Showing papers by "Stéphane Laurent published in 2014"

2013 ESH/ESC Practice guidelines for the management of arterial hypertension

Abstract: ABPMambulatory blood pressure monitoringACEangiotensin converting enzymeARBangiotensin receptor blockerA-Vatrio-ventricularBBbeta-blockerBPblood pressureCHDcoronary heart diseaseCKDchronic kidney d...

Establishing reference values for central blood pressure and its amplification in a general healthy population and according to cardiovascular risk factors

Abstract: Aims Estimated central systolic blood pressure (cSBP) and amplification (Brachial SBP-cSBP) are non-invasive measures potentially prognostic of cardiovascular (CV) disease. No worldwide, multiple-device reference values are available. We aimed to establish reference values for a worldwide general population standardizing between the different available methods of measurement. How these values were significantly altered by cardiovascular risk factors (CVRFs) was then investigated. Methods and results Existing data from population surveys and clinical trials were combined, whether published or not. Reference values of cSBP and amplification were calculated as percentiles for ‘Normal’ (no CVRFs) and ‘Reference’ (any CVRFs) populations. We included 45 436 subjects out of 82 930 that were gathered from 77 studies of 53 centres. Included subjects were apparently healthy, not treated for hypertension or dyslipidaemia, and free from overt CV disease and diabetes. Values of cSBP and amplification were stratified by brachial blood pressure categories and age decade in turn, both being stratified by sex. Amplification decreased with age and more so in males than in females. Sex was the most powerful factor associated with amplification with 6.6 mmHg (5.8–7.4) higher amplification in males than in females. Amplification was marginally but significantly influenced by CVRFs, with smoking and dyslipidaemia decreasing amplification, but increased with increasing levels of blood glucose. Conclusion Typical values of cSBP and amplification in a healthy population and a population free of traditional CVRFs are now available according to age, sex, and brachial BP, providing values included from different devices with a wide geographical representation. Amplification is significantly influenced by CVRFs, but differently in men and women.

Is Hypertension Associated With an Accelerated Aging of 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, …

Dose-dependent arterial destiffening and inward remodeling after olmesartan in hypertensives with metabolic syndrome.

Abstract: Whether angiotensin receptor blockers can dose-dependently remodel the arterial wall during long-term treatment has been largely debated. In this phase III, multicenter, randomized, double-blind, parallel-group study, 133 subjects with hypertension and metabolic syndrome were assigned to olmesartan, either 20 mg (n=44), 40 mg (n=42), or 80 mg (n=47) once a day, according to a force titration design during a 1-year period. Office blood pressure, 24-hour blood pressure, aortic stiffness (carotid-femoral pulse wave velocity), and carotid parameters were measured at baseline, 24 weeks, and 52 weeks. Pulse wave velocity significantly decreased (P<0.001) with time in each group, with no significant time-dose interaction, despite a tendency (P=0.0685) for a smaller effect of 20 mg, compared with 40 and 80 mg at week 52. When the 40 and 80 mg doses were combined (40/80 mg versus 20 mg), a significant blood pressure-independent reduction in pulse wave velocity (-0.61 m/s) was observed at week 52 (P=0.0066), whereas the nonadjusted reduction was -1.31 m/s (P<0.0001). By contrast, after 20 mg, the blood pressure-independent reduction in pulse wave velocity was not significant. Patients receiving the highest dose of olmesartan (40 and 80 mg) had an inward carotid remodeling and were shifted toward a lower elastic modulus at a given circumferential wall stress, indicating an improvement in the intrinsic elastic properties of the carotid artery wall material. These data suggest that 40 and 80 mg olmesartan were able to significantly remodel and destiffen the arterial wall material during long-term treatment, partly independently of blood pressure, compared with 20 mg.

Blood pressure and LDL-cholesterol targets for prevention of recurrent strokes and cognitive decline in the hypertensive patient: design of the European Society of Hypertension-Chinese Hypertension League Stroke in Hypertension Optimal Treatment randomized trial.

