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  • 1.
    Abedpour Dehkordi, Adel
    et al.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine.
    Nayeri, H.
    Naderi, G. A.
    Dinani, N. Jafari
    Boshtam, M.
    Interleukin-6 reduces paraoxonase-1 activity in a dose-dependent manner: evidence for a potential novel lipoprotein-based modulatory mechanism2016In: Atherosclerosis, ISSN 0021-9150, E-ISSN 1879-1484, Vol. 252, E113-E114 p.Article in journal (Other academic)
    Abstract [en]

    Objectives: The anti-oxidant/anti-inflammatory nature of HDL is mainly associated with paraoxonase-1 (PON1). Previous studies have revealed an inverse correlation between Interleukin-6 (IL-6) and PON1 expression. The current study investigates the effect of IL-6 on serum PON1 activity in vitro, given the potential structural capability of PON1 to host multiple ligands. Methods: PON1 activity was measured spectrophotometrically (234 nm) using paraoxon substrate in the presence of concentrations of IL-6 than control samples. A sequence alignment using the FASTA sequence was manually conducted to identify possible homologies between PON1 and the IL-6-binding protein. Statistical analysis was conducted using GraphPad Prism v5.0. Results: PON1 enzyme activity decreased by 15%, 26% (P<0.05) and 55% (P<0.001) in the presence of 4, 10 and 20 pg/ml of IL-6, respectively. in comparison with the controls. Student t. test was used as statistical method (p<0.05: statistically significant). There are potential homologies between PON1 active sites and know IL-6-binding residues. Conclusions: This study shows that IL-6 directly reduce the PON1 activity in a dose-dependent manner. This observation supports some studies indicating inverse correlation between PON1 and IL-6. However, as opposed to the gene-mediated approach, this study suggest that IL-6 may act directly through specific binding to PON1 (biochemical modulation). X ray crystallography can further scrutinize the present finding.

  • 2.
    Andersson, Jonas
    et al.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Medicine.
    Jansson, Jan-Håkan
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Medicine.
    Hellsten, Gideon
    Nilsson, Torbjörn K
    Hallmans, Göran
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research.
    Boman, Kurt
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Medicine.
    Effects of heavy endurance physical exercise on inflammatory markers in non-athletes2010In: Atherosclerosis, ISSN 0021-9150, E-ISSN 1879-1484, Vol. 209, no 2, 601-605 p.Article in journal (Refereed)
    Abstract [en]

    OBJECTIVES: Physical activity has beneficial effects on cardiovascular disease but the mechanisms are still somewhat unclear. One possible pathway may be through the anti-inflammatory effects attributed to regular physical activity. Our primary aim was to study the effects of endurance physical exercise on C-reactive protein (CRP), Interleukin-6 (IL-6), Tumor Necrosis Factor-alpha (TNFalpha) during the acute and recovery phases. Secondarily, we studied the impact of diet on these inflammatory markers.

    METHODS: Twenty men, aged 18-55 years, participated in a 14 days cross-country skiing tour. They traveled 12-30km per day corresponding to about 10h of heavy physical activity. The participants were randomized to a diet with either 30 or 40% of energy derived from fat. Inflammatory variables were analysed at week 0, after 1 and 2 weeks and during the recovery phase at week 6 and 8.

    RESULTS: CRP and TNFalpha increased significantly during the two weeks of exercise (1.4-5.0mg/l, p=0.00 and 6.8-8.4pg/ml, p=0.00). CRP levels were significantly lower during recovery (median 0.7mg/l) compared to baseline (median 1.4mg/l) and did not correlate to metabolic variables. There were no significant changes in IL-6 levels during the study period. For dietary groups significant CRP changes were observed only in the high fat group during recovery.

    CONCLUSIONS: CRP and TNFalpha increased significantly but reacted differently during heavy physical activity while there seemed to be no significant changes in IL-6. No significant differences regarding inflammatory variables were found between the dietary groups.

  • 3. Antoniewicz, Lukasz
    et al.
    Bosson, Jenny A.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Pulmonary Medicine.
    Kuhl, Jeanette
    Abdel-Halim, Samy M.
    Kiessling, Anna
    Mobarrez, Fariborz
    Lundback, Magnus
    Electronic cigarettes increase endothelial progenitor cells in the blood of healthy volunteers2016In: Atherosclerosis, ISSN 0021-9150, E-ISSN 1879-1484, Vol. 255, 179-185 p.Article in journal (Refereed)
    Abstract [en]

    Background and aims: The use of electronic cigarettes is increasing dramatically on a global scale and its effects on human health remain uncertain. In the present study, we measured endothelial progenitor cells (EPCs) and microvesicles (MVs) in healthy young volunteers following short-term exposure to inhalation of e-cigarette vapor (ECV) to determine vascular changes.

    Methods: Sixteen healthy seldom smokers were randomized into two groups either exposed or not exposed to 10 puffs of ECV for 10 min, in a crossover design. Blood samples were obtained at baseline and 1, 4 and 24 h following exposure. EPCs (CD34 + CD309) and MVs were analyzed by flow cytometry. MVs were phenotyped according to origin (platelet (CD41), endothelial (CD144), leukocytes (CD45), monocytes (CD14)) and nuclear content (SYTO 13 dye). In addition, expression of inflammation markers such P-selectin (CD62P), E-selectin (CD62E), CD40-ligand (CD154) and HMGB1 was investigated. Fractional exhaled nitric oxide (FeNO) was also measured at baseline and after 24 h.

    Results: EPC levels in blood were significantly increased 1 h following exposure to ECV and returned to baseline values after 24 h. Only E-selectin positive MVs (endothelial origin) were slightly elevated (p < 0.038). FeNO was unaffected by exposure to ECV. Conclusions: In healthy volunteers, ten puffs of e-cigarette vapor inhalation caused an increase in EPCs. This increase was of the same magnitude as following smoking of one traditional cigarette, as we previously demonstrated. Taken together, these results may represent signs of possible vascular changes after short e-cigarette inhalation. Further studies analyzing potential cardiovascular health effects are critical as the e-cigarette market continues to burgeon.

