Beloqui, O. (Óscar)
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- Evaluation of measured and calculated small dense low-density lipoprotein in capillary blood and association with the metabolic syndrome(Elsevier, 2024) Deza, S. (Sara); Beloqui, O. (Óscar); Colina, I. (Inmaculada); Varo, N. (Nerea); Maroto-García, J. (Julia); Gonzalez-Hernandez, A. (Alvaro); Mugueta, C. (Carmen); Martínez-Chávez, E. (Estéfani); Monreal, J.I. (José Ignacio)Background and aims: Small-dense-low-density-lipoprotein cholesterol (sdLDL-C) is proatherogenic and not commonly measured. The aims were to evaluate capillary blood and its stability for sdLDL-C measurement and measure sdLDL-C in patients with metabolic syndrome (MS). Methods: 182 patients were studied (49 with MS). sdLDL-C was measured by electrophoresis (LipoPrint®), direct measurement (Roche Diagnostics) and Sampson equation. Intima-media thickness (IMT) and presence of atheroma was evaluated. sdLDL-C was compared in paired venous and capillary blood according to CLSI-EP09c (n = 40). sdLDL-C stability was studied after 24 h at room temperature (RT). Results: sdLDL-C in capillary blood and venous blood showed agreement with the direct measurement (bias: 4.17 mg/dL, LOA 95 %:-5.66; 13.99) and estimation (bias:8.12 mg/dL, LOA 95 %:-8.59; 24.82). sdLDL-C is stable in capillary blood for 24 h at RT. The electrophoretic method yielded lower (p < 0.05) sdLDL-C than the equation or direct measurement. Patients with MS had (p < 0.05) higher sdLDL-C (%) than patients without MS. Patients with atheroma plaques had higher sdLDL-C (p < 0.05). Estimated sdLDL-C correlated with IMT (r = 0.259, p < 0.001). Conclusions: Capillary blood is an alternative to venous blood for sdLDL-C measurement and is stable for 24 h after collection. Estimated and directly measured sdLDL-C associate with the MS being accessible tools for cardiovascular risk assessment.
- Association between matrix metalloproteinase-10 concentration and smoking in individuals without cardiovascular disease(Elsevier, 2008) Paramo, J.A. (José Antonio); Beloqui, O. (Óscar); Diez-Martinez, J. (Javier); Orbe, J. (Josune); Rodriguez, J.A. (José Antonio)INTRODUCTION AND OBJECTIVES: Smoking is an important cardiovascular risk factor whose underlying mechanism is incompletely understood. However, it has been suggested that alterations in the balance between synthesis and degradation of the extracellular matrix (ECM) may play a role. The aim of this study was to determine whether there is an independent association between smoking and the concentration of circulating metalloproteinases (MMPs) in individuals without cardiovascular disease. METHODS: Metabolic parameters, the carotid intima-media thickness (IMT), inflammatory markers (fibrinogen, C-reactive protein and interleukin-6), markers of endothelial damage (e.g., von Willebrand factor), and the concentration of MMP-1, -9 and -10 and tissue inhibitor of metalloproteinase-1 (TIMP-1) were assessed in 400 asymptomatic individuals with cardiovascular risk factors. Subjects were divided into non-smokers (n=195), smokers (n=118) and former smokers (n=87). In addition, global cardiovascular risk was determined from PROCAM and REGICOR scores. RESULTS: Both MMP-1 and MMP-10 concentrations were significantly higher in smokers than non-smokers (P< .05 and P< .001, respectively), though there was no difference in the levels of MMP-9, TIMP-1, IMT and other inflammatory parameters. There were positive correlations between the MMP-10 concentration and PROCAM and REGICOR scores (P< .001). Multivariate analysis showed that there was still an association between smoking and the MMP-10 concentration after adjustment for age, sex and other cardiovascular risk factors (P< .001). Multiple regression analysis showed that smoking accounted for 28% of the variability in the MMP-10 concentration. CONCLUSIONS: There was an independent association between smoking and the MMP-10 concentration in asymptomatic individuals. This relationship between MMP-10 and the ECM may indicate a mechanism through which this MMP contributes to smoking-related atherosclerosis.
