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  • 1. Dormandy, J. A.
    et al.
    Betteridge, D. J.
    Schernthaner, G.
    Pirags, V.
    Norgren, Lars
    Örebro University, School of Health and Medical Sciences.
    Impact of peripheral arterial disease in patients with diabetes: results from PROactive (PROactive 11)2009In: Atherosclerosis, ISSN 0021-9150, E-ISSN 1879-1484, Vol. 202, no 1, p. 272-281Article in journal (Refereed)
    Abstract [en]

    We compared cardiovascular disease outcomes according to the presence of peripheral arterial disease (PAD) at baseline in a post hoc analysis from the PROactive study. Of the 5238 patients in PROactive (a study of pioglitazone versus placebo in patients with type 2 diabetes and macrovascular disease; mean follow-up=34.5 months), 1274 had PAD at baseline (619=pioglitazone; 655=placebo). Patients with PAD at baseline showed significantly higher rates of the primary endpoint, main secondary endpoint, all-cause mortality (all P<0.0001), and stroke (P=0.0175) than those with no PAD at baseline. The risk of PAD alone was similar to that of myocardial infarction alone. In patients with no PAD at baseline, the event rates of the primary endpoint (P=0.0160), main secondary endpoint (P=0.0453), and acute coronary syndrome (P=0.0287) were significantly lower with pioglitazone than with placebo. This beneficial effect of pioglitazone was not seen in patients with PAD at baseline. In the total population, there was a higher frequency of leg revascularizations with pioglitazone than placebo-this was wholly due to first events that occurred within the initial 12 months of treatment. The presence of PAD increased the risk of all major cardiovascular events. Those without PAD at baseline seemed to benefit more from pioglitazone treatment than the overall PROactive population.

  • 2.
    Lind, Monica
    et al.
    Department of Medical Sciences, Occupational and Environmental Medicine, Uppsala University, Uppsala, Sweden.
    Salihovic, Samira
    Örebro University, School of Science and Technology. Department of Medical Sciences, Molecular Epidemiology and Science for Life Laboratory, Uppsala University, Uppsala, Sweden.
    Stubleski, Jordan
    Örebro University, School of Science and Technology.
    Kärrman, Anna
    Örebro University, School of Science and Technology.
    van Bavel, Bert
    Örebro University, School of Science and Technology.
    Lind, Lars
    Department of Medical Sciences, Cardiovascular Epidemiology, Uppsala University, Uppsala, Sweden.
    The changes in plasma levels of perfluoroalkyl substances (PFASs) are related to the increase in carotid intima-media thickness over 10 years2017In: Atherosclerosis, ISSN 0021-9150, E-ISSN 1879-1484, Vol. 263, p. E18-E18Article in journal (Other academic)
    Abstract [en]

    Aim: It has previously been reported that the environmental contaminants perfluoroalkyl substances (PFASs) are linked to atherosclerosis in cross-sectional studies. Since cross-sectional studies could be subject to reverse causation, we here analyzed if the longitudinal changes in PFASs during a 10 years follow-up were related to the change in intima-media thickness (IMT) during the same period.

    Methods: In the Prospective Investigation of the Vasculature in Uppsala Seniors (PIVUS) study,1,016 individuals were investigated at age 70. 826 of those were reinvestigated at age 75 and 606 at age 80 years. Eight different PFASs and carotid artery intima-media thickness (IMT, ultrasound) were measured at the three time-points.

    Results: IMT increased 0.058 mm during the 10-year period (p<0.0001). Following adjustment for baseline values of PFASs (age 70) and sex, the changes in plasma levels of 6 of the 8 measured PFASs were significantly related to the change in IMT over the 10-year follow-up period (p<0.0062 using Bonferroni correction for 8 tests). Further adjustment for traditional CV risk factors (HDL and LDL-cholesterol, smoking, systolic blood pressure, statin use, fasting glucose and serum triglycerides) did only affect these relationships marginally.

    Conclusions: The change in plasma levels of several PFASs during 10 years was related the increase in IMT seen during the same period, giving further evidence that PFASs might interfere with the atherosclerotic process.