  • 4.
    Bengrid, Tarek
    et al.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine.
    Zhao, Y.
    Ultrasound Department, Beijing Anzhen Hospital, Beijing, China.
    Henein, Michael
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Medicine.
    Disturbed right ventricular function response to dobutamine stress in Syndrome X patients: a potential effect of coronary calcification2014In: Atherosclerosis, ISSN 0021-9150, E-ISSN 1879-1484, Vol. 235, no 2, E229-E229 p.Article in journal (Other academic)
  • 5.
    Bengrid, Tarek
    et al.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Cardiology.
    Zhao, Y.
    Ultrasound Department, Beijing Anzhen Hospital, Beijing, China.
    Henein, Michael
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Cardiology.
    Effect of coronary calcium score on subendocardial function in patients with Syndrome X: a tissue doppler dobutamine stress echocardiography study2014In: Atherosclerosis, ISSN 0021-9150, E-ISSN 1879-1484, Vol. 235, no 2, E68-E68 p.Article in journal (Other academic)
  • 6.
    Bergström, Erik
    et al.
    Umeå University, Faculty of Medicine, Department of Clinical Sciences, Paediatrics.
    Hernell, Olle
    Umeå University, Faculty of Medicine, Department of Clinical Sciences, Paediatrics.
    Persson, L A
    Vessby, B
    Serum lipid values in adolescents are related to family history, infant feeding, and physical growth.1995In: Atherosclerosis, ISSN 0021-9150, E-ISSN 1879-1484, Vol. 117, no 1, 1-13 p.Article in journal (Refereed)
    Abstract [en]

    Total serum cholesterol (TC), high density lipoprotein cholesterol (HDL-C), low density lipoprotein cholesterol (LDL-C), triglycerides (TG), apolipoprotein A-I (apo A-I), apolipoprotein B (apo B), and lipoprotein (a) (Lp(a)) were analysed in 879 14- and 17-year-old healthy adolescents (477 boys and 402 girls), and related to family history of cardiovascular disease, early feeding, weight and length at birth, and physical growth during infancy and childhood. Mean TC was significantly higher in girls than in boys (4.4 and 4.2 mmol/l, respectively, both age-groups together). High TC values ( > 5.2 mmol/l) were more prevalent in girls than in boys: 14% and 17% compared to 6% and 12% in 14- and 17-year-old girls and boys, respectively. Mean TC and LDL-C values were lower during mid-puberty in both boys and girls while, in boys but not in girls, mean HDL-C values decreased and TG values increased successively with increasing pubertal stage. Girls who were taking oral contraceptives had higher mean values of TC (4.91/4.39 mmol/l), TG (1.32/0.83 mmol/l), and apo B (0.89/0.73 g/l). Boys with a family history of early deaths ( < 55 years) from myocardial infarction and girls with a family history of cerebral haemorrhage/thrombosis in fathers had higher mean values of TC (4.55/4.17 and 5.03/4.40 mmol/l, for boys and girls, respectively), LDL-C (2.84/2.47 and 3.08/2.56 mmol/l), and apo B (0.73/0.70 and 0.86/0.73 g/l). Adolescents with short duration of breast feeding ( < 6 months), or early introduction of infant formula, had higher mean values of TC (4.29/4.14 mmol/l) and apo B (0.72/0.68 g/l). There were no significant correlations between serum lipid values and body weight or length at birth, but adolescents with high LDL-C (upper quartile) seemed to have lower attained heights during infancy and childhood. In conclusion, this study shows that serum lipids in adolescence are primarily related to age and sex but also to early determinants like family history of cardiovascular diseases, infant feeding, and early physical growth.

  • 7. Björck, M
    et al.
    Ravn, H
    Nilsson, Torbjörn K
    Department of Clinical Chemistry, Örebro University Hospital.
    Wanhainen, A
    Nilsson, P M
    Blood cell telomere length among patients with an isolated popliteal artery aneurysm and those with multiple aneurysm disease2011In: Atherosclerosis, ISSN 0021-9150, E-ISSN 1879-1484, Vol. 219, no 2, 946-950 p.Article in journal (Refereed)
    Abstract [en]

    OBJECTIVES: Short relative telomere length (RTL) is associated with vascular ageing, inflammation and cardiovascular risk factors. Previous studies have reported an association between abdominal aortic aneurysm and short RTL. The presence of atherosclerosis among patients with aneurysm disease may, however, be a confounder. The aim was to explore the associations between short RTL and aneurysm disease, by comparing patients with isolated popliteal artery aneurysms with those having multiple aneurysms.

    DESIGN AND PATIENTS: DNA was retrieved from 183 patients with popliteal artery aneurysm (PAA). They were all examined with ultrasound at the time of blood-sampling, and had a total of 423 aneurysms (range 1-7, mean 2.3/patient).

    METHODS: TL was measured with Real-Time PCR, RTL was calculated by comparing with three reference populations.

    RESULTS: Patients with bilateral PAAs had a mean RTL of 0.985 vs. 1.038 with unilateral PAAs (P = 0.326). Patients with abdominal aortic aneurysm had RTL 1.035, vs. 0.999 without (P = 0.513). No difference was seen with or without femoral or iliac aneurysms. Fifty-six patients with isolated PAA at surgery and at re-examination had RTL 0.974, vs. 1.033 who had >1 aneurysm (P = 0.308). RTL was not associated with the number of aneurysms at re-examination (P = 0.727, one-way ANOVA). There was a trend towards shorter RTL among active smokers (0.93 vs. 1.04, P = 0.066).

    CONCLUSIONS: No association between short RTL and multiple aneurysm disease was found. The previously reported association between AAA and short RTL may be secondary to cardiovascular risk factors, rather than by aneurysm disease.

  • 8.
    Eriksson, Jan. W.
    et al.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Medicine.
    Burén, Jonas
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Medicine.
    Svensson, Maria
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Medicine.
    Olivecrona, Thomas
    Umeå University, Faculty of Medicine, Department of Medical Biosciences, Physiological chemistry.
    Olivecrona, Gunilla
    Umeå University, Faculty of Medicine, Department of Medical Biosciences, Physiological chemistry.
    Postprandial regulation of blood lipids and adipose tissue lipoprotein lipase in type 2 diabetes patients and healthy control subjects2003In: Atherosclerosis, ISSN 0021-9150, E-ISSN 1879-1484, Vol. 166, no 2, 359-367 p.Article in journal (Refereed)
    Abstract [en]

    Background/aim: In type 2 diabetes and other insulin-resistant conditions, postprandial hypertriglyceridaemia is an important metabolic perturbation. To further elucidate alterations in the clearance of triglyceride-rich lipoproteins in type 2 diabetes we focused on the nutritional regulation of adipose tissue lipoprotein lipase (LPL).

    Subjects and methods: Eight subjects with type 2 diabetes and eight age-, sex- and body mass index (BMI)-matched control subjects underwent subcutaneous abdominal adipose tissue biopsies in the fasting state and 3.5 h following a standardized lipid-enriched meal. LPL activity and mass were measured in adipose tissue and also in plasma after an intravenous injection of heparin.

    Results: Postprandial, but not fasting, triglycerides were significantly higher in the diabetic subjects than in the control subjects (3.0±0.4 vs 2.0±0.2 mmol/l, P=0.028). Adipose tissue LPL activity was increased following the meal test by ∼35–55% (P=0.021 and 0.004, respectively). There was no significant difference between the groups in this respect. The specific enzyme activity of LPL was not altered in the postprandial state. Fasting and postprandial adipose tissue LPL activity as well as post-heparin plasma LPL activity tended to be lower among the diabetes patients (NS). There was a significant and independent inverse association between insulin resistance (homeostasis model assessment insulin resistance (HOMA-IR) index) vs post-heparin plasma LPL activity and postprandial triglyceride levels, respectively. Adipose tissue LPL activity was related to insulin action in vitro on adipocyte glucose transport, but not to HOMA-IR.

    Conclusion: Following food intake adipose tissue LPL activity is enhanced to a similar degree in patients with type 2 diabetes and in healthy control subjects matched for BMI, age and gender. If LPL dysregulation is involved in the postprandial hypertriglyceridaemia found in type 2 diabetes, it should occur in tissues other than subcutaneous fat.