Abstract: The SBP values to be achieved by antihypertensive therapy in order to maximize reduction of cardiovascular outcomes are unknown; neither is it clear whether in patients with a previous cardiovascular event, the optimal values are lower than in the low-to-moderate risk hypertensive patients, or a more cautious blood pressure (BP) reduction should be obtained. Because of the uncertainty whether 'the lower the better' or the 'J-curve' hypothesis is correct, the European Society of Hypertension and the Chinese Hypertension League have promoted a randomized trial comparing antihypertensive treatment strategies aiming at three different SBP targets in hypertensive patients with a recent stroke or transient ischaemic attack. As the optimal level of low-density lipoprotein cholesterol (LDL-C) level is also unknown in these patients, LDL-C-lowering has been included in the design. (Less)

Blood pressure and low-density lipoprotein-cholesterol lowering for prevention of strokes and cognitive decline: a review of available trial evidence

Abstract: It is well established by a large number of randomized controlled trials that lowering blood pressure (BP) and low-density lipoprotein cholesterol (LDL-C) by drugs are powerful means to reduce stroke incidence, but the optimal BP and LDL-C levels to be achieved are largely uncertain. Concerning BP targets, two hypotheses are being confronted: first, the lower the BP, the better the treatment outcome, and second, the hypothesis that too low BP values are accompanied by a lower benefit and even higher risk. It is also unknown whether BP lowering and LDL-C lowering have additive beneficial effects for the primary and secondary prevention of stroke, and whether these treatments can prevent cognitive decline after stroke.

Comparison of the Complior Analyse device with Sphygmocor and Complior SP for pulse wave velocity and central pressure assessment.

Abstract: BACKGROUND: The Complior device (Alam Medical, France) was used in epidemiological studies which established pulse wave velocity (PWV) as a cardiovascular risk marker. Central pressure is related, but complementary to PWV and also associated to cardiovascular outcomes. The new Complior Analyse measures both PWV and central blood pressure during the same acquisition. The aim of this study was to compare PWV values from Complior Analyse with the previous Complior SP (PWVcs) and with Sphygmocor (PWVscr; AtCor, Australia), and to compare central systolic pressure from Complior Analyse and Sphygmocor. METHOD: Peripheral and central pressures and PWV were measured with the three devices in 112 patients. PWV measurements from Complior Analyse were analysed using two foot-detection algorithms (PWVca_it and PWVca_cs). Both radial (ao-SBPscr) and carotid (car-SBPscr) approaches from Sphygmocor were compared to carotid Complior Analyse measurements (car-SBPca). The same distance and same calibrating pressures were used for all devices. RESULTS: PWVca_it was strongly correlated to PWVscr (R(2) = 0.93, P < 0.001) with a difference of 0.0 ± 0.7 m/s. PWVca_cs was also correlated to PWVcs (R(2) = 0.90, P < 0.001) with a difference of 0.1 ± 0.7 m/s. Central systolic pressures were strongly correlated. The difference between car-SBPca and ao-SBPscr was 3.1 ± 4.2 mmHg (P < 0.001), statistically equivalent to the difference between car-SBPscr and ao-SBPscr (3.9 ± 5.8 mmHg, P < 0.001), whilst the difference between car-SBPca and car-SBPscr was negligible (-0.7 ± 5.6 mmHg, P = NS). CONCLUSION: The new Complior Analyse device provides equivalent results for PWV and central pressure values to the Sphygmocor and Complior SP. It reaches Association for the Advancement of Medical Instrumentation standard for central blood pressure and grades as excellent for PWV on the Artery Society criteria. It can be interchanged with existing devices.

Large artery stiffness and carotid flow pulsatility in stroke survivors.