  • 3. Osika, Walter
    et al.
    Dangardt, Frida
    Montgomery, Scott M.
    Örebro University, School of Health and Medical Sciences.
    Volkmann, Reinhard
    Gan, Li Ming
    Friberg, Peter
    Sex differences in peripheral artery intima, media and intima media thickness in children and adolescents2008In: Atherosclerosis, ISSN 0021-9150, E-ISSN 1879-1484, Vol. 203, no 1, p. 172-177Article in journal (Refereed)
    Abstract [en]

    Objective Males have higher coronary heart disease (CHD) lifetime risk and increased magnitude of atherosclerosis, compared with women. Using very high-resolution ultrasound, we have shown that the intima thickness (IT) of radial and dorsal pedal arteries, measured separately from the media thickness (MT), increases with age. We wanted to test whether there is already a difference between the sexes in childhood for IT, MT and intima media thickness (IMT) in the radial and dorsal pedal arteries. Methods and results A total of 252 children (age 14.5 years S.D. ± 1.0 girls/boys 139/113) from two schools in Gothenburg, Sweden, participated in the study. The high-resolution (55 MHz) ultrasound measurements showed that boys had larger values than girls for the radial IT (0.057 ± 0.010 mm vs. 0.054 ± 0.008 mm, P = 0.007), MT (0.176 ± 0.033 vs. 0.153 ± 0.025, P = 0.031), IMT (0.232 ± 0.035 vs. 0.207 ± 0.026, P = 0.000), and for dorsal pedal artery MT (0.160 ± 0.039 vs. 0.149 ± 0.034, P = 0.022) and IMT (0.222 ± 0.041 vs. 0.209 ± 0.037, P = 0.016). Conclusion With this new very high-resolution ultrasound technique, we demonstrated in a large study population of children, that both intimal and medial arterial wall layers were thicker in boys than in girls. These findings may constitute an “early background” explaining why CHD starts sooner in men compared with women.

  • 4.
    Pettersson-Pablo, Paul
    et al.
    Örebro University, School of Medical Sciences. Department of Laboratory Medicine.
    Nilsson, T. K.
    Umeå University, Umeå- Sweden., Department of Medical Biosciences/Clinical Chemistry, Umeå, Sweden.
    Cao, Yang
    Örebro University, School of Medical Sciences. Örebro University Hospital. Clinical Epidemiology and Biostatistics.
    Breimer, L.
    Faculty of Medicine and Health, Örebro University, Örebro, Sweden; Department of Laboratory Medicine, Örebro, Sweden.
    Hurtig-Wennlöf, Anita
    Örebro University, School of Health Sciences.
    Cluster Analysis And Risk Score Calculation Of Surrogate Markers Of Vascular Health, And Their Association With Cardiometabolic Risk Factors In A Healthy Young Adults2019In: Atherosclerosis, ISSN 0021-9150, E-ISSN 1879-1484, Vol. 287, p. E191-E191Article in journal (Other academic)
  • 5. Sheikine, Yuri
    et al.
    Sirsjö, Allan
    Örebro University, School of Health and Medical Sciences.
    CXCL16/SR-PSOX: a friend or a foe in atherosclerosis?2008In: Atherosclerosis, ISSN 0021-9150, E-ISSN 1879-1484, Vol. 197, no 2, p. 487-495Article in journal (Refereed)
    Abstract [en]

