Jacques Blacher

Université Paris 13 Nord, Вильтанез, Île-de-France, France

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Publications (325)1021.1 Total impact

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    ABSTRACT: Hypertension (HTN) in chronic kidney disease (CKD) is influenced by blood pressure (BP) and the progression of CKD, including hemodialysis and renal transplantation. To date, the efficacy of antihypertensive drug strategies has chiefly been assessed by measuring steady-state systolic, diastolic and mean arterial pressures (MAP). However, recently elucidated features of the BP curve have highlighted other important goals, that is, the specific roles of pulse pressure (PP), arterial stiffness, pulse wave velocity (PWV) and wave reflections as potentially deleterious factors affecting the progression of HTN and CKD. Pharmacological strategies to date have included progressive withdrawal of alpha-blocking agents; efficacy of beta-blockers for coronary prevention; use of angiotensin blockade in HTN with glomerular injury, using angiotensin-converting enzyme inhibition or receptor blockade, as mono but never double-blockade, to avoid major complications; development of combination therapies with diuretics and/or calcium channel blockers. Nowadays, most clinical trials show that SBP, DBP and MAP-lowering is an effective strategy, although results no longer show preference for any specific drug class.Studies of arterial stiffness in CKD have become crucial. In older individuals, PWV is considerably elevated. The 'stiffness gradient' disappears or is inverted (normally, aortic PWV is lower than brachial PWV). Despite BP-lowering, PP is insufficiently dampened, thus promoting microcirculatory damage, progression of arterial calcifications and disturbed wave reflections, which all increase the risk of mortality. In the absence of effective hemodialysis or graft, increased arterial stiffness is therefore a major cardiovascular risk factor in CKD.
    Journal of Hypertension 07/2015; DOI:10.1097/HJH.0000000000000711 · 4.22 Impact Factor
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    ABSTRACT: The objective of the present study was to conduct the first systematic review and meta-analysis of prospective studies investigating the associations between total cholesterol (TC), HDL-cholesterol (HDL-C) and LDL-cholesterol (LDL-C) levels and the risk of breast cancer. Relevant studies were identified in PubMed (up to January 2014). Inclusion criteria were original peer-reviewed publications with a prospective design. Random-effects models were used to estimate summary hazard ratios (HR) and 95 % CI. Distinction was made between studies that did or did not exclude cancer cases diagnosed during the first years of follow-up, thereby eliminating potential preclinical bias. Overall, the summary HR for the association between TC and breast cancer risk was 0·97 (95 % CI 0·94, 1·00; dose-response per 1 mmol/l increment, thirteen studies), and that between HDL-C and breast cancer risk was 0·86 (95 % CI 0·69, 1·09; dose-response per 1 mmol/l increment, six studies), with high heterogeneity (I 2= 67 and 47 %, respectively). For studies that eliminated preclinical bias, an inverse association was observed between the risk of breast cancer and TC (dose-response HR 0·94 (95 % CI 0·89, 0·99), seven studies, I 2= 78 %; highest v. lowest HR 0·82 (95 % CI 0·66, 1·02), nine studies, I 2= 81 %) and HDL-C (dose-response HR 0·81 (95 % CI 0·65, 1·02), five studies, I 2= 30 %; highest v. lowest HR 0·82 (95 % CI 0·69, 0·98), five studies, I 2= 0 %). There was no association observed between LDL-C and the risk of breast cancer (four studies). The present meta-analysis confirms the evidence of a modest but statistically significant inverse association between TC and more specifically HDL-C and the risk of breast cancer, supported by mechanistic plausibility from experimental studies. Further large prospective studies that adequately control for preclinical bias are needed to confirm the results on the role of cholesterol level and its fractions in the aetiology of breast cancer.