Abstract: OBJECTIVE: Aortic stiffness is increased in lacunar stroke. The precise mechanism linking aortic stiffness to symptomatic lacunar stroke is not well understood. The aim of this study was to compare the effects of aortic stiffness, carotid stiffness, central blood pressure, and cerebrovascular resistance on carotid flow pulsatility according to stroke subtype. METHODS: Two hundred and one consecutive patients were examined 13 months after hospitalization for their first-ever ischemic stroke. The stroke subtype was classified using the Causative Classification of Stroke System. Carotid-femoral pulse wave velocity (PWV) was used as a measure of aortic stiffness. Common carotid flow pulsatility was expressed as resistive index. Central blood pressure was measured using applanation tonometry. RESULTS: Complete data were available for 174 patients (mean age… 67 ± 10 years, 64% men). In patients with lacunar stroke, aortic PWV was higher (13.11 ± 2.74 m/s) than in individuals with large artery atherosclerosis (9.98 ± 1.87 m/s, P <0.001), cardioembolic (11.31 ± 3.18 m/s, P = 0.04) or cryptogenic stroke (11.13 ± 3.2 m/s, P = 0.01). Similarly, central SBP and resistive index were higher in patients with lacunar stroke (145 ± 23 mmHg and 0.80 ± 0.04, respectively) than those with large artery atherosclerosis (128 ± 18 mmHg, P <0.01 and 0.74 ± 0.07, P <0.01, respectively) or cryptogenic stroke (132 ± 18 mmHg, P <0.01 and 0.76 ± 0.07, P <0.05, respectively). In multivariate analysis, aortic stiffness and central pulse pressure were the main determinants of resistive index independent of stroke subtype. CONCLUSION: Our results suggest that aortic stiffening, by reducing the buffering function of the aorta and thereby increasing the transmission of pressure and flow pulsatility into the cerebral arterioles, may contribute to the pathogenesis of lacunar stroke.

Destiffening effect of valsartan and atenolol: influence of heart rate and blood pressure.

Abstract: Objective:We investigated data in 373 patients from the EXPLOR trial to determine the influence of heart rate (HR) and blood pressure (BP) on aortic stiffness in response to beta-blockade or angiotensin 2 type 1 receptor antagonism, administered during 24 weeks.Methods:Carotid–femoral pulse wave vel

ARB-based single-pill platform to guide a practical therapeutic approach to hypertensive patients

Abstract: Hypertension is a major modifiable risk for the development of cardiovascular, cerebrovascular and renal diseases. Thus, effective treatment of high blood pressure is an important strategy for reducing disease burden; however, in spite of the availability of numerous effective therapies only 30–40 % of patients with hypertension achieve the recommended blood pressure goals of <140/90 mmHg. Lack of adherence to therapy and reluctance to intensify therapy are cited frequently to explain the discrepancy between potential and attained outcomes. Adherence is closely related to the tolerability, effectiveness and complexity of therapy. Therapeutic inertia may be influenced by concerns over tolerability, as well as the lack of clear preferences for therapies when managing patients with risk factors and comorbidities. Effective and well-tolerated single pill combination therapies are now available that improve adherence and simplify treatment. The combination of a renin-angiotensin system blocker with a calcium channel blocker and a diuretic improves adherence to therapy. We have devised a practical tool for orienting the application of well-tolerated single pill 2/3 drug fixed dose combination therapies in clinical situations commonly encountered when treating hypertensive patients. This approach employs the angiotensin receptor blocker olmesartan alone or in combinations with amlodipine and/or hydrochlorothiazide. This platform is based on clinical evidence, guidelines, best practice, and clinical experience where none of these is available. We believe it will increase the percentage of hypertensive patients who achieve blood pressure control when applied as part of an integrative approach that includes regular follow-up and instruction on lifestyle changes.

Non-hemodynamically significant renal artery stenosis predicts cardiovascular events in persons with ischemic heart disease.