- Does the metabolic syndrome need more descriptive studies or more evidence of its involvement in secondary prevention? Response(2011) Landecho, M.F. (Manuel F.); Beloqui, O. (Óscar); Fortuño, A. (Ana); Zalba, G. (Guillermo)
- Oxidative stress in hypertension: from the SNPs to the clinical phenotype(Sociedad Española de Nefrología, 2004) Moreno, M.U. (María Ujué); Beloqui, O. (Óscar); Fortuño, A. (Ana); Diez-Martinez, J. (Javier); San-Jose, G. (Gorka); Zalba, G. (Guillermo); Olivan, S. (Sara)
- Oxidative stress, endothelial dysfunction and cerebrovascular disease(Karger, 2007) Moreno, M.U. (María Ujué); Beloqui, O. (Óscar); Fortuño, A. (Ana); Diez-Martinez, J. (Javier); San-Jose, G. (Gorka); Zalba, G. (Guillermo)Endothelial dysfunction is a marker of atherosclerosis and contributes to the atherogenic process and the development of atherothrombotic complications. Oxidative stress has been implicated in the development of endothelial dysfunction through alterations of the nitric oxide metabolism. A number of evidence suggests a role for phagocytic-cell-mediated oxidative stress in diminished nitric oxide availability that is present in patients with atherosclerotic risk factors such as arterial hypertension. Thus, the combination of an excessive production of reactive oxygen species, namely superoxide anion, with an impaired antioxidant defense capacity leading to oxidative stress may facilitate the development and progression of atherosclerosis. Findings from recent clinical studies suggest that this mechanism can be operative in patients with cerebrovascular disease. This view may increase our capabilities to understand the pathophysiology of cerebrovascular disease, as well as to stimulate the design of new therapeutic strategies aimed to prevent and control the atherosclerotic process in patients presenting this condition.
- Association of the peroxisome proliferator-activated receptor α gene L162V polymorphism with stage C heart failure(Lippincott, Williams & Wilkins, 2011) Valencia-Serrano, F. (Félix); Beloqui, O. (Óscar); Arias, T. (Teresa); Lopez-Salazar, M.B. (María Begoña); Diez-Martinez, J. (Javier); Gomez-Doblas, J.J. (Juan José); Barba, J. (Joaquín); Teresa, E. (Eduardo) de; Beaumont, J. (Javier); Zalba, G. (Guillermo)OBJECTIVE: To analyze whether genetic variants of PPARA are associated with the development of stage C heart failure. METHODS: We analyzed the distribution of the rs1800206, rs4253778 and rs135551 polymorphisms in genomic DNA extracted from peripheral blood cells of 534 patients in different heart failure stages and 63 healthy individuals. The mRNA expression of the peroxisome proliferator-activated receptor (PPAR)α target genes long-chain 3-hydroxyacyl-CoA dehydrogenase (LCHAD) and medium-chain acyl-CoA dehydrogenase (MCAD) was measured in myocardial biopsies of a subgroup of stage B and C patients. Functional studies were performed in HL-1 cardiomyocytes. RESULTS: The V162 allele of the rs1800206 polymorphism was more frequent in stage C patients than in stage A and B patients and healthy individuals. Patients with the V162 allele exhibited decreased myocardial LCHAD and MCAD mRNA expression as compared to L162 homozygote patients. In addition, stage C patients exhibited lower myocardial LCHAD and MCAD mRNA expression than stage B patients. Cardiomyocytes transfected with the V162 allele presented decreased PPARα transcriptional activity, LCHAD mRNA expression and ATP production compared to cardiomyocytes transfected with the L162 variant. CONCLUSIONS: These findings suggest that the V162 allele of the human PPARA gene can be a new risk factor in the development of stage C heart failure, likely via depressed cardiac PPARα activity