    The British journal of nutrition 07/2015; DOI:10.1017/S000711451500183X · 3.34 Impact Factor
  • C Chi · C Tai · J Wang · A Protogerou · J Blacher · M E Safar · Y Zhang · Y Xu
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    ABSTRACT: Current clinical evidence and latest guidelines recommended the combination antihypertensive therapy with angiotensin-converting enzyme (ACE) inhibitor / angiotensin receptor blocker (ARB) and calcium channel blocker (CCB) in patients with grade 2 to 3 hypertension. However, data are scarce in the comparison between the ACE inhibitor / ARB + CCB (A+C) therapy and other combinations. We therefore conducted a meta-analysis to see if ACE inhibitor/ARB combined with CCB is superior to other combinations.(Figure is included in full-text article.) DESIGN AND METHOD:: A meta-analysis was conducted in 20,669 hypertensives from 9 randomized controlled trials and we compared the A+C therapy with other combinations, in terms of blood pressure (BP) reduction, clinical outcomes and adverse effects. BP reduction did not differ significantly between the A+C therapy and other combination therapies, neither in systolic nor in diastolic BP, with P = 0.43 and P = 0.41, respectively. However, A+C strategy, compared with other combination therapies, achieved a significantly lower incidence of cardiovascular composite endpoints, including cardiovascular mortality, non-fatal myocardial infarction and non-fatal stroke (Risk ratio [RR] and 95% confidential interval [CI]: 0.80 [0.70, 0.91], P < 0.001, see as Figure), but similar all-cause mortality (0.90 [0.77, 1.04], P = 0.15) and stroke rate (0.90 [0.77, 1.04], P = 0.09). Moreover, A+C combination therapy exhibited a 3.10 ml/min/1.73m2 greater estimated glomerular filtration rate than other combinations (P = 0.01). Lastly, A+C therapy showed a similar incidence of adverse effects as other combinations (P = 0.34), but had a significantly lower incidence of severe adverse effects (0.85 [0.73, 0.98], P = 0.03). In summary, clinical evidences favor A+C therapy, which is superior to other combinations, in current anti-hypertensive strategy, with greater clinical benefit in cardiovascular outcome and reservation of renal function.
    Journal of Hypertension 06/2015; 33 Suppl 1 - ESH 2015 Abstract Book:e19-e20. DOI:10.1097/01.hjh.0000467402.25796.00 · 4.22 Impact Factor
  • J. Blacher
    Journal des Maladies Vasculaires 03/2015; 40(2). DOI:10.1016/j.jmv.2014.12.078 · 0.24 Impact Factor
  • J. Blacher
    Journal des Maladies Vasculaires 03/2015; 40(2). DOI:10.1016/j.jmv.2014.12.149 · 0.24 Impact Factor
  • J. Blacher
    Journal des Maladies Vasculaires 03/2015; 40(2). DOI:10.1016/j.jmv.2014.12.013 · 0.24 Impact Factor
  • Diabetes & Metabolism 03/2015; 41:A36-A37. DOI:10.1016/S1262-3636(15)30129-4 · 2.85 Impact Factor
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    ABSTRACT: In recent clinical investigations, visit-to-visit systolic blood pressure (SBP) variability was proven as a predictor of cardiovascular events and all-cause mortality. However, inconsistent results exist in this association. A meta-analysis of 13 prospective studies was conducted to evaluate the prognostic value of visit-to-visit SBP variability by different parameters in 77,299 patients with a mean follow-up of 6.3 years. The pooled age- and mean SBP-adjusted hazard ratios (HRs) for all-cause mortality were 1.03 (95% confidence interval [CI], 1.02-1.04; P<.001) per 1-mm Hg increase in SBP standard deviation (SD) and 1.04 (1.02-1.06, P<.001) per 1% in SBP coefficient of variation, and the corresponding values of cardiovascular mortality were 1.10 (1.02-1.17, P<.001) and 1.01 (0.99-1.03, P=.32), respectively. Moreover, a 1-mm Hg increase in SD was significantly associated with stroke, with an HR of 1.02 (1.01-1.03, P<.001). Visit-to-visit SBP variability, independent of age and mean SBP, is a predictor of cardiovascular and all-cause mortality and stroke. ©2015 Wiley Periodicals, Inc.