Abstract: Background/Aims: Recently, we reported that small renal arteries, defined by a low reference diameter (RD) or minimal luminal diameter (MD), are independently associated with a low GFR, resistant hypertension, and onset of contrast-induced nephropathy and suggested a post-hoc analysis of CORAL trial based on RD categories Here we hypothesized that RD and MD are markers of nontraditional cardiovascular risk factors and tested whether low RD and MD could impact the prognosis of patients with ischemic heart disease Methods: Prospective cohort study We used proportional hazards models to analyze the first onset of cardiovascular events in relation with RD, MD, or percentage of renal artery stenosis (RAS) in those with low-to-moderate RAS (10-70%) (n = 181) Results: During the median follow-up of 45 (range, 01-5) years, 278% participants (n = 623; mean age, 64 years; 29% women) experienced a cardiovascular event (354% in those with RAS 10-70%) The presence of low-to-moderate RAS was associated with cardiovascular events In these subjects, those with low MD were associated with a higher risk of cardiovascular events (MD >42 mm, HR: 1; MD 32-42 mm, HR: 166, 95% CI: 074-372, p = 022; MD Conclusions: In patients with ischemic heart disease and low-to-moderate RAS, MD is a significant predictor of cardiovascular events, improves risk prediction, and may represent a valuable biomarker of cardiovascular disease risk i 2014 S Karger AG, Basel

Aortic stiffness measurement improves the prediction of asymptomatic coronary artery disease in stroke/transient ischemic attack patients.

Abstract: BackgroundAortic stiffness is an independent predictor of coronary events.AimsWe assessed the predictive value of aortic stiffness for ⩾50% asymptomatic coronary artery disease in a stroke/transient ischemic attack population.MethodsWe enrolled 300 consecutive patients aged 45–75 years with nondisabling, noncardioembolic ischemic stroke or transient ischemic attack, and no prior history of coronary artery disease. Coronary artery disease was assessed with 64-section computed tomography coronary angiography and all patients had a detailed cervicocephalic arterial work-up. Aortic stiffness was determined from carotid-femoral pulse wave velocity with 9·6 m/s as cutoff value. The predictive value of aortic stiffness was assessed by logistic regression and reclassification tables method after adjustment for the Framingham Risk Score and the presence of cervicocephalic stenosis, which were previously shown to be independent predictor of ⩾50% asymptomatic coronary artery disease.ResultsAmong the 274 included pat...

Erratum to: ARB-Based Single-Pill Platform to Guide a Practical Therapeutic Approach to Hypertensive Patients

Abstract: In Fig. 2 of the article, when referring to Coronary artery disease with Grade 2 or Grade 3 hypertension the abbreviation ‘‘OLM’’ was used instead of ‘‘OM’’ to indicate olmesartan, as defined in the footnote. In addition, referring to Nephropathy with Grade 1 hypertension, ‘‘2040 mg’’ should be ‘‘20–40 mg’’. This has been corrected in the new Fig. 2 (see below). The authors apologise for this oversight.

Response to Varol et al.'s letter.

Abstract: I read the article by Calvet et al. with great interest (1). They investigated the predictive value of aortic stiffness for ≥50% asymptomatic coronary artery disease (CAD) in a stroke/transient ischemic attack patients. They found that aortic pulse wave velocity improves the prediction of >50% asymptomatic CAD in stroke/transient ischemic attack patients. I congratulate the authors for this important study. However, I want to make minor criticism for this study from the methodological aspect. It is known that arterial stiffness is a complex process, and it is closely associated with confounding factors. Recently, Cecelja and Chowienczyk published a systematic review that showed that the contribution of cardiovascular risk factors other than age and blood pressure to aortic stiffness measured by carotid– femoral pulse wave velocity is small or insignificant, and age and blood pressure were consistently independently associated with aortic stiffness (2). As a result, this systematic review showed that age and blood pressure were consistently independently associated with aortic stiffness in majority of studies. It has also been shown that some antihypertensive drugs like angiotensin-converting enzyme inhibitors, calcium channel blockers, and spiranolactone reduce arterial stiffness (3,4). When we look at the study, there is no data of blood pressure and antihypertensive drugs used. Also statins reduce arterial stiffness, and there is also no data about statin use (3). It would have been useful if the authors had provided this information. Arterial stiffness describes the reduced capability of an artery to expand and contract in response to pressure changes, and it is an independent predictor of cardiovascular morbidity and all-cause mortality (3). It has been suggested that aortic stiffness occurs as a result of atherosclerosis along the aorta. However, it is closely associated with confounding factors especially blood pressure. Hypertension and some antihypertensive drugs can greatly influence arterial stiffness, and these factors should be considered in arterial stiffness evaluation.

