL;DR: In this article, a randomized controlled trial of Aliskiren in the Prevention of Major Cardiovascular Events in Elderly people was presented. But the authors did not discuss the effect of the combination therapy in patients living with systolic hypertension.
Abstract: ABCD
: Appropriate Blood pressure Control in Diabetes
ABI
: ankle–brachial index
ABPM
: ambulatory blood pressure monitoring
ACCESS
: Acute Candesartan Cilexetil Therapy in Stroke Survival
ACCOMPLISH
: Avoiding Cardiovascular Events in Combination Therapy in Patients Living with Systolic Hypertension
ACCORD
: Action to Control Cardiovascular Risk in Diabetes
ACE
: angiotensin-converting enzyme
ACTIVE I
: Atrial Fibrillation Clopidogrel Trial with Irbesartan for Prevention of Vascular Events
ADVANCE
: Action in Diabetes and Vascular Disease: Preterax and Diamicron-MR Controlled Evaluation
AHEAD
: Action for HEAlth in Diabetes
ALLHAT
: Antihypertensive and Lipid-Lowering Treatment to Prevent Heart ATtack
ALTITUDE
: ALiskiren Trial In Type 2 Diabetes Using Cardio-renal Endpoints
ANTIPAF
: ANgioTensin II Antagonist In Paroxysmal Atrial Fibrillation
APOLLO
: A Randomized Controlled Trial of Aliskiren in the Prevention of Major Cardiovascular Events in Elderly People
ARB
: angiotensin receptor blocker
ARIC
: Atherosclerosis Risk In Communities
ARR
: aldosterone renin ratio
ASCOT
: Anglo-Scandinavian Cardiac Outcomes Trial
ASCOT-LLA
: Anglo-Scandinavian Cardiac Outcomes Trial—Lipid Lowering Arm
ASTRAL
: Angioplasty and STenting for Renal Artery Lesions
A-V
: atrioventricular
BB
: beta-blocker
BMI
: body mass index
BP
: blood pressure
BSA
: body surface area
CA
: calcium antagonist
CABG
: coronary artery bypass graft
CAPPP
: CAPtopril Prevention Project
CAPRAF
: CAndesartan in the Prevention of Relapsing Atrial Fibrillation
CHD
: coronary heart disease
CHHIPS
: Controlling Hypertension and Hypertension Immediately Post-Stroke
CKD
: chronic kidney disease
CKD-EPI
: Chronic Kidney Disease—EPIdemiology collaboration
CONVINCE
: Controlled ONset Verapamil INvestigation of CV Endpoints
CT
: computed tomography
CV
: cardiovascular
CVD
: cardiovascular disease
D
: diuretic
DASH
: Dietary Approaches to Stop Hypertension
DBP
: diastolic blood pressure
DCCT
: Diabetes Control and Complications Study
DIRECT
: DIabetic REtinopathy Candesartan Trials
DM
: diabetes mellitus
DPP-4
: dipeptidyl peptidase 4
EAS
: European Atherosclerosis Society
EASD
: European Association for the Study of Diabetes
ECG
: electrocardiogram
EF
: ejection fraction
eGFR
: estimated glomerular filtration rate
ELSA
: European Lacidipine Study on Atherosclerosis
ESC
: European Society of Cardiology
ESH
: European Society of Hypertension
ESRD
: end-stage renal disease
EXPLOR
: Amlodipine–Valsartan Combination Decreases Central Systolic Blood Pressure more Effectively than the Amlodipine–Atenolol Combination
FDA
: U.S. Food and Drug Administration
FEVER
: Felodipine EVent Reduction study
GISSI-AF
: Gruppo Italiano per lo Studio della Sopravvivenza nell'Infarto Miocardico-Atrial Fibrillation
HbA1c
: glycated haemoglobin
HBPM
: home blood pressure monitoring
HOPE
: Heart Outcomes Prevention Evaluation
HOT
: Hypertension Optimal Treatment
HRT
: hormone replacement therapy
HT
: hypertension
HYVET
: HYpertension in the Very Elderly Trial
IMT
: intima-media thickness
I-PRESERVE
: Irbesartan in Heart Failure with Preserved Systolic Function
INTERHEART
: Effect of Potentially Modifiable Risk Factors associated with Myocardial Infarction in 52 Countries
INVEST
: INternational VErapamil SR/T Trandolapril
ISH
: Isolated systolic hypertension
JNC
: Joint National Committee
JUPITER
: Justification for the Use of Statins in Primary Prevention: an Intervention Trial Evaluating Rosuvastatin
LAVi
: left atrial volume index
LIFE
: Losartan Intervention For Endpoint Reduction in Hypertensives
LV
: left ventricle/left ventricular
LVH
: left ventricular hypertrophy
LVM
: left ventricular mass
MDRD
: Modification of Diet in Renal Disease
MRFIT
: Multiple Risk Factor Intervention Trial
MRI
: magnetic resonance imaging
NORDIL
: The Nordic Diltiazem Intervention study
OC
: oral contraceptive
OD
: organ damage
ONTARGET
: ONgoing Telmisartan Alone and in Combination with Ramipril Global Endpoint Trial
PAD
: peripheral artery disease
PATHS
