G Bricca

Claude Bernard University Lyon 1, Villeurbanne, Rhône-Alpes, France

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Publications (15)48.75 Total impact

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    ABSTRACT: Orthostatic blood pressure (BP) variations have been related with cardiovascular events in hypertensive patients; they are associated with autonomic and neurohormonal abnormalities. Large vessels damages, i.e. aortic atherosclerosis (ATS), may exaggerate this BP deregulation and thus, amplify its prognostic consequence. This study aimed at investigating the interaction of ATS on the prognostic value of postural BP changes. In a cohort of 958 hypertensive patients with an aortography available (mean age 44 ± 11 years, 61% of men, 26.5% of secondary prevention), BP was measured with a manual sphygmomanometer after 10 minutes of rest in the supine position and in the standing position, one minute after assuming the upright position. Supine and standing SBP were each the average of six measurements. Postural BP change was recalculated as absolute value of the difference between mean supine SBP and mean standing SBP. ATS was assessed by a 2-modality score: absent or mild vs. moderate or severe. All-cause and cardiovascular deaths were assessed after 15 years of follow-up. BP was 182/110 mm Hg, on average. During the follow-up, 167 cardiovascular and 280 all-cause death occurred. As illustrated in the figure, an increased risk of death was observed across tertiles of increasing level of postural BP changes in the presence of moderate or severe ATS but not if ATS was absent or mild. In a multivariable Cox Regression analysis adjusted for major cardiovascular risk factors, postural BP change was statistically associated with all-cause and cardiovascular mortality only in the presence of moderate or severe ATS: tertile 2 vs. 1: 2.19 [1.10-4.39] and 2.02 [0.82-4.96] respectively; tertile 3 vs. 1: 3.21 [1.73-5.94] and 4.65 [2.20-9.80] respectively (P for interaction 0.006 for all-cause mortality and 0.002 for cardiovascular mortality). We did not observe such interaction with ECG left ventricular hypertrophy, history of heart failure and anti-hypertensive treatment. The prognostic significance of postural BP changes is markedly influenced by aortic damage in hypertensive patients.(Figure is included in full-text article.).
    Journal of Hypertension 06/2015; 33 Suppl 1 - ESH 2015 Abstract Book:e41. DOI:10.1097/01.hjh.0000467456.01139.e9 · 4.72 Impact Factor
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    ABSTRACT: Objective: During atherogenesis, vascular smooth muscle cells (VSMCs) undergo a phenotypic modulation leading to migration and loss of contractility. Here we propose a gene regulatory network specific of the contractile phenotype of the carotid VSMCs from transcriptomic data. Design and method: Human carotid atheroma plaque (ATH, Stary>4) and nearby macroscopically intact tissue (MIT, Stary<3) of 32 patients were analysed by microarrays (Affymetrix HuGene-1.0ST). Histological analysis ensured the large predominance of VSMCs in MIT. Vascular smooth muscle contraction (VSMcontr) involved 119 genes (KEGG database). Transcriptional regulators (TRs) were obtained from Genomatix
    Journal of Hypertension 06/2015; 33 Suppl 1 - ESH 2015 Abstract Book:e1-e2. DOI:10.1097/01.hjh.0000467353.66660.d4 · 4.72 Impact Factor
  • Diabetes & Metabolism 03/2015; 41:A77. DOI:10.1016/S1262-3636(15)30289-5 · 3.27 Impact Factor
  • Journal des Maladies Vasculaires 09/2010; 35(5):317-317. DOI:10.1016/j.jmv.2010.07.070 · 0.24 Impact Factor
  • V Paget · N Gaudebout · L Legedz · MO Rial · H Milon · G Bricca · P Lantelme
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    ABSTRACT: Objective: Transglutaminase 2 (TG2) is ubiquitously expressed and induces transamidation and cross-linking of proteins. This process is important for cell-matrix interactions and vascular remodeling, and is modulated by angiotensin II (Ang II). We hypothesized that Ang II through the angiotensin type 1 receptor (AT1R) modulates TG2 expression, which differentially regulates MAP kinase expression in rat vascular smooth muscle cells (VSMCs). Methods: Mesenteric artery-derived VSMCs from Wistar Kyoto (WKY) and spontaneously hypertensive rats (SHR) were studied. Cells were stimulated with Ang II (100 nM) ± the AT1R blocker valsartan (Val 10 μM) or ± the TG2 inhibitor cystamine (CYS 10 μM). Expression of TG2, p38 MAPK, AT1R and AT2R was evaluated by immunoblotting. Results: Basal TG2 expression in SHR VSMCs was significantly higher compared to basal TG2 expression in WKY VSMCs (+28 ± 12%, p < 0.05). Ang II significantly increased TG2 expression only in SHR VSMCs compared to vehicle (+57 ± 19%, p < 0.05). Val significantly