Determination of Systemic and Regional Arterial Structure and Function

Abstract: Large artery stiffness can be measured through direct and indirect techniques. Measurement of pulse wave propagation is among the most direct techniques, either through pulse wave velocity or through artificial pressure wave propagation. Measurement of strain and stress through echotracking techniques gives also direct, hypothesis-free measurement of arterial stiffness. Other techniques are derived from models of circulation and can approximate arterial stiffness. Details about techniques, parameter definition, are given here to help researchers and practitioners to make the best choice of technique for their applications.

Large Artery Remodeling and Chronic Kidney Disease

Abstract: In recent years, many studies emphasized the role of arterial remodeling in the development of cardiovascular diseases, and it was shown that stiffening of arteries is associated with increased cardiovascular mortality and morbidity. Moreover, arterial stiffening is linked to decreased glomerular filtration rate, and is predictive of kidney-disease progression and the patient’s cardiovascular outcome. Early vascular aging and arterial stiffening are observed with progression of chronic kidney disease (CKD) and in end-stage renal disease (ESRD). This accelerated aging is associated with outward remodeling of large vessels, characterized by increased arterial radius not totally compensated for by artery wall hypertrophy. The mechanisms involved in large artery remodelling associated with CKD are complex including arterial calcification, inflammation, oxidative stress in association with mineral and bone metabolism disorders. Arterial stiffening in CKD and ESRD patients is of multifactorial origin with extensive arterial calcifications representing a major covariate. With aging, arterial stiffening is more pronounced in the aorta than peripheral conduit arteries, leading to the disappearance or inversion of the arterial stiffness gradient and less protection of the microcirculation from high-pressure transmission. Various non-pharmacological or pharmacological interventions can modestly slow the progression of arterial stiffness, but arterial stiffness is, in part, pressure-dependent and treatments able to stop the process mainly include antihypertensive drugs.

Predictive Value of Arterial Stiffness for Cardiovascular Events

Abstract: A major reason for measuring arterial stiffness “routinely” in clinical practice comes from the recent demonstration that arterial stiffness has an independent predictive value for cardiovascular events. Several longitudinal epidemiological studies have demonstrated the predictive value of arterial stiffness as intermediate endpoints, i.e. the higher the arterial stiffness, the higher the number of cardiovascular events. The largest amount of evidence has been given for aortic stiffness, measured through carotid-femoral pulse wave velocity which is considered as gold standard. Aortic stiffness has independent predictive value for all-cause and cardiovascular mortality, fatal and nonfatal coronary events and fatal strokes not only in patients with uncomplicated essential hypertension but also in patients with type 2 diabetes or end-stage renal disease, in elderly subjects and in the general population. Currently, as many as 21 studies consistently showed the independent predictive value of aortic stiffness for fatal and nonfatal cardiovascular events in various populations. Aortic stiffness can thus be considered as an intermediate endpoint for cardiovascular events.