  • 9.
    Gistera, A.
    et al.
    Medicine Solna, Karolinska Institutet, Stockholm, Sweden.
    Robertson, A. K.
    Medicine Solna, Karolinska Institutet, Stockholm, Sweden.
    Andersson, J.
    Medicine Solna, Karolinska Institutet, Stockholm, Sweden.
    Ketelhuth, D. F. J.
    Medicine Solna, Karolinska Institutet, Stockholm, Sweden.
    Oychinnikova, O.
    Medicine Solna, Karolinska Institutet, Stockholm, Sweden.
    Nilsson, Stefan K
    Umeå University, Faculty of Medicine, Department of Medical Biosciences, Physiological chemistry.
    Lundberg, A. M.
    Medicine Solna, Karolinska Institutet, Stockholm, Sweden.
    Li, M. O.
    Department of Immunobiology, Yale University School of Medicine, New Haven CT, USA.
    Flavell, R. A.
    Department of Immunobiology, Yale University School of Medicine, New Haven CT, USA.
    Hansson, G. K.
    Medicine Solna, Karolinska Institutet, Stockholm, Sweden.
    Transforming growth factor-beta signaling in t cells promotes stabilization of atherosclerotic plaques through an interleukin-17 dependent pathway2014In: Atherosclerosis, ISSN 0021-9150, E-ISSN 1879-1484, Vol. 235, no 2, E88-E89 p.Article in journal (Other academic)
  • 10.
    Gonzalez, Manuel
    et al.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Cardiology.
    Lind, Lars
    Uppsala Univ, Dept Med, Uppsala, Sweden.
    Söderberg, Stefan
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Cardiology.
    Leptin and endothelial function in the elderly: the Prospective Investigation of the Vasculature in Uppsala Seniors (PIVUS) study2013In: Atherosclerosis, ISSN 0021-9150, E-ISSN 1879-1484, Vol. 228, no 2, 485-490 p.Article in journal (Refereed)
    Abstract [en]

    Background: Leptin levels are elevated in obese humans. Several studies have shown an association between hyperleptinemia and development of atherosclerosis and cardiovascular disease (CVD), but the relationship between leptin and vascular function remains unclear.

    Aim: To evaluate associations between circulating plasma leptin and measures of vascular function in a large sample of elderly individuals from the community.

    Methods: This cross-sectional study included 1016 subjects aged 70 (50% women) from the Prospective Investigation of the Vasculature in Uppsala Seniors (PIVUS). The invasive technique forearm plethysmography with intra-arterial infusions of acetylcholine and sodium nitroprusside was used for estimation of endothelial dependent vasodilatation (EDV) and endothelial independent vasodilatation (EIDV), respectively, in resistance arteries, and the non-invasive technique ultrasound assessed flow mediated vasodilation (FMD) in conduit arteries. The aortic augmentation index (AoAI), a surrogate measure of arterial stiffness, was evaluated by pulse wave analysis. Associations of vascular function, arterial stiffness and blood pressure with leptin were explored.

    Results: In sex-adjusted models, high levels of leptin were inversely associated with EDV and EIDV. These associations remained after stratification for sex, traditional risk factors of CVD and insulin resistance, but were attenuated after taking a measure of obesity (body mass index) into account. In addition, leptin associated with arterial stiffness and systolic and diastolic blood pressure.

    Conclusion: Hyperleptinemia associated inversely with vasodilatation in resistance arteries. Furthermore, hyperleptinemia associated with arterial stiffness and hypertension. These associations were attenuated after adjusting for body mass index suggesting that leptin may be the mediator between obesity and impaired vascular function. (C) 2013 Elsevier Ireland Ltd. All rights reserved.

  • 11. Hansen, T
    et al.
    Ahlström, H
    Söderberg, Stefan
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Medicine.
    Hulthe, J
    Wikström, J
    Lind, L
    Johansson, L
    Visceral adipose tissue, adiponectin levels and insulin resistance are related to atherosclerosis as assessed by whole-body magnetic resonance angiography in an elderly population2009In: Atherosclerosis, ISSN 0021-9150, E-ISSN 1879-1484, Vol. 205, no 1, 163-167 p.Article in journal (Refereed)
    Abstract [en]

    OBJECTIVE: The principal aim of this study was to determine whether the amount of visceral adipose tissue (VAT) is more related than subcutaneous adipose tissue (SAT) to atherosclerosis assessed by whole-body MRA (WBMRA). A further objective was to investigate whether traditional risk factors, inflammation, or adipokines could explain the hypothesized relationship between VAT and atherosclerosis. METHODS: Men and women aged 70 were recruited from the general population into the Prospective Investigation of The Vasculature in Uppsala Seniors (PIVUS) and 306 of them underwent WBMRA in a clinical 1.5-T scanner. The arterial tree was assessed for degree of stenosis or occlusion and a total atherosclerotic score (TAS) was established. Information on risk factors and BMI and on SAT and VAT, segmented on an axial MR scan was collected. Adiponectin, leptin, and high sensitive C-reactive protein (hsCRP) were measured in serum. HOMA index was used as a marker of insulin resistance. RESULTS: VAT was related to TAS independently of gender, total obesity (BMI), amount of SAT, hsCRP and also to the traditional risk factors included in the Framingham risk score (FRS) in an elderly population. Adiponectin or the HOMA insulin resistance, but not leptin or VAT, together with FRS was significantly related to TAS in a multiple censored regression model. CONCLUSION: Adiponectin attenuated the relationship between VAT and TAS, suggesting that adiponectin and insulin resistance is an important link between visceral adiposity and atherosclerosis.

  • 12.
    Henein, Michael
    et al.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Cardiology.
    Bengrid, Tarek
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Cardiology.
    Nicoll, Rachel
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Cardiology.
    Zhao, Y.
    Ultrasound Department, Capital Medical University, Beijing, China.
    Johansson, Bengt
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Cardiology.
    Schmermund, A.
    Medicine, Bethanien Hospital, Frankfurt, Germany.
    Extensive coronary calcification compromises myocardial perfusion in the absence of high grade stenosis2014In: Atherosclerosis, ISSN 0021-9150, E-ISSN 1879-1484, Vol. 235, no 2, E68-E68 p.Article in journal (Other academic)
  • 13.
    Henein, Michael
    et al.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Cardiology.
    Hällgren, Peter
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Cardiology.
    Holmgren, Anders
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Cardiology.
    Sörensen, Karen
    Umeå University, Faculty of Medicine, Department of Radiation Sciences, Diagnostic Radiology.
    Ibrahimi, Pranvera
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Cardiology.
    Kofoed, Klaus Fuglsang
    Larsen, Linnea Hornbech
    Hassager, Christian
    Aortic root, not valve, calcification correlates with coronary artery calcification in patients with severe aortic stenosis: a two-center study2015In: Atherosclerosis, ISSN 0021-9150, E-ISSN 1879-1484, Vol. 243, no 2, 631-637 p.Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: The underlying pathology in aortic stenosis (AS) and coronary artery stenosis (CAS) is similar including atherosclerosis and calcification. We hypothesize that coronary artery calcification (CAC) is likely to correlate with aortic root calcification (ARC) rather than with aortic valve calcification (AVC), due to tissue similarity between the two types of vessel rather than with the valve leaflet tissue.

