liu.seSearch for publications in DiVA
Change search
Refine search result
1234 1 - 50 of 185
CiteExportLink to result list
Permanent link
Cite
Citation style
  • apa
  • harvard1
  • ieee
  • modern-language-association-8th-edition
  • vancouver
  • oxford
  • Other style
More styles
Language
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Other locale
More languages
Output format
  • html
  • text
  • asciidoc
  • rtf
Rows per page
  • 5
  • 10
  • 20
  • 50
  • 100
  • 250
Sort
  • Standard (Relevance)
  • Author A-Ö
  • Author Ö-A
  • Title A-Ö
  • Title Ö-A
  • Publication type A-Ö
  • Publication type Ö-A
  • Issued (Oldest first)
  • Issued (Newest first)
  • Created (Oldest first)
  • Created (Newest first)
  • Last updated (Oldest first)
  • Last updated (Newest first)
  • Disputation date (earliest first)
  • Disputation date (latest first)
  • Standard (Relevance)
  • Author A-Ö
  • Author Ö-A
  • Title A-Ö
  • Title Ö-A
  • Publication type A-Ö
  • Publication type Ö-A
  • Issued (Oldest first)
  • Issued (Newest first)
  • Created (Oldest first)
  • Created (Newest first)
  • Last updated (Oldest first)
  • Last updated (Newest first)
  • Disputation date (earliest first)
  • Disputation date (latest first)
Select
The maximal number of hits you can export is 250. When you want to export more records please use the 'Create feeds' function.
  • 1.
    Angelin, Bo
    et al.
    Karolinska University, Sweden; Karolinska University, Sweden.
    Kristensen, Jens D.
    Karo Bio AB, Sweden.
    Eriksson, Mats
    Karolinska University, Sweden; Karolinska University, Sweden.
    Carlsson, Bo
    Karo Bio AB, Sweden.
    Klein, Irwin
    NYU, NY USA.
    Olsson, Anders
    Linköping University, Department of Medical and Health Sciences, Division of Cardiovascular Medicine. Linköping University, Faculty of Health Sciences. Region Östergötland, Heart and Medicine Center, Department of Endocrinology. Stockholm Heart Centre, Sweden.
    Chester Ridgway, E.
    University of Colorado, CO USA.
    Ladenson, Paul W.
    Johns Hopkins University, MD 21205 USA.
    Reductions in serum levels of LDL cholesterol, apolipoprotein B, triglycerides and lipoprotein(a) in hypercholesterolaemic patients treated with the liver-selective thyroid hormone receptor agonist eprotirome2015In: Journal of Internal Medicine, ISSN 0954-6820, E-ISSN 1365-2796, Vol. 277, no 3, p. 331-342Article in journal (Refereed)
    Abstract [en]

    BackgroundLiver-selective thyromimetic agents could provide a new approach for treating dyslipidaemia. MethodsWe performed a multicentre, randomized, placebo-controlled, double-blind study to evaluate the efficacy and safety of eprotirome, a liver-selective thyroid hormone receptor agonist, in 98 patients with primary hypercholesterolaemia. After previous drug wash-out and dietary run-in, patients received 100 or 200gday(-1) eprotirome or placebo for 12weeks. The primary end-point was change in serum LDL cholesterol; secondary end-points included changes in other lipid parameters and safety measures. ResultsEprotirome treatment at 100 and 200g daily reduced serum LDL cholesterol levels by 235% and 31 +/- 4%, respectively, compared with 2 +/- 6% for placebo (Pless than0.0001). Similar reductions were seen in non-HDL cholesterol and apolipoprotein (apo) B, whereas serum levels of HDL cholesterol and apo A-I were unchanged. There were also considerable reductions in serum triglycerides and lipoprotein(a), in particular in patients with elevated levels at baseline. There was no evidence of adverse effects on heart or bone and no changes in serum thyrotropin or triiodothyronine, although the thyroxine level decreased. Low-grade increases in liver enzymes were evident in most patients. ConclusionIn hypercholesterolaemic patients, the liver-selective thyromimetic eprotirome decreased serum levels of atherogenic lipoproteins without signs of extra-hepatic side effects. Selective stimulation of hepatic thyroid hormone receptors may be an attractive way to modulate lipid metabolism in hyperlipidaemia.