- Association of cystatin C with heart failure with preserved ejection fraction in elderly hypertensive patients: potential role of altered collagen metabolism(Lippincott Williams & Wilkins, 2016) Huerta, A. (Ana); Brugnolaro, C. (Cristina); Beloqui, O. (Óscar); Zubillaga, E. (Elena); Querejeta, R. (Ramón); Ravassa, S. (Susana); Gonzalez, A. (Arantxa); Rabago, G. (Gregorio); San-Jose, G. (Gorka); López, B. (Begoña); Diez, J. (Javier)Objectives: Cystatin C has been shown to be associated with heart failure with preserved ejection fraction (HFPEF). In addition, myocardial fibrosis has been involved in diastolic dysfunction in HFPEF. Therefore, we hypothesized that increased cystatin C levels may be associated with altered collagen metabolism, contributing to diastolic dysfunction in patients with HFPEF. Methods: One hundred and forty-one elderly hypertensive patients with HFPEF were included. Cardiac morphology and function was assessed by echocardiography. Circulating levels of cystatin C, biomarkers of collagen type I synthesis (carboxy-terminal propeptide of procollagen type I) and degradation [matrix metalloproteinase-1 (MMP- 1) and its inhibitor TIMP-1] and osteopontin were analyzed by ELISA. Twenty elderly sex-matched patients with no identifiable cardiac disease were used as controls. In-vitro studies were performed in human cardiac fibroblasts. Results: Compared with controls, cystatin C was increased (P < 0.001) in patients with HFPEF, even in those with a normal estimated glomerular filtration rate (eGFR; P < 0.05). Cystatin C was directly correlated with the estimated pulmonary capillary wedge pressure (P < 0.01), TIMP-1 and osteopontin (P < 0.001) and inversely correlated with MMP-1:TIMP-1 (P < 0.01), but not with carboxy-terminal propeptide of procollagen type I or MMP- 1 in all patients with HFPEF. These associations were independent of eGFR. In vitro, osteopontin (P < 0.01) and TIMP-1 (P < 0.001) increased in the supernatant of cardiac fibroblasts exposed to cystatin C. Conclusion: In patients with HFPEF of hypertensive origin, cystatin C is increased and associated with diastolic dysfunction and alterations in collagen metabolism independently of eGFR. An excess of cystatin C might contribute to diastolic dysfunction in HFPEF by facilitating myocardial fibrosis via accumulation of osteopontin and TIMP-1.
- The C242T CYBA polymorphism of NADPH oxidase is associated with essential hypertension(Lippincott, Williams & Wilkins, 2006) Moreno, M.U. (María Ujué); Beloqui, O. (Óscar); Fortuño, A. (Ana); Diez-Martinez, J. (Javier); San-Jose, G. (Gorka); Zalba, G. (Guillermo)OBJECTIVE: Oxidative stress is implicated in hypertension. The reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidases are the main source of superoxide in phagocytic and vascular cells. The C242T polymorphism of CYBA, the human gene that encodes p22phox, has been found to be functionally associated with vascular NADPH oxidase activity in atherosclerotic patients. We investigated the association of the C242T polymorphism with hypertension and its potential impact on NADPH oxidase activity. We also analysed the interaction of C242T polymorphism with the -930A/G CYBA variant. DESIGN: Case-control study in a random sample of 623 subjects (326 hypertensive patients and 297 normotensive controls) from the general population. METHODS: CYBA polymorphisms were determined by restriction fragment length polymorphism (RFLP) or allelic discrimination. NADPH oxidase activity and p22phox expression were quantified in phagocytic cells by chemiluminescence and by northern and western blots, respectively. RESULTS: The prevalence of the CC genotype and the C allele frequency were significantly higher (P < 0.05) in hypertensives than in normotensives. CC genotype remained associated with hypertension after adjusting for potential confounders in a logistic regression analysis. Increased phagocytic NADPH oxidase activity was observed in CC hypertensives compared with CT and TT hypertensives (P < 0.05). Enhanced plasma levels of von Willebrand factor were found in CC hypertensives compared with TT hypertensives (P < 0.05). The C242T polymorphism was not in linkage disequilibrium with the -930A/G CYBA promoter variation, which also associates with hypertension. CONCLUSION: The C242T CYBA polymorphism is associated with essential hypertension. Furthermore, hypertensives carrying the CC genotype of this polymorphism exhibit features of NADPH oxidase-mediated oxidative stress and endothelial damage.