    MATERIAL AND METHODS: We studied 212 consecutive patients (age 72.5 ± 7.9 years, 91 females) with AS requiring aortic valve replacement (AVR) in two Heart Centers, who underwent multidetector cardiac CT preoperatively. CAC, AVC and ARC were quantified using Agatston scoring. Correlations were tested by Spearman's test and Mann-Whitney U-test was used for comparing different subgroups; bicuspid (BAV) vs tricuspid (TAV) aortic valve.

    RESULTS: CAC was present in 92%, AVC in 100% and ARC in 82% of patients. CAC correlated with ARC (rho = 0.51, p < 0.001) but not with AVC. The number of calcified coronary arteries correlated with ARC (rho = 0.45, p < 0.001) but not with AVC. 29/152 patients had echocardiographic evidence of BAV and 123 TAV, who were older (p < 0.001) but CAC was associated with TAV even after adjusting for age (p = 0.01). AVC score was associated with BAV after adjusting for age (p = 0.03) but ARC was not. Of the total cohort, 82 patients (39%) had significant coronary stenosis (>50%), but these were not different in the pattern of calcification from those without CAS. CAC was consistently higher in patients with risk factors for atherosclerosis compared to those without.

    CONCLUSION: The observed relationship between coronary and aortic root calcification suggests a diffuse arterial disease. The lack of relationship between coronary and aortic valve calcification suggests a different pathology.

  • 14.
    Hultin, M
    et al.
    Umeå University, Faculty of Medicine, Department of Medical Biosciences, Physiological chemistry.
    Olivecrona, T
    Umeå University, Faculty of Medicine, Department of Medical Biosciences, Physiological chemistry.
    Conversion of chylomicrons into remnants.1998In: Atherosclerosis, ISSN 0021-9150, E-ISSN 1879-1484, Vol. 141 Suppl 1, S25-9 p.Article in journal (Refereed)
    Abstract [en]

    The turnover of chylomicrons in the blood is the sum of several processes. The native chylomicron is synthesized in the intestine out of available substrates. When the chylomicron enters the circulation exchanges of apolipoproteins with other lipoproteins, it also binds to the vascular endothelium where the chylomicron is lipolyzed by lipoprotein lipase. After a short period in the circulation the chylomicron/chylomicron remnant appears to be available for receptor mediated uptake. In this paper several of the processes involved in generation and clearance of chylomicron remnants are discussed.

  • 15.
    Ibrahimi, Pranvera
    et al.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Cardiology.
    Jashari, Fisnik
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Cardiology.
    Johansson, Elias
    Umeå University, Faculty of Medicine, Department of Pharmacology and Clinical Neuroscience, Clinical Neuroscience. Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Medicine.
    Grönlund, Christer
    Umeå University, Faculty of Medicine, Department of Radiation Sciences, Radiation Physics.
    Bajraktari, Gani
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Cardiology.
    Wester, Per
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Medicine.
    Henein, Michael Y
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Cardiology.
    Vulnerable plaques in the contralateral carotid arteries in symptomatic patients: a detailed ultrasound analysis2014In: Atherosclerosis, ISSN 0021-9150, E-ISSN 1879-1484, Vol. 235, no 2, 526-531 p.Article in journal (Refereed)
    Abstract [en]

    BACKGROUND AND AIM: Carotid plaques may represent a generalized atherosclerotic syndrome or a localized disease. The aim of this study was to assess the morphological and textural features of carotid plaques located contralateral to the symptomatic side and compare them with the symptomatic side and with plaques from asymptomatic patients. METHODS: We studied 66 arteries in 39 patients (mean age 70 ± 7 year, 33% females). Arterial plaques were classified as either symptomatic (n = 30), contralateral to symptomatic (n = 25) or asymptomatic (n = 11). We compared several plaque features between these groups including the mean values of the grey scale median (GSM), entropy, juxtaluminal black area (JBA) without visible echogenic cap, GSM of the JBA and surface irregularity. RESULTS: The plaques contralateral to symptomatic arteries had similar morphological and textural features to those in the symptomatic arteries. In contrast, they had more vulnerable morphological and textural features than those in asymptomatic arteries: less smooth plaques (12% vs. 55%) and instead more often mildly irregular (60% vs 36%) or markedly irregular (28% vs. 9%; p = 0.03), lower GSM (26.2 ± 8 vs. 49.4 ± 14, p < 0.001) and lower GSM of the JBA (5.0 ± 3.6 vs. 11.4 ± 2.1, p = 0.008). The frequency of entropy and plaque calcification was similar in all groups. CONCLUSION: Symptomatic patients with carotid artery disease seem to have similar morphological and textural features of vulnerability in the symptomatic and the contralateral carotid arteries, which are profound compared with asymptomatic carotid arteries. These findings support the concept of generalized carotid atherosclerotic pathology rather than incidental unilateral disease, and also emphasize a need for aggressive measures for plaque stabilization, particularly in symptomatic patients.

  • 16.
    Ibrahimi, Pranvera
    et al.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Cardiology.
    Jashari, Fisnik
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Cardiology.
    Johansson, Elias
    Umeå University, Faculty of Medicine, Department of Pharmacology and Clinical Neuroscience, Clinical Neuroscience.
    Grönlund, Christer
    Umeå University, Faculty of Medicine, Department of Radiation Sciences.
    Wester, Per
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Medicine.
    Henein, Michael Y.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Cardiology.
    Common carotid intima-media measurements determine distal disease structure and vulnerability in asymptomatic patients2015In: Atherosclerosis, ISSN 0021-9150, E-ISSN 1879-1484, Vol. 241, no 1, E164-E164 p.Article in journal (Other academic)
  • 17.
    Ibrahimi, Pranvera
    et al.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Cardiology.
    Jashari, Fisnik
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Cardiology.
    Nicoll, Rachel
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Cardiology.
    Bajraktari, Gani
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Cardiology.
    Wester, Per
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Medicine.
    Henein, Michael Y
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Cardiology.
    Coronary and carotid atherosclerosis: how useful is the imaging?2013In: Atherosclerosis, ISSN 0021-9150, E-ISSN 1879-1484, Vol. 231, no 2, 323-333 p.Article in journal (Refereed)
    Abstract [en]

    The recent advancement of imaging modalities has made possible visualization of atherosclerosis disease in all phases of its development. Markers of subclinical atherosclerosis or even the most advanced plaque features are acquired by invasive (IVUS, OCT) and non-invasive imaging modalities (US, MRI, CTA). Determining plaques prone to rupture (vulnerable plaques) might help to identify patients at risk for myocardial infarction or stroke. The most accepted features of plaque vulnerability include: thin cap fibroatheroma, large lipid core, intimal spotty calcification, positive remodeling and intraplaque neovascularizations. Today, research is focusing on finding imaging techniques that are less invasive, less radiation and can detect most of the vulnerable plaque features. While, carotid atherosclerosis can be visualized using noninvasive imaging, such as US, MRI and CT, imaging plaque feature in coronary arteries needs invasive imaging modalities. However, atherosclerosis is a systemic disease with plaque development simultaneously in different arteries and data acquisition in carotid arteries can add useful information for prediction of coronary events.