    Journal of Clinical Hypertension 02/2015; 17(2). DOI:10.1111/jch.12484 · 2.96 Impact Factor
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    ABSTRACT: Cardiac involvement in eosinophilia is potentially fatal and requires early diagnosis and prompt treatment. We report here the case of a 71-year-old female patient with eosinophilia > 10,000/mm3 for 2 months due to a myeloproliferative/myelodysplastic syndrome, with a rapidly progressive exertional dyspnea explained by an important circumferential eosinophilic pericarditis. Due to a rapid evolution to a tamponade, an emergent surgical drainage was performed. Subsequent medical treatment combined high-dose corticosteroids (1 mg/kg/day) with hydroxyurea and imatinib. The outcome was favourable with regression of the effusion, of the volume overload symptoms and decrease in eosinophilia.
    Annales de cardiologie et d'angeiologie 01/2015; DOI:10.1016/j.ancard.2014.12.002 · 0.30 Impact Factor
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    ABSTRACT: Background/Aims: Renal function decreases over time as a result of reduction in the number of functioning nephrons with age. In recipients and donors of kidney grafts, renal function decline may be linked differently to various parameters, namely arterial stiffness. Methods: We conducted a prospective cohort study including 101 recipients of kidney grafts and their donors aiming at determining the factors correlating with renal function decline over time. Aortic stiffness was evaluated by the non-invasive measurement of aortic pulse wave velocity. Glomerular filtration rate was estimated using the Modification of Diet in Renal Disease equation and the annualized change was determined. Results: Decline in renal function was estimated at 1-year post-transplantation and annually thereafter (median follow-up 8 years, range 3.6-18.3), as the mean of the annualized decrease in the glomerular filtration rate. In recipients, filtration rate decreased by 4.8 ± 19.7 mL/min/1.73m2 the first post-transplant year, and at a yearly rate of 2.2 ± 3.8 mL/min/1.73m2 thereafter. The first year decline was related to smoking and acute rejection. Later decline was significantly associated with donor age and aortic stiffness. In living donors, renal function decline after the first year corresponded to 0.7 mL/min/1.73m2, was significantly lower than that of recipients (p<0.001), and was determined by donor age at nephrectomy. Conclusion: Recipients of kidney grafts show a glomerular filtration rate decline over time that is significantly associated with donor age and aortic stiffness after the first post-transplant year, while donors demonstrate a lower decline that is mostly determined by age at nephrectomy.
    American Journal of Nephrology 12/2014; 41(1). DOI:10.1159/000371858 · 2.65 Impact Factor
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    ABSTRACT: It has been hypothesized that arterial stiffness leads to generalized microvascular dysfunction and that individuals with type 2 diabetes mellitus (T2DM) are particularly prone to the detrimental effects of arterial stiffness. However, evidence for an association between stiffness and markers of generalized microvascular dysfunction is lacking. We therefore investigated the association between arterial stiffness and skin microvascular function in individuals without and with T2DM. Cross-sectional data were used of The Supplementation en Vitamines et Mineraux Antioxydants 2 (SUVIMAX2) Study (n = 284/62.2 years/48.6% women/0% T2DM (by design)) and The Maastricht Study (n = 737/59.7 years/45.2% women/28.8% T2DM (by design)). Arterial stiffness was determined by carotid-femoral pulse wave velocity (cfPWV). Skin capillaroscopy was used to determine capillary density at baseline, and during reactive hyperemia and venous congestion. Laser Doppler flowmetry was used to assess acetylcholine- and local heating-induced vasoreactivity, and skin flowmotion. In The SUVIMAX2 Study, cfPWV (per +1 SD) was not associated with baseline capillary density (regression coefficient: -0.48 (95% confidence interval: 2.37; 1.41)) or capillary recruitment during venous congestion (0.54% (-0.74; 1.81%)). In addition, cfPWV was not associated with acetylcholine (-0.02% (-0.14; 0.10%)) or local heating-induced vasoreactivity (0.03% (-0.07; 0.12%)). In The Maastricht Study, in individuals without T2DM, cfPWV was not associated with baseline capillary density (-1.20 (-3.17; 0.77)), and capillary recruitment during reactive hyperemia (1.22% (-0.41; 2.84%)) or venous congestion (1.50% (-0.25; 3.25%)). In addition, cfPWV was not associated with flowmotion (-0.01 (-0.07; 0.06)). Results were adjusted for age and sex. Additional adjustments for confounders did not materially change these results. Results were qualitatively similar in individuals with T2DM. Arterial stiffness is not associated with skin microvascular function, irrespective of the presence of T2DM. © American Journal of Hypertension, Ltd 2014. All rights reserved. For Permissions, please email: journals.permissions@oup.com.
