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: Age-dependent effect of exposure and the fact that, to fully evaluate its impact, hypertension should be assessed several decades before the onset of dementia have made it remarkably more complex to study the role of hypertension on the brain.
Abstract: One of the first studies to examine the question of a potential negative impact of hypertension on the brain was published in 1971 in Science .1 Subsequently, many studies have been published, mainly on the relationship of blood pressure (BP) with cognitive performance, cognitive decline, and dementia.2 Their results were sometimes contradictory, some studies even suggesting that high BP could protect against the risk of dementia. This apparent contradiction created some confusion and a sense that this issue should not deserve much attention. The accumulation of data from high-quality population-based studies has helped us to decipher this riddle. Indeed, they have shown that the impact of hypertension on the brain strongly depends on when BP is measured in life. High BP in middle age is a risk factor for dementia, but not when measured at an old age. This age-dependent effect of exposure and the fact that, to fully evaluate its impact, hypertension should be assessed several decades before the onset of dementia have made it remarkably more complex to study the role of hypertension on the brain.
Because of global aging, the number of dementia cases is skyrocketing around the world. The last World Health Organization report estimates that in 2010, 7.7 million persons have developed dementia, 1 new case every 4 seconds.3 The total number of people with dementia worldwide was estimated at 35.6 million in 2010 and is projected to reach 115.4 million in 2050. This ongoing epidemic of dementia and the absence of any preventive or curative treatment revived interest in studying modifiable risk factors of dementia, even if this relationship is complex as for hypertension. Indeed, simulation studies have shown that delaying by just a few months the entry into the clinical phase of the disease could enable, at the population level, …
106 citations
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TL;DR: This Brief Review will discuss experimental designs of randomized clinical trials demonstrating that a therapeutic strategy that normalizes arterial stiffness is more effective in preventing CV events than usual care, and suggest additional studies to demonstrate its value as surrogate end point.
Abstract: Classic risk scores may underestimate the risk of cardiovascular (CV) events in specific risk groups suitable for primary prevention, such as asymptomatic hypertensive subjects.1 Particularly, those considered as at intermediate risk may benefit the most from a reassessment of their CV risk using novel biomarkers.2 In primary prevention, some imaging biomarkers, such as arterial stiffness, enhance risk prediction to a higher extent than circulating biomarkers.3 Whether novel biomarkers are ready for routine clinical use is a matter of controversy.1–4 Particularly, whether an imaging biomarker can be substituted to clinical events in outcome trials and be considered as surrogate end point has rarely been demonstrated.1–4 The aims of the present Brief Review are to address the concepts of “imaging biomarker” and “surrogate end point”; to focus on arterial stiffness as putative surrogate end point for future CV events; and to suggest additional studies to demonstrate its value as surrogate end point. Particularly, we will discuss experimental designs of randomized clinical trials demonstrating that a therapeutic strategy that normalizes arterial stiffness is more effective in preventing CV events than usual care.
### “Circulating” Biomarkers Versus “Tissue” or “Imaging” Biomarkers
Although classic risk scores, such as the Framingham risk score5 and the European Systematic Coronary Risk Evaluation,6 detect patients at high risk of CV events, they are largely influenced by aging, leading to undermanagement of CV risk in other risk groups, particularly those considered as at intermediate risk. A very large number of newer biomarkers have been proposed in the literature2,4 to increase risk prediction beyond classic risk scores. According to the Biomarkers Definition Working Group of the National Institutes of Health,7 a biomarker is “a characteristic that is objectively measured and evaluated as an indicator of normal biological processes, pathogenic processes, or pharmacological responses to …
105 citations
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TL;DR: The results suggest that active mechanisms compensate for intrinsic viscosity under physiological conditions, and one of these energy-saving mechanisms might be dependent on normal endothelial function.
Abstract: Arterial wall viscosity (AWV) is a potential source of energy dissipation in circulation. That arteries, which are known to be markedly viscous in vitro, have lower viscosity in vivo has been suggested but not demonstrated under similar pressure conditions. Endothelium, which may modulate AWV through smooth muscle tone, could contribute to the low level of viscosity in vivo. Our objectives were first to compare AWV of the rat abdominal aorta, in vivo and in vitro, with similar pulse-pressure waves, and second, to determine whether endothelial function influences AWV in vivo and in vitro. The diameter of the abdominal aorta and distending pressure were measured in vivo and in vitro with a high-resolution echotracking system and a micromanometer, respectively. AWV was calculated as the area of the pressure-volume curve hysteresis. After in vivo examination, the arterial segments were isolated in vitro and submitted to resynthesized pressure waves identical to those recorded in vivo. Deendothelializ...
105 citations
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TL;DR: The present review discusses the concept of vascular aging, that structural and functional changes occur in the large arteries with aging; and EVA; that such age-associated changes are accelerated in individuals at increased cardiovascular risk; and their metrics.
Abstract: Whereas vascular aging has been identified as an emerging cardiovascular risk factor, definitions of 'normal' and 'early' vascular aging (EVA) and their precise relationship with cardiovascular risk are currently equivocal. The present review discusses the concept of vascular aging; that structural and functional changes occur in the large arteries with aging; and EVA; that such age-associated changes are accelerated in individuals at increased cardiovascular risk; and their metrics; indeed, in order to provide a definition of when EVA occurs in clinical practice, reference values of normal and accelerated vascular aging are needed. Due to the complex nature of age-associated changes in the large arteries described above, there are different parameters relating to vascular aging which can be measured. These broadly include aortic and carotid stiffening; aortic and carotid lumen dilation; endothelial dysfunction (usually measured via brachial flow-mediated dilatation); and carotid intima-media thickness.
102 citations
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TL;DR: Modifications in the stiffness of the aorta and other large arteries must be considered to understand reversion of cardiac hypertrophy as a result of antihypertensive treatment.
102 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