  • 18.
    Jashari, Fisnik
    et al.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Cardiology.
    Ibrahimi, Pranvera
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Cardiology.
    Johansson, Elias
    Umeå University, Faculty of Medicine, Department of Pharmacology and Clinical Neuroscience.
    Grönlund, Christer
    Umeå University, Faculty of Medicine, Department of Radiation Sciences.
    Wester, Per
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Medicine.
    Henein, Michael Y.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Cardiology.
    Carotid im-gsm is related to multisite atherosclerosis disease2015In: Atherosclerosis, ISSN 0021-9150, E-ISSN 1879-1484, Vol. 241, no 1, E164-E164 p.Article in journal (Other academic)
  • 19.
    Jashari, Fisnik
    et al.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Cardiology.
    Ibrahimi, Pranvera
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Cardiology.
    Nicoll, Rachel
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Cardiology.
    Bajraktari, Gani
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Cardiology.
    Wester, Per
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Medicine.
    Henein, Michael Y.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Cardiology.
    Coronary and carotid atherosclerosis: similarities and differences2013In: Atherosclerosis, ISSN 0021-9150, E-ISSN 1879-1484, Vol. 227, no 2, 193-200 p.Article in journal (Refereed)
    Abstract [en]

    Although a relationship is commonly accepted between coronary and carotid arterial disease, suggesting that atherosclerosis is a systemic condition, the extent of this association and correspondence has not been fully elucidated. This review discusses recent research in this field and highlights areas for future study. The prevalence of severe carotid stenosis increases with prevalence of coronary stenosis, with the latter being found in a significant number of stroke patients, while those with carotid stenosis may be at higher risk of myocardial infarction than stroke. There also appear to be common risk factors (age, diabetes, hypertension, smoking and dyslipidemia), although the effects in both vascular systems may not be identical. Furthermore, while the degree of stenosis in the coronary artery has little ability to predict acute coronary syndrome, which is caused by local thrombosis from a ruptured or eroded plaque, severe carotid stenosis causing hypoperfusion is highly predictive of stroke, although this effect may be time-limited. This apparent difference in event mechanism in the two arteries is interesting as is the difference in the rate of development of collaterals. Overall, the evidence shows that a clear relationship exists between disease in the coronary and carotid arteries, since conventional risk factors and the extent of stenosis and/or previous events emanating from one artery have a strong bearing on the prevalence of events in the other artery. Nevertheless, the exact correspondence between the two arteries is unclear, with sometimes contradictory study results. More research is needed to identify the full extent of risk factors for severe stenosis and cardio- or cerebral vascular events, among which, inflammatory biomarkers such as hs-CRP and prior vascular events are likely to play a key role.

  • 20. Labayen, Idoia
    et al.
    Olsson, Lovisa A
    Ortega, Francisco B
    Nilsson, Torbjörn K
    Department of Clinical Chemistry, Örebro University Hospital.
    Sjöström, Michael
    Lucia, Alejandro
    Ruiz, Jonatan R
    Cardiorespiratory fitness modifies the association between the UCP3-55C>T (rs1800849) polymorphism and plasma homocysteine in Swedish youth2010In: Atherosclerosis, ISSN 0021-9150, E-ISSN 1879-1484, Vol. 210, no 1, 183-187 p.Article in journal (Refereed)
    Abstract [en]

    OBJECTIVE: Whether the polymorphisms in the UCP3 gene have an influence on plasma homocysteine levels during youth is not known, and to elucidate the putative modifying role of fitness is also of clinical interest. We analysed the association between polymorphisms in the UCP3 gene and plasma homocysteine in youth and to examine whether fitness modifies this association.

    METHODS: The study population comprised 267 Swedish children (8-10 years) and 305 adolescents (14-16 years). Fasting total plasma homocysteine was the outcome variable. We genotyped five UCP3 polymorphisms (rs1800849, rs1800006, rs2075577, rs647126, and rs591758) and one MTHFR 677C>T (rs1801133) polymorphism. Cardiorespiratory fitness was measured with a maximal ergometer bike test.

    RESULTS: Youth homozygous or heterozygous for the T allele of the rs1800849 polymorphism had significantly higher levels of homocysteine than those carrying the CC genotype (8.56+/-4.72 micromol/L vs. 7.72+/-2.73 micromol/L, respectively, P=0.011) after adjusting for gender, age, pubertal status, folate and vitamin B(12) intake and MTHFR 677C>T polymorphism, whereas no association was observed for the other analysed polymorphisms. There was a significant interaction effect of fitnessxrs1800849 polymorphism (P=0.042). The effect of the rs1800849 polymorphism on homocysteine levels persisted in youth with low fitness, whereas it was abolished in those with moderate or high cardiorespiratory fitness (P>0.1).

    CONCLUSIONS: Cardiorespiratory fitness modifies the association between the rs1800849 polymorphism and homocysteine so that the negative effect of the T allele does not persist in youth with moderate to high levels of fitness.

  • 21. Lindskog Jonsson, Annika
    et al.
    Fåk Hållenius, Frida
    Akrami, Rozita
    Johansson, Elias
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine. Umeå University, Faculty of Medicine, Department of Pharmacology and Clinical Neuroscience.
    Wester, Per
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine. Karolinska Institute Danderyds Hospital, Department of Clinical Sciences, Stockholm, Sweden.
    Arnerlöv, Conny
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences.
    Bäckhed, Fredrik
    Bergström, Göran
    Bacterial profile in human atherosclerotic plaques2017In: Atherosclerosis, ISSN 0021-9150, E-ISSN 1879-1484, Vol. 263, 177-183 p.Article in journal (Refereed)
    Abstract [en]

    Background and aims: Several studies have confirmed the presence of bacterial DNA in atherosclerotic plaques, but its contribution to plaque stability and vulnerability is unclear. In this study, we investigated whether the bacterial plaque-profile differed between patients that were asymptomatic or symptomatic and whether there were local differences in the microbial composition within the plaque. Methods: Plaques were removed by endarterectomy from asymptomatic and symptomatic patients and divided into three different regions known to show different histological vulnerability: A, upstream of the maximum stenosis; B, site for maximum stenosis; C, downstream of the maximum stenosis. Bacterial DNA composition in the plaques was determined by performing 454 pyrosequencing of the 16S rRNA genes, and total bacterial load was determined by qPCR. Results: We confirmed the presence of bacterial DNA in the atherosclerotic plaque by qPCR analysis of the 16S rRNA gene but observed no difference (n.s.) in the amount between either asymptomatic and symptomatic patients or different plaque regions A, B and C. Unweighted UniFrac distance metric analysis revealed no distinct clustering of samples by patient group or plaque region. Operational taxonomic units (OTUs) from 5 different phyla were identified, with the majority of the OTUs belonging to Proteobacteria (48.3%) and Actinobacteria (40.2%). There was no difference between asymptomatic and symptomatic patients, or plaque regions, when analyzing the origin of DNA at phylum, family or OTU level (n.s.). Conclusions: There were no major differences in bacterial DNA amount or microbial composition between plaques from asymptomatic and symptomatic patients or between different plaque regions, suggesting that other factors are more important in determining plaque vulnerability.