    American Journal of Hypertension 12/2014; 28(7). DOI:10.1093/ajh/hpu246 · 3.40 Impact Factor
  • Artery Research 12/2014; 8(4):141. DOI:10.1016/j.artres.2014.09.132
  • Artery Research 12/2014; 8(4). DOI:10.1016/j.artres.2014.09.080
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    ABSTRACT: Aortic blood pressure (BP) and 24-h ambulatory BP are both better associated with target organ damage than office brachial BP. However, it remains unclear whether a combination of these two techniques would be the optimal methodology to evaluate patients' BP in terms of left ventricular diastolic dysfunction (LVDD) prevention. In 230 participants, office brachial and aortic BPs were measured by a validated BP monitor and a tonometry-based device, respectively. 24-h ambulatory brachial and aortic BPs were measured by a validated ambulatory BP monitor (Mobil-O-Graph, Germany). Systematic assessment of patients' LVDD was performed. After adjustment for age, gender, hypertension and antihypertensive treatment, septum and lateral E/Ea were significantly associated with office aortic systolic BP (SBP) and pulse pressure (PP) and 24-h brachial and aortic SBP and PP (P⩽0.04), but not with office brachial BP (P⩾0.09). Similarly, 1 standard deviation in SBP was significantly associated with 97.8±20.9, 86.4±22.9, 74.1±23.3 and 51.3±22.6 in septum E/Ea and 68.6±20.1, 54.2±21.9, 37.9±22.4 and 23.1±21.4 in lateral E/Ea, for office and 24-h aortic and brachial SBP, respectively. In qualitative analysis, except for office brachial BP, office aortic and 24-h brachial and aortic BPs were all significantly associated with LVDD (P⩽0.03), with the highest odds ratio in 24-h aortic SBP. Furthermore, aortic BP, no matter in the office or 24-h ambulatory setting, showed the largest area under receiver operating characteristic curves (P⩽0.02). In conclusion, 24-h aortic BP is superior to other BPs in the association with LVDD.Journal of Human Hypertension advance online publication, 13 November 2014; doi:10.1038/jhh.2014.101.
    Journal of Human Hypertension 11/2014; 29(7). DOI:10.1038/jhh.2014.101 · 2.69 Impact Factor
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    ABSTRACT: Although the clinical relevance of brachial blood pressure (BP) measurement for cardiovascular (CV) risk stratification is nowadays widely accepted, this approach can nevertheless present several limitations. Pulse pressure (PP) amplification accounts for the notable increase in PP from central to peripheral arterial sites. Target organs are more greatly exposed to central hemodynamic changes than peripheral organs. The pathophysiological significance of local BP pulsatility, which has a role in the pathogenesis of target organ damage in both the macro- and the microcirculation, may therefore not be accurately captured by brachial BP as traditionally evaluated with cuff measurements. The predictive value of central systolic BP and PP over brachial BP for major clinical outcomes has been demonstrated in the general population, in elderly adults and in patients at high CV risk, irrespective of the invasive or non-invasive methods used to assess central BP. Aortic stiffness, timing and intensity of wave reflections, and cardiac performance appear as major factors influencing central PP. Great emphasis has been placed on the role of aortic stiffness, disturbed arterial wave reflections and their intercorrelation in the pathophysiological mechanisms of CV diseases as well as on their capacity to predict target organ damage and clinical events. Comorbidities and age-related changes, together with gender-related specificities of arterial and cardiac parameters, are known to affect the predictive ability of central hemodynamics on individual CV risk.