reduced Ang II-induced TG2 expression in SHR VSMCs. Basal AT1R expression in cells from WKY was lower compared to SHR (1.15 ± 0.2 AU vs 1.8 ± 0.1 AU, p < 0.05). Basal AT2R expression was 2-fold higher in SHR cells than in WKY (p < 0.05). Ang II had no effect on AT1R expression in either WKY or SHR. In presence of Ang II, AT2R expression was significantly increased in WKY and reduced in SHR (224.6 ± 65.13% vs 47.87 ± 11.95%, p < 0.05). After one-hour stimulation, Ang II increased p38 MAPK expression only in SHR (3-fold increase vs vehicle, p < 0.05). Ang II-induced p38 MAPK expression was significantly reduced by CYS. Conclusions: Ang II positively regulates TG2 expression in rat VSMCs via AT1R. TG2 plays a role in Ang II-induced p38 MAPK long-term production. These effects are particularly evident in SHR VSMCs which presented high basal levels of Ang II receptors and TG2.
    Journal of Hypertension 06/2010; 28. DOI:10.1097/01.hjh.0000378280.44189.0d · 4.72 Impact Factor
  • P Lantelme · V Paget · L Legedz · MO Rial · H Milon · G Bricca
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    ABSTRACT: Objective: Large arterial remodeling in CKD patients has been extensively described in the last years and is mainly characterized by an outward remodeling. However, the predictive value of arterial remodeling and stiffening is still debated in CKD stages 3–5. Methods: 180 patients (mean age 59.6 years) with CKD (mean mGFR 32 mL/min/1.73m2) were included in this longitudinal study (mean follow-up 4.6 years). Patients underwent a yearly check-up including arterial evaluation (carotido-femoral pulse wave velocity (SphygmoCor®), carotid thickness, diameter and stiffness (Art-Lab system®)) and GFR measurement with the 51Cr-EDTA clearance. Results: Changes overtime of arterial parameters estimated by a linear mixed-model regression with adjustment for age and sex were characterized by a stability of aortic stiffness, a significant decrease in carotid compliance and distensibility (adjusted slope −24 ± 9, P = 0.007, −1.46 ± 0.35, P < 0.0001, respectively), a significant carotid wall thinning (adjusted slope −25 ± 4, P < 0.0001) associated with an increase in carotid internal diameter (adjusted slope 0.09 ± 0.02, P < 0.0001) without modification of carotid external diameter. Carotid circumferential wall stress increased significantly over time (adjusted slope 2.5 ± 0.4, P < 0.0001). In multivariate COX analyses, after stepwise selection of significant variables, circumferential wall stress, Log UACR and alfacalcidol treatment remained independent determinants of the occurrence of renal event defined by a 20% reduction in GFR in 5 years or start dialysis. Conclusion: In stage 3–5 CKD patients, increased circumferential wall stress, due to an inadaptative remodeling, has a predictive value of CKD progression, independently of major determinants of CKD progression such as blood pressure, proteinuria.
    Journal of Hypertension 06/2010; 28. DOI:10.1097/01.hjh.0000378292.05179.25 · 4.72 Impact Factor
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    ABSTRACT: Lipogenesis is expressed in vascular smooth muscle cells (VSMCs), and such in situ lipogenesis could be providing the fatty acids for triglyceride synthesis and cholesterol esterification, and contributing to lipid accumulation in the arterial wall. This study investigated both the expression and regulation of lipogenesis in VSMCs to determine if they are modified in Psammomys obesus gerbils fed a high-fat diet as a model of insulin resistance and diabetes. Aortas were collected from diabetic and non-diabetic P. obesus for histological examination, measurement of lipogenic gene expression and VSMC culture. The aortas of diabetic animals exhibited lipid deposits and foam cells as well as disorganization of elastic fibres. However, lipogenic gene expression was not modified. VSMCs in vitro from the aortas of diabetic animals had, compared with cells from non-diabetic animals, lower mRNA levels of SREBP-1c and ChREBP. An adipogenic medium stimulated moderate FAS and ACC1 expression in cells from both diabetic and non-diabetic animals, but glucose and insulin on their own had no such stimulatory action. Also, triiodothyronine (T3) had a clear stimulatory action, while angiotensin II had a moderate effect, in cells from non-diabetic P. obesus, but not from diabetic animals, whereas LXR agonists stimulated lipogenesis in cells from both animal groups. Lipogenesis is expressed in the arterial walls and VSMCs of P. obesus. However, its expression was not increased in diabetes, and did not respond to either T3 or angiotensin II. Therefore, lipogenesis in situ is unlikely to contribute to the accumulation of lipids in the arterial walls of diabetic P. obesus gerbils.