  • 22.
    Neuger, Lucyna
    et al.
    Umeå University, Faculty of Medicine, Medical Biosciences.
    Ruge, Toralph
    Umeå University, Faculty of Medicine, Medical Biosciences.
    Makoveichuk, Elena
    Umeå University, Faculty of Medicine, Medical Biosciences.
    Vlodavsky, Israel
    Olivecrona, Gunilla
    Umeå University, Faculty of Medicine, Medical Biosciences.
    Effects of the heparin-mimicking compound RG-13577 on lipoprotein lipase and on lipase mediated binding of LDL to cells2001In: Atherosclerosis, ISSN 0021-9150, Vol. 157, no 1, 13-21 p.Article in journal (Refereed)
    Abstract [en]

    Lipoprotein lipase (LPL) has high affinity for heparin and heparin-like compounds. In vivo the enzyme is attached to heparan sulfate proteoglycans on the endothelium of capillaries and larger blood vessels. The enzyme is released from these sites after intravenous injection of heparin. One has here investigated the effects of RG-13577 on LPL, both after intravenous injection to rats and under cell culture conditions. RG-13577 is a heparin-mimicking compound known to prevent angiogenesis by interference with binding of growth factors to cells. It has therefore been considered for use in cancer therapy as well as for prevention of atherosclerosis and restenosis. It was found that intravenously injected RG-13577 released both LPL and hepatic lipase (HL) to the blood. Binding of LPL in extrahepatic tissues was prevented and clearance of radiolabeled LPL from the circulation was delayed. Furthermore, RG-13577 released LPL from extracellular matrix (ECM) produced by endothelial cells and from THP-1 monocyte-derived macrophages. Lipase-mediated binding and uptake of human LDL in these cells was also prevented by RG-13577. Thus, in the test systems RG-13577 had the same effects as heparin, but on a molar basis RG-13577 was in all cases less effective.

  • 23.
    Nicoll, Rachel
    et al.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Cardiology.
    Wiklund, Urban
    Umeå University, Faculty of Medicine, Department of Radiation Sciences, Radiation Physics.
    Schmermund, A.
    Cardiology, Bethanian Hospital, Frankfurt, Germany.
    Diederichsen, A.
    Cardiology, Odense University Hospital, Odense, Denmark.
    Mickley, H.
    Cardiology, Odense University Hospital, Odense, Denmark.
    Overhus, K.
    Cardiology, Odense University Hospital, Odense, Denmark.
    Zamorano, P.
    Cardiology, University Hospital Ramón y Cajal Carretera, Madrid, Spain.
    Gueret, P.
    Cardiology, Hôpital Henri Mondor Creteil, France.
    Maffi, E.
    Cardiology, Giovanni XXIII Hospital, Italy.
    Cademartiri, F.
    Cardiology, Giovanni XXIII Hospital, Italy.
    Henein, Michael
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Cardiology.
    Euro-ccad: Differing conventional atherosclerosis risk factors for coronary calcification depending on degree of luminal stenosis2014In: Atherosclerosis, ISSN 0021-9150, E-ISSN 1879-1484, Vol. 235, no 2, E81-E82 p.Article in journal (Other academic)
  • 24.
    Nicoll, Rachel
    et al.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Cardiology.
    Wiklund, Urban
    Umeå University, Faculty of Medicine, Department of Radiation Sciences.
    Zhao, Ying
    Diederichsen, A.
    Mickley, H.
    Ovrehus, K.
    Zamorano, J.
    Gueret, P.
    Schmermund, A.
    Maffei, E.
    Cademartiri, F.
    Budoff, M.
    Henein, Michael
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Cardiology.
    Gender and age effects on risk factor-based prediction of coronary artery calcium in symptomatic patients: a Euro-CCAD study2016In: Atherosclerosis, ISSN 0021-9150, E-ISSN 1879-1484, Vol. 252, 32-39 p.Article in journal (Refereed)
    Abstract [en]

    Background and aims: The influence of gender and age on risk factor prediction of coronary artery calcification (CAC) presence in symptomatic patients is unclear.

    Methods: From the European Calcific Coronary Artery Disease (EURO-CCAD) cohort, we retrospectively investigated 6309 symptomatic patients, 62% male, from Denmark, France, Germany, Italy, Spain and USA. All had risk factor assessment and CT scanning for CAC scoring.

     Results: The prevalence of CAC among females was lower than among males in all age groups. Using multivariate logistic regression, age, dyslipidaemia, hypertension, diabetes and smoking were independently predictive of CAC presence in both genders. In addition to a progressive increase in CAC with age, the most important predictors of CAC presence were dyslipidaemia and diabetes (β = 0.64 and 0.63 respectively) in males and diabetes (β = 1.08) followed by smoking (β = 0.68) in females; these same risk factors were also important in predicting increasing CAC scores. There was no difference in the predictive ability of diabetes, hypertension and dyslipidaemia in either gender for CAC presence in patients aged <50 and 50-70 years. However, in patients aged >70, only dyslipidaemia predicted CAC presence in males and only smoking and diabetes were predictive in females. 

     

    Conclusion:  In symptomatic patients, there are significant differences in the ability of conventional risk factors to predict CAC presence between genders and between patients aged <70 and ≥70, indicating the important role of age in predicting CAC presence.

  • 25.
    Nilsson, Stefan K
    et al.
    Umeå University, Faculty of Medicine, Department of Medical Biosciences, Physiological chemistry.
    Heeren, Joerg
    Olivecrona, Gunilla
    Umeå University, Faculty of Medicine, Department of Medical Biosciences, Physiological chemistry.
    Merkel, Martin
    Apolipoprotein A-V; a potent triglyceride reducer2011In: Atherosclerosis, ISSN 0021-9150, E-ISSN 1879-1484, Vol. 219, no 1, 15-21 p.Article in journal (Refereed)
    Abstract [en]

    Since its discovery, apolipoprotein A-V has been considered to be a potent factor affecting plasma triglycerides (TG) in humans and mice. Several single nucleotide polymorphisms in the APOA5 gene are associated with increased TG levels in humans, and some nonsense mutations affecting protein structure predispose for familial hypertriglyceridemia and late onset chylomicronemia. It is not clear, how apoA-V decreases plasma TG. There are three major hypotheses: apolipoprotein A-V could work through (1) an intracellular mechanism affecting VLDL production in the liver, (2) stimulation of proteoglycan-bound lipoprotein lipase at the endothelium of capillaries in peripheral organs, or (3) enhancing the clearance of TG-rich lipoproteins via lipoprotein receptors in the liver. There is good evidence for a role of apoA-V in extracellular TG metabolism and increasing support for an additional function of ApoA-V as a receptor ligand. The intracellular role of apoA-V for lipoprotein assembly and secretion is still speculative. This review discusses these possible mechanisms.