: Prevention And Treatment of Hypertension Study
PCI
: percutaneous coronary intervention
PPAR
: peroxisome proliferator-activated receptor
PREVEND
: Prevention of REnal and Vascular ENdstage Disease
PROFESS
: Prevention Regimen for Effectively Avoiding Secondary Strokes
PROGRESS
: Perindopril Protection Against Recurrent Stroke Study
PWV
: pulse wave velocity
QALY
: Quality adjusted life years
RAA
: renin-angiotensin-aldosterone
RAS
: renin-angiotensin system
RCT
: randomized controlled trials
RF
: risk factor
ROADMAP
: Randomized Olmesartan And Diabetes MicroAlbuminuria Prevention
SBP
: systolic blood pressure
SCAST
: Angiotensin-Receptor Blocker Candesartan for Treatment of Acute STroke
SCOPE
: Study on COgnition and Prognosis in the Elderly
SCORE
: Systematic COronary Risk Evaluation
SHEP
: Systolic Hypertension in the Elderly Program
STOP
: Swedish Trials in Old Patients with Hypertension
STOP-2
: The second Swedish Trial in Old Patients with Hypertension
SYSTCHINA
: SYSTolic Hypertension in the Elderly: Chinese trial
SYSTEUR
: SYSTolic Hypertension in Europe
TIA
: transient ischaemic attack
TOHP
: Trials Of Hypertension Prevention
TRANSCEND
: Telmisartan Randomised AssessmeNt Study in ACE iNtolerant subjects with cardiovascular Disease
UKPDS
: United Kingdom Prospective Diabetes Study
VADT
: Veterans' Affairs Diabetes Trial
VALUE
: Valsartan Antihypertensive Long-term Use Evaluation
WHO
: World Health Organization
### 1.1 Principles
The 2013 guidelines on hypertension of the European Society of Hypertension (ESH) and the European Society of Cardiology …
14,173 citations
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TL;DR: Authors/Task Force Members: Piotr Ponikowski* (Chairperson) (Poland), Adriaan A. Voors* (Co-Chair person) (The Netherlands), Stefan D. Anker (Germany), Héctor Bueno (Spain), John G. F. Cleland (UK), Andrew J. S. Coats (UK)
13,400 citations
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TL;DR: 2007 Guidelines for the Management of Arterial Hypertension : The Task Force for the management of Arterspertension of the European Society ofhypertension (ESH) and of theEuropean Society of Cardiology (ESC).
Abstract: 2007 Guidelines for the Management of Arterial Hypertension : The Task Force for the Management of Arterial Hypertension of the European Society of Hypertension (ESH) and of the European Society of Cardiology (ESC).
9,932 citations
01 Jan 2014
TL;DR: These standards of care are intended to provide clinicians, patients, researchers, payors, and other interested individuals with the components of diabetes care, treatment goals, and tools to evaluate the quality of care.
Abstract: XI. STRATEGIES FOR IMPROVING DIABETES CARE D iabetes is a chronic illness that requires continuing medical care and patient self-management education to prevent acute complications and to reduce the risk of long-term complications. Diabetes care is complex and requires that many issues, beyond glycemic control, be addressed. A large body of evidence exists that supports a range of interventions to improve diabetes outcomes. These standards of care are intended to provide clinicians, patients, researchers, payors, and other interested individuals with the components of diabetes care, treatment goals, and tools to evaluate the quality of care. While individual preferences, comorbidities, and other patient factors may require modification of goals, targets that are desirable for most patients with diabetes are provided. These standards are not intended to preclude more extensive evaluation and management of the patient by other specialists as needed. For more detailed information, refer to Bode (Ed.): Medical Management of Type 1 Diabetes (1), Burant (Ed): Medical Management of Type 2 Diabetes (2), and Klingensmith (Ed): Intensive Diabetes Management (3). The recommendations included are diagnostic and therapeutic actions that are known or believed to favorably affect health outcomes of patients with diabetes. A grading system (Table 1), developed by the American Diabetes Association (ADA) and modeled after existing methods, was utilized to clarify and codify the evidence that forms the basis for the recommendations. The level of evidence that supports each recommendation is listed after each recommendation using the letters A, B, C, or E.
9,618 citations