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Träfflista för sökning "WFRF:(Lundman Pia) srt2:(2010-2014)"

Sökning: WFRF:(Lundman Pia) > (2010-2014)

  • Resultat 1-4 av 4
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1.
  • Bennermo, Marie, et al. (författare)
  • Genetic and environmental influences on the plasma interleukin-6 concentration in patients with a recent myocardial infarction : a case-control study
  • 2011
  • Ingår i: Journal of Interferon and Cytokine Research. - : Mary Ann Liebert Inc. - 1079-9907 .- 1557-7465. ; 31:2, s. 259-264
  • Tidskriftsartikel (refereegranskat)abstract
    • The aim was to study the stimuli responsible for triggering and sustaining the plasma concentration of the inflammatory marker interleukin-6 (IL-6) in patients with a first myocardial infarction before the age of 60 and healthy control subjects matched for age and sex. The plasma IL-6 concentration, antibodies against Chlamydia pneumoniae, cytomegalovirus, Epstein-Barr virus, Helicobacter pylori, herpes simplex type 1 and 2, and genotype for the IL6-174 G>C single-nucleotide polymorphism were determined 3 months after the acute event. The results showed that patients had higher IL-6 levels than control subjects, whereas there were no differences regarding individual or total number (pathogen burden) of positive antibody tests against the different pathogens or IL6 genotype distribution. The plasma IL-6 concentration was associated with the number of positive antibody tests in patients and control subjects, whereas patients irrespective of IL6 genotype had increased IL-6. Multivariate analysis, including traditional coronary heart disease risk factors, antibodies against pathogens, and IL6 genotype, explained 17% of the variation of the plasma IL-6 concentration. Neither pathogen burden nor IL6 genotype did contribute to the variation of plasma IL-6 levels, whereas smoking, body-mass index, hypertension, case-control status, and age were determinants of the plasma IL-6 concentration.
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2.
  • Paramel, Geena, 1985-, et al. (författare)
  • CARD8 gene encoding a protein of innate immunity is expressed in human atherosclerosis and associated with markers of inflammation
  • 2013
  • Ingår i: Clinical Science. - London, United Kingdom : Portland Press. - 0143-5221 .- 1470-8736. ; 125:8, s. 401-407
  • Tidskriftsartikel (refereegranskat)abstract
    • Inflammation is a key factor in the development of atherosclerotic coronary artery disease. It is promoted through the inflammasome, a molecular machine that produces IL (interleukin)-1 beta in response to cholesterol crystal accumulation in macrophages. The CARD8 (caspase recruitment domain 8) protein modulates this process by suppressing caspase 1 and the transcription factor NF-kappa B (nuclear factor kappa B). The expression of CARD8 mRNA was examined in atherosclerotic vascular tissue and the impact on MI (myocardial infarction) of a polymorphism in the CARD8 gene determined. CARD8 mRNA was analysed by microarray of human atherosclerotic tissue and compared with transplant donor arterial tissue. Microarray analysis was performed for proximal genes associated with the rs2043211 locus in plaque. The CARD8 rs2043211 polymorphism was analysed by genotyping of two Swedish MI cohorts, FIA (First Myocardial Infarction in Northern Sweden) and SCARF (Stockholm Coronary Atherosclerosis Risk Factor). The CRP (C-reactive protein) level was measured in both cohorts, but the levels of the pro-inflammatory cytokines IL-1 beta, IL-18, TNF (tumour necrosis factor) and MCP-1 (monocyte chemoattractant protein) were measured in sera available from the SCARF cohort. CARD8 mRNA was highly expressed in atherosclerotic plaques compared with the expression in transplant donor vessel (P < 0.00001). The minor allele was associated with lower expression of CARD8 in the plaques, suggesting that CARD8 may promote inflammation. Carriers of the minor allele of the rs2043211 polymorphism also displayed lower circulating CRP and lower levels of the pro-atherosclerotic chemokine MCP-1. However, no significant association could be detected between this polymorphism and MI in the two cohorts. Genetic alterations in the CARD8 gene therefore seem to be of limited importance for the development of MI.
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3.
  • Szummer, Karolina, et al. (författare)
  • Association between statin treatment and outcome in relation to renal function in survivors of myocardial infarction
  • 2011
  • Ingår i: KIDNEY INTERNATIONAL. - : Nature Publishing Group. - 0085-2538 .- 1523-1755. ; 79:9, s. 997-1004
  • Tidskriftsartikel (refereegranskat)abstract
    • As statins are recommended at discharge to all patients following myocardial infarction (MI), we studied their use and efficacy in renal disease by analyzing the data, in the nationwide SWEDEHEART registry, of 42,814 consecutive survivors of MI with available creatinine/dialysis data but without statin therapy on admission. The estimated glomerular filtration rate (eGFR) was determined by the Modification of Diet in Renal Disease Study formula and the patients classified into the five traditional stages of kidney disease. The 1-year survival in relation to prescription of statin at discharge was assessed in a Cox regression analysis adjusted by a propensity score that described each individuals likelihood of being treated with a statin, established by 36 baseline characteristics and in-hospital therapies. Statin use at discharge decreased with increased renal impairment from 81% in eGFR stage 1 to 31% in eGFR stage 5. After adjusting for the propensity score and discharge medication, statin use was associated with a significant reduction in overall risk of death (hazard ratio 0.63), with a statistically significant interaction between statin therapy and the stage of renal function. Thus, statin use at discharge was associated with improved 1-year survival of patients in stages 2-4 (mild-to-severe) of renal insufficiency. This effect appears attenuated in those with stage 5 renal failure.
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4.
  • Szummer, Karolina, et al. (författare)
  • Cockcroft-Gault is better than the Modification of Diet in Renal Disease study formula at predicting outcome after a myocardial infarction : Data from the Swedish Web-system for Enhancement and Development of Evidence-based care in Heart disease Evaluated According to Recommended Therapies (SWEDEHEART)
  • 2010
  • Ingår i: American Heart Journal. - : Elsevier BV. - 0002-8703 .- 1097-6744. ; 159:6, s. 979-986
  • Tidskriftsartikel (refereegranskat)abstract
    • Background The aim was to examine whether the Modification of Diet in Renal Disease (MDRD) or the Cockcroft-Gault (CG) formula is better at predicting prognosis in myocardial infarction (MI) patients. Methods All consecutive MI patients entered in a nationwide registry between 2003 and 2006 with glomerular filtration rate (eGFR) estimated by both the MDRD and CG formula (N = 36,137) were analyzed. Results Cockcroft-Gault classified a larger proportion of patients as having at least a moderate (39.8% vs 31.1%, P<.001) or at least a severe renal dysfunction (7.6% vs 4.4%, P<.001) compared with the MDRD. The largest difference between the estimations was seen when patients were divided according to gender, age, and weight, where CG estimated a lower eGFR in women, the elderly, and those with low body weight. In a receiver operating characteristic analysis, CG had a stronger association to 1-year mortality (area under the curve 0.78, 95% CI 0.77-0.79) than MDRD (area under the curve 0.73, 95% CI 0.72-0.74). Within each renal function stage classified with the MDRD, there were patients identified with the CG as having both a worse renal function and a higher mortality. After multivariable adjustment, CG predicted 1-year mortality better than the MDRD (renal failure vs normal renal function: hazard ratio 3.00, 95% CI 2.42-3.71 with the CG; hazard ratio 2.56, 95% CI 2.10-3.11 with the MDRD). Conclusion Cockcroft-Gault is better than the MDRD equation at predicting mortality after a MI. This is mainly explained by differences in the coefficients and variables included in the eGFR equations, and less to differences in various subgroups of patients.
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