  • 26.
    Nyman, Emma
    et al.
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Clinical Physiology.
    Grönlund, Christer
    Umeå University, Faculty of Medicine, Department of Radiation Sciences.
    Vanoli, Davide
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Clinical Physiology.
    Lindqvist, Per
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Clinical Physiology.
    Näslund, Ulf
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Cardiology.
    Carotid artery plaque assessment within the Västerbotten intervention programme: VIPVIZA2015In: Atherosclerosis, ISSN 0021-9150, E-ISSN 1879-1484, Vol. 241, no 1, E159-E159 p.Article in journal (Other academic)
  • 27.
    Nyman, Emma
    et al.
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Clinical Physiology.
    Vanoli, Davide
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Clinical Physiology.
    Grönlund, Christer
    Umeå University, Faculty of Medicine, Department of Radiation Sciences.
    Näslund, Ulf
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Cardiology.
    Lindqvist, Per
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Clinical Physiology.
    Area measurement of carotid plaque comparing B-MODE, Doppler color and contrast-enhanced ultrasound imaging2016In: Atherosclerosis, ISSN 0021-9150, E-ISSN 1879-1484, Vol. 252, E191-E191 p.Article in journal (Other academic)
    Abstract [en]

    Objectives: Carotid plaque characteristic analysis are suggested to improve risk stratification. Plaque area and echolucent plaques have shown to correlate with increased risk for cardiovascular diseases. A limitation with B-mode imaging is the uncertainty that the whole plaque area is identified, primarily on echolucent plaques. Contrast-enhanced ultrasound (CEUS) is used to improve carotid imaging including better plaque area measurement. Aim: Evaluate if CEUS could improve accurate plaque area measurement compared with B-mode and Doppler color flow imaging. Methods: The study included 28 participants (50% females, mean age 58 years) with identified asymptomatic carotid plaques. We performed B-mode, Doppler color and CEUS ultrasound imaging whereas the plaque area was manually outdrawn by a single operator. Plaques were also subjectively classified as 1 echogenic, 2 echolucent, or 3 mixed plaques. Results: We did not find a significant difference in plaque area measurements between different ultrasound image modalities having all plaque types included. In the group of echolucent plaques (n= 11) we found a significant different between B-mode and CEUS (p=0.049) and also between B-mode and Doppler color imaging (p=0.039) (Illustrated in Fig 1). Conclusions: Echolucent plaque can be underestimated with B-mode imaging. Use of contrast-enhanced ultrasound should be considered in carotid plaque imaging on echolucent plaques when plaque outline is difficult to identify.

  • 28. Paju, S
    et al.
    Pussinen, PJ
    Sinisalo, J
    Mattila, K
    Dogan, B
    Ahlberg, J
    Valtonen, V
    Nieminen, MS
    Asikainen, Sirkka
    Umeå University, Faculty of Medicine, Odontology, Oral Microbiology.
    Clarithromycin reduces recurrent cardiovascular events in subjects without periodontitis.2006In: Atherosclerosis, ISSN 0021-9150, Vol. 188, no 2, 412-419 p.Article in journal (Refereed)
    Abstract [en]

    Inflammation leading to acute coronary syndrome may be triggered by bacteria causing periodontal infection. We investigated if recurrence of cardiovascular events in unstable coronary patients are associated with periodontitis or microbiological/serological markers of it. Periodontitis-related parameters of 141 patients with acute non-Q-wave infarction or unstable angina pectoris, who participated in a double-blind, placebo-controlled study with clarithromycin for 3 months, were adjusted to the occurrence of a recurrent cardiovascular event during a follow-up period (average 519 days). In the age group under 65 years the patients with periodontitis had a univariate odds ratios (OR) 95% confidence intervals (95% CI) of 5.0 (1.02-24.55) for a recurrent cardiovascular event in comparison with patients without periodontitis. Dental status correlated positively with serum lipopolysaccharide concentrations and combined IgG antibody response to Actinobacillus actinomycetemcomitans and Porphyromonas gingivalis. The end point frequency did not differ between clarithromycin and placebo groups in bacterium-positive, seropositive, or periodontitis patients. Fewer end points in clarithromycin group were seen in bacterium-negative, seronegative, edentulous, and non-periodontitis patients. Periodontitis and edentulousness are associated with recurrent cardiovascular events, especially in younger patients. Long-term clarithromycin therapy seems to be beneficial in prevention of recurrent cardiovascular events in non-periodontitis but not in periodontitis patients.

  • 29. Silveira, Angela
    et al.
    McLeod, Olga
    Strawbridge, Rona J.
    Gertow, Karl
    Sennblad, Bengt
    Baldassarre, Damiano
    Veglia, Fabrizio
    Deleskog, Anna
    Persson, Jonas
    Leander, Karin
    Gigante, Bruna
    Kauhanen, Jussi
    Rauramaa, Rainer
    Smit, Andries J.
    Mannarino, Elmo
    Giral, Philippe
    Gustafsson, Sven
    Söderberg, Stefan
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Cardiology.
    Ohrvik, John
    Humphries, Steve E.
    Tremoli, Elena
    de Faire, Ulf
    Hamsten, Anders
    Plasma IL-5 concentration and subclinical carotid atherosclerosis2015In: Atherosclerosis, ISSN 0021-9150, E-ISSN 1879-1484, Vol. 239, no 1, 125-130 p.Article in journal (Refereed)
    Abstract [en]

    Objective: Genetic variants robustly associated with coronary artery disease were reported in the vicinity of the interleukin (IL)-5 locus, and animal studies suggested a protective role for IL-5 in atherosclerosis. Therefore, we set this work to explore IL-5 as a plasma biomarker for early subclinical atherosclerosis, as determined by measures of baseline severity and change over time of carotid intima-media thickness (cIMT).

    Methods: We used biobank and databases of IMPROVE, a large European prospective cohort study of high-risk individuals (n = 3534) free of clinically overt cardiovascular disease at enrollment, in whom composite and segment-specific measures of cIMT were recorded at baseline and after 15 and 30 months. IL-5 was measured with an immunoassay in plasma samples taken at baseline.

    Results: IL-5 levels were lower in women than in men, lower in the South than in North of Europe, and showed positive correlations with most established risk factors. IL-5 showed significant inverse relationships with cIMT change over time in the common carotid segment in women, but no significant relationships to baseline cIMT in either men or women.

    Conclusions: Our results suggest that IL-5 may be part of protective mechanisms operating in early atherosclerosis, at least in women. However, the relationships are weak and whereas IL-5 has been proposed as a potential molecular target to treat allergies, it is difficult to envisage such a scenario in coronary artery disease.