    Current Pharmaceutical Design 10/2014; 21(6). DOI:10.2174/1381612820666141023164125 · 3.29 Impact Factor
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    ABSTRACT: Reduction strategies of blood pressure, as a modifiable cardiovascular risk, are currently based on office assessment of brachial artery blood pressure. However, antihypertensive treatment based on brachial BP values reduces cardiovascular risk but cannot completely reverse the hypertension-induced risk of morbidity events. As is well known, BP varies in different arterial systems and invasive and non-invasive studies have demonstrated that brachial BP does not necessarily reflect central aortic BP. Emerging evidences now suggest that central pressure may predict cardiovascular diseases better than brachial BP; moreover, it may differently respond to certain antihypertensive drugs. The potential effects beyond peripheral BP control may be due to specific protective properties of different antihypertensive drugs in affecting central aortic pressure and arterial stiffness. Although data on direct cardiovascular benefit impact of central blood pressure treatment in randomized clinical trials are still lacking, it is likely that the improvement of quality of care and the individualized assessment of the hypertension-associated cardiovascular risk are achievable with the use of central hemodynamics. Therefore, basing antihypertensive treatment guidance on central pressures rather than on peripheral blood pressure may be the key for future antihypertensive strategies.
    Current Pharmaceutical Design 10/2014; 21(6). DOI:10.2174/1381612820666141023164530 · 3.29 Impact Factor
  • Goël Fenech · Gérald Rajzbaum · Mikaël Mazighi · Jacques Blacher
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    ABSTRACT: Hyperuricaemia is commonly found in subjects with cardiovascular disease, but its role as risk factor is very controversial. Although several studies reported serum uric acid as a marker of an underlying pathophysiological process, other studies hypothesis a potential causal link between serum uric acid and cardiovascular diseases. Some studies suggest that uric acid is biologically active and may have an atherogenesis role in development of cardiovascular diseases, although the mechanisms are not fully understood. Other studies have shown that uric acid can independently predict the development of some cardiovascular risk factors such as hypertension and metabolic syndrome, as well as myocardial infarction and stroke. The relations between serum uric acid and established cardiovascular risk factors are complex, and these latter could be considered as confounding factors. In this report, we review the inextricably link of serum uric acid to known cardiovascular risk factors, and we describe the possible mechanisms and potential causative role between serum uric acid and cardiovascular events in the general population, in subjects with cardiovascular risk factors and in those with pre-existing cardiovascular diseases. Limited information however is available concerning the impact of urate-lowering treatments on cardiovascular events, whereas only a positive therapeutic trial could give definite answers to the difficult problem of causality of uric acid in relation to cardiovascular risk. Thus, it is time to propose the design of a therapeutic trial, integrating cardiologists and rheumatologists, in order to further decrease cardiovascular risk.
    Joint, bone, spine: revue du rhumatisme 10/2014; 81(5). DOI:10.1016/j.jbspin.2014.01.008 · 3.22 Impact Factor
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    ABSTRACT: During year 2013, several recommendations for the management of hypertension were published: recommendations of the French and European Societies of Hypertension and two recommendations from the USA, those from the ACC/AHA/CDC groups and those from the JNC 8. The recommendations of the JNC 8 are not, strictly speaking, the recommendations of JNC 8, since they are neither endorsed by their sponsor: the National Heart, Lung and Blood Institute (NHLBI), nor by any other supervisor. They only commit their authors. Just before the publication of the JNC 8, "competing" recommendations, jointly produced by the AHA, ACC and CDC, were jointly published in Hypertension and in the Journal of American College of Cardiology, with different preferred treatment choices and significantly different algorithms. The authors of the JNC 8 have only included in their literature review randomized controlled trials of sufficient power. Randomized controlled trials are clearly the gold standard of comparative trials in medicine, but can they summarize all the knowledge? The authors of the JNC 8 propose in subjects over 60, a therapeutic threshold and target blood pressure of 150/90mmHg. This original threshold is poorly supported by the evidence and possibly increases the risk of physicians' inertia. The issue of experts' conflicts of interest has greatly changed the rules of drafting guidelines for clinical practice. Knowing that the vast majority of clinical trials is promoted by drug industry, could guidelines be strictly without any conflict of interest? Finally, recommendations for practice should have as primary, if not unique, objective to improve the practice.