  • 2.
    Assman, Gerd
    et al.
    Tyskland.
    Cullen, Paul
    Tyskland.
    Fruchart, Jean-Charles
    Frankrike.
    Greten, Heiner
    Tyskland.
    Naruszewicz, Marek
    Polen.
    Olsson, Anders
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Care, Internal Medicine. Östergötlands Läns Landsting, Centre for Medicine, Department of Endocrinology and Gastroenterology UHL.
    Paoletti, Rudolfo
    Italien.
    Riesen, Walter
    Schweiz.
    Stoll, Monika
    Tyskland.
    Tikkanen, Matti
    Finland.
    Von Eckardstein, Arnold
    Schweiz.
    Implications of emerging risk factors for therapeutic intervention2005In: NMCD. Nutrition Metabolism and Cardiovascular Diseases, ISSN 0939-4753, E-ISSN 1590-3729, Vol. 15, no 5, p. 373-381Article in journal (Refereed)
    Abstract [en]

    Recently, the National Cholesterol Education Panel (NCEP) of the United States of America commented on the implications of new clinical trials for the Adult Treatment Panel III (ATP III) guidelines [Grundy SM, Cleeman JI, Merz CN, Brewer Jr HB, Clark LT, Hunninghake DB, et al. Implications of recent clinical trials for the National Cholesterol Education Program Adult Treatment Panel III guidelines. Circulation 2004,110:227-39]. In this commentary, new categories of "moderately high" and "very high" coronary risk were proposed with new "therapeutic options" for low-density lipoprotein (LDL) cholesterol of ≤ 100 mg/dL and ≤70 mg/dL respectively. In ATP III, these "moderately high" risk patients had been classified as moderate risk with an LDL treatment goal of ≤130 mg/dL, while the "very high" risk patients had been classified as high risk with a treatment goal of ≤100 mg/dL. Risk classification in the new NCEP publication is based essentially on the combination of the Framingham risk score plus counting of classical risk factors. In the present document, the International Task Force for Prevention of Coronary Heart Disease responds to this NCEP commentary and supports the suggestion of more intensive LDL cholesterol lowering in particular cases. However, the Task Force feels that a classification based on a combination of a risk score plus a count of emerging risk factors is a more logical way to identify such patients requiring lower LDL cholesterol levels than a scheme in which classical risk factors are taken into account twice, once in a count and once in a risk score. © 2005 Elsevier B.V. All rights reserved.

  • 3.
    Ballantyne, Christie M.
    et al.
    Baylor Coll Med, Dept Med, Houston, TX 77030 USA Linkoping Univ Hosp, Dept Internal Med, S-58185 Linkoping, Sweden Merck Res Labs, Rahway, NJ USA Aker Hosp, Med Clin, Oslo, Norway Natl Hosp Norway, Dept Med, Oslo, Norway.
    Olsson, Anders
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medical and Health Sciences, Internal Medicine. Östergötlands Läns Landsting, Centre for Medicine, Department of Endocrinology and Gastroenterology UHL.
    Cook, Thomas J.
    Baylor Coll Med, Dept Med, Houston, TX 77030 USA Linköping Univ Hosp, Dept Internal Med, S-58185 Linkoping, Sweden Merck Res Labs, Rahway, NJ USA Aker Hosp, Med Clin, Oslo, Norway Natl Hosp Norway, Dept Med, Oslo, Norway.
    Mercuri, Michele F.
    Baylor Coll Med, Dept Med, Houston, TX 77030 USA Linkoping Univ Hosp, Dept Internal Med, S-58185 Linkoping, Sweden Merck Res Labs, Rahway, NJ USA Aker Hosp, Med Clin, Oslo, Norway Natl Hosp Norway, Dept Med, Oslo, Norway.
    Pedersen, Terje R.
    Baylor Coll Med, Dept Med, Houston, TX 77030 USA Linkoping Univ Hosp, Dept Internal Med, S-58185 Linkoping, Sweden Merck Res Labs, Rahway, NJ USA Aker Hosp, Med Clin, Oslo, Norway Natl Hosp Norway, Dept Med, Oslo, Norway.
    Kjekshus, John
    Baylor Coll Med, Dept Med, Houston, TX 77030 USA Linkoping Univ Hosp, Dept Internal Med, S-58185 Linkoping, Sweden Merck Res Labs, Rahway, NJ USA Aker Hosp, Med Clin, Oslo, Norway Natl Hosp Norway, Dept Med, Oslo, Norway.
    Low high-density lipoprotein cholesterol and response to simvastatin therapy in Scandinavian Simvastatin Survival Study (4S) - Response2002In: Circulation, ISSN 0009-7322, E-ISSN 1524-4539, Vol. 106, no 2, p. E8-E8article id e8Article in journal (Other academic)
  • 4. Ballantyne, CM
    et al.
    Olsson, Anders
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Care, Internal Medicine. Östergötlands Läns Landsting, MKC-2, GE: endomed.
    Cook, TJ
    Mercuri, MF
    Pedersen, TR
    Kjekshus, J
    Influence of low high-density lipoprotein cholesterol and elevated triglyceride on coronary heart disease events and response to simvastatin therapy in 4S2001In: Circulation, ISSN 0009-7322, E-ISSN 1524-4539, Vol. 104, no 25, p. 3046-3051Article in journal (Refereed)
    Abstract [en]