Response to Balta et al. letter

Abstract: This letter is a reply to the Letter to the Editor, ‘Arterial stiffness in patients with ischemic attack’ that was published in the International Journal of Stroke volume 9 issue 2 (1). In our study, we showed that measurement of carotid-femoral pulse wave velocity (PWV) improves the prediction of ≥50% asymptomatic coronary artery disease provided by the Framingham Risk Score and the presence of cervicocephalic stenosis in patients aged 45–75 years with nondisabling, noncardioembolic ischemic stroke or TIA (2). Our findings are consistent with many large epidemiological studies (3–6). Indeed, several studies have shown that aortic stiffness assessed by PWV is associated with higher cardiovascular event rates in high-risk and community-based samples, and that its predictive value is in addition to traditional vascular risk factor, including Framingham Risk Score (4–6). The 2013 ESH/ESC guidelines for the management of arterial hypertension pointed out that all available data are a relevant argument in favor of using assessment of arterial stiffness, using PWV, in daily practice (7). Obviously, identifying patients at high risk of a cardiovascular event still needs to be refined and the potential additional value of other vascular risk factors as discussed by Balta et al. will need to be assessed in large studies.

Decreasing Arterial Stiffness and/or Wave Reflections Independently of Mean Arterial Pressure: Effect of Non-antihypertensive Drugs (Part 2)

Abstract: Change in arterial stiffness with drugs is a major end point in clinical trials, although evidence for arterial stiffness as a therapeutic target still needs to be confirmed. Drugs which affect arterial stiffness include antihypertensive drugs, mostly blockers of the renin–angiotensin–aldosterone system. Other drugs will be addressed in Chap. 40. Whether the reduction in arterial stiffness after antihypertensive treatment is only due to the blood pressure (BP) lowering which unloads the stiff components of the arterial wall such as collagen, or additional BP-independent effects are involved, has been largely debated. Currently, an increasing body of evidence, including theoretical aspects of arterial mechanics, long-term observational studies in humans and recent meta-analyses of double-blind, randomized, controlled trials, suggests that only part of aortic stiffness could be reduced through the normalization of BP by pharmacological treatment, and further reduction of aortic stiffness would require arterial structural changes, including reduction in collagen density and rearrangement of the wall materials. Mechanistic pharmacological studies are required to demonstrate that novel pharmacological classes have true “de-stiffening” properties.

Can we learn about the hypertension-induced decline in renal function from noninvasive haemodynamics?

Abstract: N ormal arterial aging is characterized by arterial enlargement, wall-thickening and stiffening, which predominate at large arteries [1]. Arterial enlargement and stiffening occur in parallel with glomerular filtration rate (GFR) decline in patients with chronic kidney disease (CKD) [2]. In CKD patients, arterial enlargement is associated with a lack of arterial wall-thickening, resulting in an increased circumferential wall stress [3,4]. The relationships between central hemodynamics [either arterial stiffness or central blood pressure (BP)] and GFR decline are complex, and depend mainly on both the stage of the disease – early CKD, advanced CKD or endstage renal disease – and the level of BP – optimal BP, high normal and grade I-II hypertension [2–4]. O’Rourke and Safar [5] suggested that the torrential flow and low resistance to flow in the kidney expose small arterial vessels of the glomerulus to the high-pressure fluctuations that exist in the renal arteries. Such fluctuations, measurable as central pulse pressure, increase three-fold to four-fold with age. Exposure of small vessels to highly pulsatile pressure and flow may explain microvascular damage to the glomerulus through altered myogenic tone and result in renal insufficiency [5]. In addition, aortic stiffness and central BP are associated with higher risk of incident hypertension [6]. Thus, it is tempting to speculate that a vicious pathophysiological circle, involving large/ small artery cross-talk [7], can start from any rise in BP, leading to higher aortic stiffness, which itself increases central BP pulsatility, damaging in turn the renal function, which may ultimately exaggerate the rise in BP, thus increasing the incidence of sustained hypertension. An important issue is the degree of involvement of renal dysfunction in this pathophysiological pathway, that is