    La Presse Médicale 09/2014; 43(10). DOI:10.1016/j.lpm.2014.03.031 · 1.17 Impact Factor
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    ABSTRACT: BACKGROUND Hypertension is the most prevalent chronic disease worldwide. Lifestyle behaviors for its prevention and control are recommended within worldwide guidelines. Nevertheless, their combined relationship with blood pressure (BP) level, particularly in the general population, would need more investigations. Our aim in this study was to evaluate the relative impact of lifestyle and nutritional factors on BP level.
    American Journal of Hypertension 09/2014; 28(3). DOI:10.1093/ajh/hpu164 · 3.40 Impact Factor

Publication Stats

10k Citations
1,021.10 Total Impact Points


  • 2010–2015
    • Université Paris 13 Nord
      • Unité de recherche en épidémiologie nutritonnelle - UREN (UMR 557) Inserm - INRA - CNAM
      Вильтанез, Île-de-France, France
    • Hotel Dieu Hospital
      Kingston, Ontario, Canada
    • Hôpital "René-Muret - Bigottini" – Hôpitaux Universitaires Paris-Seine-Saint-Denis
      Île-de-France, France
  • 2007–2015
    • Université René Descartes - Paris 5
      • Faculté de Médecine
      Lutetia Parisorum, Île-de-France, France
    • Hôpital "Sainte-Périne - Rossini - Chardon-Lagache" – Hôpitaux universitaires Paris Ile-de-France Ouest
      Lutetia Parisorum, Île-de-France, France
  • 2004–2014
    • Hôtel-Dieu de Paris – Hôpitaux universitaires Paris Centre
      Lutetia Parisorum, Île-de-France, France
    • Hopital Hôtel-Dieu Grace
      Windsor, Ontario, Canada
    • Centre Hospitalier Universitaire de Montpellier
      Montpelhièr, Languedoc-Roussillon, France
  • 2013
    • Université Mouloud Mammeri de Tizi Ouzou
      Tizi Uzu, Tizi Ouzou, Algeria
    • National and Kapodistrian University of Athens
      • Department of Medicine
      Athínai, Attica, Greece
  • 2009–2013
    • Conservatoire National des Arts et Métiers
      Lutetia Parisorum, Île-de-France, France
  • 2002–2012
    • Assistance Publique – Hôpitaux de Paris
      Lutetia Parisorum, Île-de-France, France
  • 2011
    • St. James's Hospital
      Dublin, Leinster, Ireland
  • 2008
    • Pierre and Marie Curie University - Paris 6
      Lutetia Parisorum, Île-de-France, France
  • 2005–2006
    • French Institute of Health and Medical Research
      Lutetia Parisorum, Île-de-France, France
    • Institut Pasteur de Lille
      Lille, Nord-Pas-de-Calais, France
    • Hôpital Paul-Brousse – Hôpitaux universitaires Paris-Sud
      Villejuif, Île-de-France, France
  • 1999–2004
    • Unité Inserm U1077
      Caen, Lower Normandy, France
    • University of Lyon
      Lyons, Rhône-Alpes, France
  • 2003
    • Centre Hospitalier Sainte Anne
      Lutetia Parisorum, Île-de-France, France
  • 1998
    • University of Leuven
      • Division of Hypertension and Cardiovascular
      Louvain, Flemish, Belgium