    Background - Patients with low HDL cholesterol (HDL-C) and elevated triglyceride had an increased risk for coronary heart disease (CHD) events and received the greatest benefit with fibrate therapy in substudy analyses of the Helsinki Heart Study and the Bezafibrate Infarction Prevention Study. Methods and Results - In this post hoc analysis of the Scandinavian Simvastatin Survival Study, which enrolled patients with elevated LDL cholesterol (LDL-C) and CHD, subgroups defined by HDL-C and triglyceride quartiles were compared to examine the influence of HDL-C and triglyceride on CHD events and response to therapy. Patients in the lowest HDL-C (<1.00 mmol/L [39 mg/dL]) and highest triglyceride (>1.80 mmol/L [159 mg/dL]) quartiles (lipid triad, n=458) had increased proportions of other features of the metabolic syndrome (increased body mass index, hypertension, diabetes), men, prior myocardial infarction, prior revascularization, and ▀-blocker use than patients in the highest HDL-C (>1.34 mmol/L [52 mg/dL]) and lowest triglyceride (<1.11 mmol/L [98 mg/dL]) quartiles (isolated LDL-C elevation, n=545). The major coronary event rate was highest in lipid triad patients on placebo (35.9%), and this subgroup had the greatest event reduction (relative risk 0.48, 95% CI 0.33 to 0.69), a significant treatment-by-subgroup interaction (P=0.03) indicated a greater treatment effect in the lipid triad subgroup than the isolated LDL-C elevation subgroup. Conclusions - Patients with elevated LDL-C, low HDL-C, and elevated triglycerides were more likely than patients with isolated LDL-C elevation to have other characteristics of the metabolic syndrome, had increased risk for CHD events on placebo, and received greater benefit with simvastatin therapy.

  • 5.
    Blomqvist, Henrik
    et al.
    Linköping University, Department of Medicine and Care, Internal Medicine. Linköping University, Faculty of Health Sciences.
    Olsson, Anders
    Linköping University, Department of Medicine and Care, Internal Medicine. Linköping University, Faculty of Health Sciences.
    Monocyte chemoattractant protein‐1 and CC‐chemokine receptor‐2 in severe hypercholesterolaemia2003In: Scandinavian Journal of Clinical and Laboratory Investigation, ISSN 0036-5513, E-ISSN 1502-7686, Vol. 63, no 7-8, p. 513-519Article in journal (Refereed)
    Abstract [en]

    Objectives: To investigate whether plasma concentrations of monocyte chemoattractant protein‐1 (MCP‐1) and the gene expression of its receptor on the monocyte cell surface CCR‐2 were elevated above normal in subjects with asymptomatic, isolated hypercholesterolaemia and if statin treatment could influence this cytokine.

    Methods: The investigation was designed as a cross sectional study followed by a single, blind, treatment study of patients receiving pravastatin 80 mg/day for 8 weeks. The study included 23 patients with severe hypercholesterolaemia (LDL>5.2 mmol/L) and 39 normocholesterolaemic controls. Blood samples were obtained from patients and controls at baseline and from patients at end of the study and analysed for lipoproteins and inflammatory mediators: MCP‐1, high‐sensitivity C‐reactive protein (HS‐CRP). Isolated peripheral mononuclear cells were analysed for CCR‐2 gene expression.