    Chemokines, scavenger receptors and adhesion molecules have long been known as important players in the pathogenesis of atherosclerosis. A series of studies conducted in the past few years described CXCL16/SR-PSOX—a new molecule combining those three functions, and suggested that CXCL16/SR-PSOX can be a potential player in atherogenesis. Initial ex vivo studies showed that CXCL16/SR-PSOX is abundant in human and murine atherosclerotic lesions. Following in vitro studies suggested that as an adhesion molecule CXCL16/SR-PSOX might mediate T-cell adhesion to the endothelium, as a chemokine – drive T-cell migration, stimulate cell proliferation and elicit inflammatory phenotype in smooth muscle cells (SMC) and, finally, as a scavenger receptor – mediate uptake of atherogenic lipoproteins by macrophages and SMC. All these effects are known to be pro-atherogenic. Surprisingly, in vivo studies performed in murine models of atherosclerosis suggested that CXCL16/SR-PSOX is atheroprotective, while its receptor CXCR6 is harmful. In addition, studies investigating the association of circulating CXCL16/SR-PSOX plasma concentrations with the presence and extent of coronary artery disease (CAD) in humans are controversial suggesting both positive, negative and no association. To finally answer the question whether CXCL16/SR-PSOX can serve as a causative factor, biomarker or even a therapeutic target in atherosclerosis, we are currently in need of carefully designed animal and human studies investigating the effects of CXCL16/SR-PSOX and CXCR6 deficiency, inhibition and over-expression on the progression of atherosclerosis. Such complex approach will help us unravel the mystery of CXCL16/SR-PSOX in atherosclerosis and hopefully develop better ways of treating atherosclerosis by targeting this interesting molecule.

  • 6.
    Östman, Maja Eriksson
    et al.
    Department of Cardiology, , Faculty of Health and Medical Sciences, Örebro University, Örebro, Sweden.
    Calais, Fredrik
    Örebro University, School of Medical Sciences. Department of Cardiology, Faculty of Health and Medical Sciences, Örebro University, Örebro, Sweden.
    Rosenblad, Andreas
    Centre for Clinical Research, Västmanland County Hospital, Uppsala University, Västerås, Sweden.
    Fröbert, Ole
    Örebro University, School of Medical Sciences. Department of Cardiology, Faculty of Health and Medical Sciences, Örebro University, Örebro, Sweden.
    Leppert, Jerzy
    Centre for Clinical Research, Västmanland County Hospital, Uppsala University, Västerås, Sweden.
    Hedberg, Pär
    Centre for Clinical Research, Västmanland County Hospital, Uppsala University, Västerås, Sweden.
    Prognostic impact of subclinical or manifest extracoronary artery diseases after acute myocardial infarction2017In: Atherosclerosis, ISSN 0021-9150, E-ISSN 1879-1484, Vol. 263, p. 53-59Article in journal (Refereed)
    Abstract [en]

    Background and aims: In patients with coronary artery disease (CAD), clinically overt extracoronary artery diseases (ECADs), including claudication or previous strokes, are associated with poor outcomes. Subclinical ECADs detected by screening are common among such patients. We aimed to evaluate the prognostic impact of subclinical versus symptomatic ECADs in patients with acute myocardial infarction (AMI).

    Methods: In a prospective observational study, 654 consecutive patients diagnosed with AMI underwent ankle brachial index (ABI) measurements and ultrasonographic screening of the carotid arteries and abdominal aorta. Clinical ECADs were defined as prior strokes, claudication, or extracoronary artery intervention. Subclinical ECADs were defined as the absence of a clinical ECAD in combination with an ABI <= 0.9 or >1.4, carotid artery stenosis, or an abdominal aortic aneurysm.

    Results: At baseline, subclinical and clinical ECADs were prevalent in 21.6% and 14.4% of the patients, respectively. Patients with ECADs received evidence-based medication more often at admission but similar medications at discharge compared with patients without ECADs. During a median follow-up of 5.2 years, 166 patients experienced endpoints of hospitalization for AMI, heart failure, stroke, or cardiovascular death. With ECAD-free cases as reference and after adjustment for risk factors, a clinical ECAD (hazard ratio [HR] 2.10, 95% confidence interval [CI] 1.34-3.27, p = 0.001), but not a subclinical ECAD (HR 1.35, 95% CI 0.89-2.05, p = 0.164), was significantly associated with worse outcomes.

    Conclusions: Despite receiving similar evidence-based medication at discharge, patients with clinical ECAD, but not patients with a subclinical ECAD, had worse long-term prognosis than patients without an ECAD after AMI. (C) 2017 The Authors. Published by Elsevier Ireland Ltd.

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