  • 30.
    Söderström, Elisabet
    et al.
    Umeå University, Faculty of Medicine, Department of Medical Biosciences, Clinical chemistry.
    Schneede, Jörn
    Umeå University, Faculty of Medicine, Department of Pharmacology and Clinical Neuroscience.
    Palmqvist, Richard
    Umeå University, Faculty of Medicine, Department of Medical Biosciences, Pathology.
    Johansson, Ingegerd
    Umeå University, Faculty of Medicine, Department of Odontology.
    Hultdin, Johan
    Umeå University, Faculty of Medicine, Department of Medical Biosciences, Clinical chemistry.
    Homocysteine and cotinine levels in smokers and snus users2015In: Atherosclerosis, ISSN 0021-9150, E-ISSN 1879-1484, Vol. 241, no 1, E129-E129 p.Article in journal (Other academic)
  • 31.
    Vanoli, Davide
    et al.
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Clinical Physiology. Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine.
    Lindqvist, Per
    Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Clinical Physiology.
    Plaque characterisation and analysis in the risk stratifying patients with symptomatic carotis stenosis2016In: Atherosclerosis, ISSN 0021-9150, E-ISSN 1879-1484, Vol. 252, E191-E191 p.Article in journal (Other academic)
  • 32.
    Vorkas, P.
    et al.
    Section of Biomolecular Medicine, Imperial College, London, United Kingdom.
    Want, E.
    Section of Biomolecular Medicine, Imperial College, London, United Kingdom.
    Holmes, E.
    Section of Biomolecular Medicine, Imperial College, London, United Kingdom.
    Holmgren, Anders
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Cardiology.
    Näslund, Ulf
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Cardiology. ulf.naslund@medicin.umu.se.
    Issac, G.
    Corporation, Waters Corporation, Milford, USA.
    Millar, A.
    Corporation, Waters Corporation, Milford, USA.
    Henein, Michael
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Cardiology.
    Apoptosis is a potential mechanism for severe calcific coronary artery disease2014In: Atherosclerosis, ISSN 0021-9150, E-ISSN 1879-1484, Vol. 235, no 2, E157-E158 p.Article in journal (Other academic)
  • 33.
    Vorkas, P.
    et al.
    Section of Biomolecular Medicine, Imperial College, London, United Kingdom.
    Want, E.
    Section of Biomolecular Medicine, Imperial College, London, United Kingdom.
    Holmes, E.
    Section of Biomolecular Medicine, Imperial College, London, United Kingdom.
    Holmgren, Anders
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Cardiology.
    Näslund, Ulf
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Cardiology. ulf.naslund@medicin.umu.se.
    Issac, G
    Corporation, Waters Corporation, Milford, USA.
    Millar, A
    Corporation, Waters Corporation, Milford, USA.
    Henein, Michael
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Cardiology.
    Significant inflammation pathophysiology features calcific coronary artery disease2014In: Atherosclerosis, ISSN 0021-9150, E-ISSN 1879-1484, Vol. 235, no 2, E140-E140 p.Article in journal (Other academic)
  • 34. Zhang, Lei
    et al.
    Qiao, Qing
    Tuomilehto, Jaakko
    Hammar, Niklas
    Ruotolo, Giacomo
    Stehouwer, Coen D A
    Heine, Robert J
    Eliasson, Mats
    Umeå University, Faculty of Medicine, Public Health and Clinical Medicine, Medicine.
    Zethelius, Björn
    The impact of dyslipidaemia on cardiovascular mortality in individuals without a prior history of diabetes in the DECODE Study.2009In: Atherosclerosis, ISSN 0021-9150, Vol. 206, no 1, 298-302 p.Article in journal (Refereed)
    Abstract [en]

    OBJECTIVE: To evaluate the impact of dyslipidaemia on cardiovascular disease (CVD) mortality in relation to fasting (FPG) and 2-h (2hPG) plasma glucose levels in individuals without a prior history of diabetes. METHODS: Data from 14 European population-based prospective studies of 9132 men and 8631 women aged 25-89 years were jointly analysed. A total of 871 CVD deaths occurred during the average 10 years of follow-up. Subjects were classified into normoglycaemia, isolated fasting hyperglycaemia (IFH, FPG> or =6.10 mmol/l and 2hPG<7.80 mmol/l), isolated post-load hyperglycaemia (IPH, FPG<6.10 mmol/l and 2hPG> or =7.80 mmol/l) and combined fasting and post-load hyperglycaemia (CH, FPG> or =6.10 mmol/l and 2hPG> or =7.80 mmol/l). Multivariate-adjusted hazard ratios (HRs) and 95% confidence intervals (CIs) for CVD mortality were estimated using Cox proportional hazard analysis. RESULTS: Multivariate-adjusted HRs (95% CIs) for high-density lipoprotein cholesterol (HDL-C) were 0.84 (0.75-0.94), 0.66 (0.48-0.92), 1.03 (0.84-1.27) and 0.67 (0.51-0.89) in individuals with normoglycaemia, IFH, IPH and CH, respectively. For total cholesterol (TC) to HDL-C ratio they were 1.14 (1.03-1.27), 1.44 (1.13-1.84), 0.94 (0.77-1.15) and 1.26 (1.05-1.50), respectively. HRs for TC and triglycerides (TG) were not significant in most of the glucose categories except for TG in those with CH [HR 1.12 (1.00-1.27)]. CONCLUSIONS: Low HDL-C and high TC/HDL-C increase CVD mortality in either diabetic or non-diabetic individuals defined based on the fasting glucose criteria, but not the 2-h criteria. TG is a significant CVD risk predictor only in the presence of combined hyperglycaemia or diabetes. The difference between fasting and post-load hyperglycaemia with regard to the lipid-CVD relation may suggest a different pathophysiology underlying these two prediabetic states.

  • 35. Zhao, Ying
    et al.
    Nicoll, Rachel
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Cardiology.
    He, Yi Hua
    Henein, Michael Y.
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Cardiology.
    The effect of statins on valve function and calcification in aortic stenosis: A meta-analysis2016In: Atherosclerosis, ISSN 0021-9150, E-ISSN 1879-1484, Vol. 246, 318-324 p.Article in journal (Refereed)
    Abstract [en]

    Background: Aortic calcification has been shown to share the same risk factors as atherosclerosis which suggested a potential benefit from statins therapy. In view of the existing conflicting results, we aimed to provide objective evidence on the effect of statins in aortic stenosis (AS).

    Methods and results: A meta-analysis of eligible studies that used statins in AS was performed. Fourteen studies were identified, 5 randomized controlled trials (RCTs) and 9 observational studies. In the 14 studies as a whole, no significant differences were found in all cause mortality (OR = 0.98, p = 0.91), cardiovascular mortality (OR = 0.80, P = 0.23) or the need for valve replacement (OR = 0.93, p = 0.45) between the statins and the control groups. LDL-cholesterol dropped in the statins groups in both <24 months and ≥24 months follow-up (p < 0.001 for both) but not in controls (p = 0.35 and p = 0.33, respectively). In the <24 months statins group, the annual increase in peak aortic velocity and peak gradient was less (p < 0.0001 and p = 0.004, respectively), but the mean gradient, valve area and calcification score were not different from controls. In the ≥24 months statins group, none of the above parameters was different from controls.

    Conclusions: Despite the consistent beneficial effect of statins on LDL-cholesterol levels, the available evidence showed no effect on aortic valve structure, function or calcification and no benefit for clinical outcomes.

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