    Results: Mean plasma LDL‐C was significantly higher in patients than in controls. No difference in plasma MCP‐1 levels or CCR‐2 gene expression was seen between the groups at baseline, nor were there any differences in plasma concentrations of CRP. After treatment with pravastatin, LDL‐C decreased by 31%. Treatment did not significantly affect the levels of MCP‐1 or CCR‐2 gene expression, nor was CRP affected by treatment with pravastatin.

    Conclusions: Our study does not support the view that MCP‐1 plasma levels and CCR‐2 gene expression in circulating monocytes are directly responsible for the monocyte recruitment into the arterial intima in patients with severe asymptomatic hypercholesterolaemia. In addition, the inflammatory response of a high concentration of LDL‐C in isolated asymptomatic hypercholesterolaemia is minute.

  • 6.
    Chen, Fabian
    et al.
    Merck, Clin, Whitehouse Stn, NJ USA .
    Maccubbin, Darbie
    Merck, Clin, Whitehouse Stn, NJ USA .
    Weimer Anderson, Jennifer
    Merck, Clin, Whitehouse Stn, NJ USA .
    McCrary Sisk, Christine
    Merck, GSMP, Whitehouse Stn, NJ USA.
    Kher, Uma
    Merck, Stat, Whitehouse Stn, NJ USA .
    Olsson, Anders
    Linköping University, Department of Medical and Health Sciences, Internal Medicine. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Heart and Medicine Centre, Department of Endocrinology and Gastroenterology UHL.
    Bays, Harold E
    L MARC, Louisville, KY USA .
    Following Stable Therapy with Extended Release Niacin/Laropiprant, Continued Extended Release Niacin/Laropiprant Use Reduced Flushing versus Extended Release Niacin Alone in Dyslipidemic Patients in CIRCULATION, vol 124, issue 21, pp2011In: CIRCULATION, American Heart Association , 2011, Vol. 124, no 21Conference paper (Refereed)
    Abstract [en]

    n/a

  • 7. Cherfan, P
    et al.
    Olsson, Anders
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Care, Internal Medicine. Östergötlands Läns Landsting, Centre for Medicine, Department of Endocrinology and Gastroenterology UHL.
    Jonasson, Lena
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Care, Cardiology. Östergötlands Läns Landsting, Heart Centre, Department of Cardiology.
    Effects of simvastatin on human t-cells in vivo2005In: European Atherosclerosis Society Congress,2005, 2005Conference paper (Other academic)
  • 8.
    Chisalita, Simona Ioana
    et al.
    Linköping University, Department of Clinical and Experimental Medicine, Cell Biology. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Local Health Care Services in Central Östergötland, Department of Acute Internal Medicine.
    Lindström, Torbjörn
    Linköping University, Department of Medical and Health Sciences, Internal Medicine. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Centre for Medicine, Department of Endocrinology and Gastroenterology UHL.
    Eson Jennersjö, Pär
    Borensberg Health Centre, Linköping.
    Paulsson, Johan
    Linköping University, Department of Clinical and Experimental Medicine, Cell Biology. Linköping University, Faculty of Health Sciences.
    Westermark, Gunilla
    Linköping University, Department of Clinical and Experimental Medicine, Cell Biology. Linköping University, Faculty of Health Sciences.
    Olsson, Anders
    Linköping University, Department of Medical and Health Sciences, Internal Medicine. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Centre for Medicine, Department of Endocrinology and Gastroenterology UHL.
    Arnqvist, Hans
    Linköping University, Department of Clinical and Experimental Medicine, Cell Biology. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Centre for Medicine, Department of Endocrinology and Gastroenterology UHL.
    Differential lipid profile and hormonal response in type 2 diabetes by exogenous insulin aspart versus the insulin secretagogue repaglinide, at the same glycemic control2009In: Acta Diabetologica, ISSN 0940-5429, E-ISSN 1432-5233, Vol. 46, no 1, p. 35-42Article in journal (Refereed)
    Abstract [en]