    Diabetes & Metabolism 03/2010; 36(3):221-8. DOI:10.1016/j.diabet.2010.01.003 · 3.27 Impact Factor
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    ABSTRACT: Arterial stiffness is a strong predictor of cardiovascular events and particularly of stroke. A likely explanation is the development of atherosclerotic lesions at the carotid level, favored by increased local stiffness. Another possibility involves cardiac consequences of aortic stiffness and particularly left atrial dilatation with its subsequent risk of atrial fibrillation (AF) and cerebral embolism. The present study investigated the link between arterial stiffness, pulse pressure and left atrial size, a determinant of AF risk. Arterial stiffness was determined from pulse wave velocity (PWV) and pulse pressure (PP). Left atrial size was also measured. Several potential confounders were taken into account including indices of ventricular remodeling and diastolic function (estimated by NT-Pro brain natriuretic peptide (NT-proBNP) levels). Three-hundred and ten hypertensive patients, aged 53 +/- 13 years, were included. Mean 24-h blood pressure (BP) was 154 +/- 20 over 93 +/- 13 mmHg. Significant relationships were found between left atrial diameter (LAD) and PWV (r=0.27, P<0.001) and between LAD and 24-h PP (r=0.32, P<0.001). LAD was also correlated significantly, although not always tightly, with left ventricular dimensions, geometry and NT-proBNP. In two different multivariate models, LAD remained significantly correlated with PWV or with 24-h PP, independently of classical determinants like age, gender, body mass index, ventricular remodeling (i.e. dimensions and geometry) and filling pressure. These results led us to propose AF as a new possible pathophysiological link between arterial stiffness and stroke. These results also emphasize the cardiac consequences of arterial stiffness which can fuel a new approach to AF prevention.
    Archives of Cardiovascular Diseases 01/2008; 101(1):35-40. DOI:10.1016/S1875-2136(08)70253-5 · 1.84 Impact Factor
  • Atherosclerosis Supplements 06/2006; 7(3):355-355. DOI:10.1016/S1567-5688(06)81400-5 · 2.29 Impact Factor
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    ABSTRACT: Accumulation of cholesterol in foam cells of atheroma plaques depends on the balance between uptake and efflux of cholesterol. It may also depend on proteins surrounding lipid droplets, adipophilin, and perilipins. They favor triglyceride storage in adipocytes and could play a similar role for cholesterol in atheroma. We measured in human atheroma and nearby macroscopically intact tissue (MIT) the expression of perilipin, adipophilin, and regulatory factors of cholesterol metabolism. We identified perilipin A in human arterial wall. Its expression was largely increased in atheroma compared with MIT, and perilipin was present in macrophages and vascular smooth muscle cells. Adipophilin, ACAT1, and CD36 were also overexpressed in atheroma. mRNA levels of low-density lipoprotein receptor, 3-hydroxy-3-methylglutaryl coenzyme A reductase, and SREBP-2 were unchanged. With respect to efflux of cholesterol, the mRNA levels of NCEH and ABCA-1 were unchanged, whereas CLA-1 mRNA was slightly higher in atheroma. Importantly, immunoblotting of ABCA-1 showed a dramatic decrease of ABCA1 protein, the key molecule of cholesterol efflux, in atheroma compared with MIT. We show the presence and induction of perilipin in atheroma. This overexpression and the coordinated modifications of expression of key regulatory factors for cholesterol metabolism could favor cholesterol accumulation.