- Ultrasonic backscatter and diastolic function in hypertensive patients(American Heart Association, 2002) Beloqui, O. (Óscar); Maceira, A.M. (Alicia M.); Diez-Martinez, J. (Javier); Barba, J. (Joaquín)This study was designed to assess whether ultrasonic reflectivity, evaluated by a real-time integrated backscatter analysis, was related to the severity of diastolic dysfunction, as studied by Doppler echocardiography in patients with essential hypertension. One hundred nine subjects were included in the study. Diastolic function was assessed by mitral-inflow Doppler ultrasound recordings. Backscatter cyclic variation and maximal intensity were measured in 6 regions throughout the left ventricle. The subjects were classified in 5 groups according to blood pressure and diastolic function: 29 normotensives with normal diastolic function (group 1), 18 hypertensives with normal diastolic function (group 2), 47 hypertensives with a delayed relaxation pattern (group 3), 11 hypertensives with a pseudonormal filling pattern (group 4), and 4 hypertensives with a restrictive filling pattern (group 5). The highest cyclic variation was found in groups 1 and 2, the lowest in groups 4 and 5 (5.7+/-0.2 dB in group 1 and 5.7+/-0.2 dB in group 2 versus 2.9+/-0.3 dB in group 4 and 2.1+/-0.4 dB in group 5; P<0.001), with intermediate values in group 3 (5.2+/-0.2 dB). Cyclic variation was inversely correlated with left ventricular chamber stiffness (P<0.05) and directly correlated with midwall fractional shortening (P<0.02) in all hypertensives. No differences in maximal intensity were found among the 5 groups of subjects. These results show an association between diminished cyclic variation of backscatter and deterioration of diastolic function in hypertensive patients. Thus, alterations in this parameter may be useful for the assessment of diastolic dysfunction in hypertension.
- Association of age, inflammatory markers and subclinical atherosclerosis in subjects free from cardiovascular disease(Elsevier, 2008) Paramo, J.A. (José Antonio); Benito-Boilos, A. (Alberto); Beloqui, O. (Óscar); Colina, I. (Inmaculada); Diez-Martinez, J. (Javier); Orbe, J. (Josune); Rodriguez, J.A. (José Antonio)BACKGROUND AND OBJECTIVE: We assessed whether an independent association between inflammatory markers and age-related subclinical atherosclerosis could be found in subjects free from cardiovascular disease. PATIENTS AND METHOD: Metabolic parameters, inflammatory and endothelial markers, such as high-sensitivity C-reactive protein, interleukin-6, fibrinogen and von Willebrand factor, as well as the carotid intima-media thickness were assessed in 890 asymptomatic subjects (mean age: 55 years; range: 20-80 years; 80% men) with cardiovascular risk factors. RESULTS: Subjects in the upper quartile (age 61-80 years) showed a significant increase of traditional risk factors, particularly arterial pressure and glucose levels (p < 0.01) as compared with lower quartiles. We also found a significant increase in the levels on inflammatory and endothelial markers (p < 0.001) and intima-media thickness (p < 0.001) in older adults. In the multivarate analysis, after adjustment for cardiovascular risk factors, intima-media thickness was independently associated with inflammation and endothelial dysfunction in older adults (p < 0.01). CONCLUSIONS: Besides age, systemic inflammation and vascular damage are associated with subclinical atherosclerosis in asymptomatic subjects. The age-related inflammatory profile may predispose to cardiovascular complications.