    Arteriosclerosis Thrombosis and Vascular Biology 09/2005; 25(8):1711-7. DOI:10.1161/01.ATV.0000174123.19103.52 · 6.00 Impact Factor
  • L Legedz · H Vidal · E Loizon · P Feugier · G Bricca
    European Journal of Clinical Investigation 10/2004; 34(9):643-4. DOI:10.1111/j.1365-2362.2004.01397.x · 2.73 Impact Factor
  • M. Kurdi · C. Cerutti · J. Randon · G. Bricca
    Journal of Hypertension 06/2004; 22(Suppl. 2):S18. DOI:10.1097/00004872-200406002-00052 · 4.72 Impact Factor
  • Journal of Hypertension 06/2004; 22(Suppl. 2):S43. DOI:10.1097/00004872-200406002-00141 · 4.72 Impact Factor
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    ABSTRACT: Our goal was to study the relative influence of systolic blood pressure (SBP) and plasmatic markers of sympathetic and renin-aldosterone systems (RAS) activities to left atrial diameter (LAD), left ventricular posterior wall thickness (LVPWT) and pulse wave velocity (PWV), which reflect cardiovascular remodeling in hypertension. In 227 consecutive patients with hypertension (mean age +/- SD: 53.3 years +/- 13.4, 126 men), we measured: PWV, LAD, LVPWT, mean 24-hours SBP, plasma renin activity, and plasma aldosterone and catecholamine levels. Multiples linear regression analyses were performed to test statistical associations between hemodynamic and neurohumoral factors, and cardiovascular remodeling parameters, after adjustment for age, gender and body mass index. LVPWT was positively correlated to SBP as well as to plasma aldosterone and meta-noradrenaline (p < 0.001). LAD and PWV were related to SBP but not to any of the biological variables. Moreover, LAD correlated to PWV independently of SBP (p < 0.05), whereas after SBP inclusion in the model, there was not significant correlation between LAD and LVPWT nor between LVPWT and PWV. In hypertension, the development of cardiac hypertrophy depends on SBP and the sympathetic and renin-aldosterone systems activities. The RAS is not involved in the PWV nor LAD modifications. Strong association between LAD and PWV suggest that left atrial enlargement, that may be considered as a marker of diastolic function, may results more from arterial stiffness than from ventricular hypertrophy.
    Archives des maladies du coeur et des vaisseaux 07/2003; 96(7-8):729-33. · 0.40 Impact Factor
  • M Kurdi · N Dizerens · C Cerutti · G Bricca · J Randon
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    ABSTRACT: Variations in the expression of cytokines from the interleukin-6 (IL-6) family: ciliary neurotrophic factor (CNTF), leukaemia inhibitory factor (LIF), and cardiotrophin 1 (CT-1) were studied during cardiac remodelling leading to left ventricular hypertrophy (LVH) in TGR(mRen2)27 rats at the age of 8 and 20 weeks. The cytokines mRNA levels within the free wall of the left ventricle were measured by semi-quantitative RT-PCR standardised with 18S. They were compared between heterozygous rats for the mRen2 transgene (TG+/-) and control rats (TG-/-). No significant difference was observed between results obtained at 8 and 20 weeks of age. At 20 weeks of age, TGR(mRen2)27 rats showed higher levels of mRNA LIF and IL-6 respectively by 52 and 55% compared to the control rats [LIF TG+/-: 3.17 +/- 0.21, TG-/-: 2.09 +/- 0.03; p < 0.001; n = 5; and IL-6 TG+/-: 1.53 +/- 0.13; TG-/-: 0.99 +/- 0.17; p < 0.05; n = 5]. By contrast, no variation of mRNAs levels of CT-1 and gp 130 genes was observed between control and transgenic rats. Concerning the cytokine receptors, the levels of mRNA for IL-6R did not vary while those of receptor subunits LIFR and CNTFR were decreased respectively by 48 and 42% in transgenic rats vs controls [LIFR TG+/-: 0.48 +/- 0.01; TG-/-: 0.92 +/- 0.08 p < 0.001; n = 5; and CNTFR TG+/-: 1.07 +/- 0.08; TG-/-: 1.85 +/- 0.18; p < 0.01; n = 5]. Therefore, these results show a specific pattern of activation of the cytokines pathway in the LVH of the TGR(mRen2)27 rat.
    Archives des maladies du coeur et des vaisseaux 01/2003; 96(7-8):811-4. · 0.40 Impact Factor