    Our aim was to study, at the same glycemic control, how treatment with either the insulin secretagogue repaglinide or exogenous insulin aspart affects endogenous insulin secretion, plasma insulin and IAPP (islet amyloid polypeptide) levels, GH-IGF (growth hormone-insulin-like growth factor) axis and plasma lipoprotein concentrations in patients with type 2 diabetes. Five patients, age 65.0 +/- A 4.1 years (mean +/- A SE), body weight 82.5 +/- A 5.0 kg, BMI (body mass index) 27.7 +/- A 1.5 kg/m(2) were treated for 10 weeks with repaglinide or insulin aspart in a randomized, cross-over study. At the end of each treatment a 24-h metabolic profile was performed. Blood glucose, C-peptide, free human insulin, free total (human and analogue) insulin, proinsulin, IAPP, IGF-I, IGFBP-1 (IGF binding protein-1), GHBP (growth hormone binding protein) and plasma lipoprotein concentrations were measured. Similar 24-h blood glucose profiles were obtained with repaglinide and insulin aspart treatment. During the repaglinide treatment, the meal related peaks of C-peptide and free human insulin were about twofold higher than during treatment with insulin aspart. Proinsulin, GHBP were higher and IAPP levels tended to be higher during repaglinide compared to insulin aspart. Postprandial plasma total cholesterol, triglycerides and apolipoprotein B concentrations were higher on repaglinide than on insulin aspart treatment. Our results show that, at the same glycemic control, treatment with exogenous insulin aspart in comparison with the insulin secretagogue repaglinide result in a lower endogenous insulin secretion, and a tendency towards a less atherogenic postprandial lipid profile.

  • 9.
    Crisby, Milita
    et al.
    Karolinska Institutet, Stockholm.
    Olsson, Anders
    Linköping University, Department of Medicine and Health Sciences, Internal Medicine . Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Local Health Care Services in Central Östergötland, Department of Endocrinology and Gastroenterology.
    Statin i hög dos vid ischemisk stroke minskar risken för ny stroke2008In: Läkartidningen, ISSN 0023-7205, E-ISSN 1652-7518, Vol. 105, no 48-49, p. 3541-3543Article in journal (Refereed)
  • 10.
    Ekman, Bertil
    et al.
    Linköping University, Department of Medicine and Care, Internal Medicine. Linköping University, Faculty of Health Sciences.
    Lindström, Torbjörn
    Linköping University, Department of Medicine and Care, Internal Medicine. Linköping University, Faculty of Health Sciences.
    Nyström, Fredrik
    Linköping University, Department of Medicine and Care, Internal Medicine. Linköping University, Faculty of Health Sciences.
    Olsson, Anders
    Linköping University, Department of Medicine and Care, Internal Medicine. Linköping University, Faculty of Health Sciences.
    Toss, Göran
    Linköping University, Department of Medicine and Care, Internal Medicine. Linköping University, Faculty of Health Sciences.
    Arnqvist, Hans
    Linköping University, Department of Biomedicine and Surgery, Cell biology. Linköping University, Faculty of Health Sciences.
    A dose titration model for recombinant GH substitution aiming at normal plasma concentrations of IGF-I in hypopituitary adults2002In: European Journal of Endocrinology, ISSN 0804-4643, E-ISSN 1479-683X, Vol. 147, no 1, p. 49-57Article in journal (Refereed)
    Abstract [en]

    OBJECTIVE: To evaluate a dose titration model for recombinant human GH substitution in adult patients with GH deficiency, aiming at normal plasma levels of IGF-I.

    DESIGN AND METHODS: Eighteen patients participated and a start dose of 0.17 mg GH/day was used except by two men who started with 0.33 mg/day. To demonstrate a clear GH effect the patients were first titrated, with steps of 0.17 mg GH/day every 6-8 weeks, to IGF-I levels in the upper range of age-adjusted reference values. The GH dose was then reduced 1 dose step and kept for a further 6 months. For comparison we investigated 17 healthy control subjects.

    RESULTS: Plasma IGF-I was increased after 2 weeks on the start dose and did not increase further for up to 8 weeks. Women had significantly lower GH sensitivity than men measured as net increment of IGF-I on the start dose of GH. GH sensitivity was not changed by age. The plasma IGF-I levels increased from 76.3+/-47.0 (s.d.) to 237+/-97 microg/l at the end of the study (P<0.001), and similar IGF-I levels were obtained in both sexes. The maintenance median GH dose was 0.33 mg/day in males and 0.83 mg/day in females (P=0.017). The GH dose correlated negatively with age in both sexes. Body weight, very low density triglycerides, lipoprotein(a) (Lp(a)), and fasting insulin increased, whereas insulin sensitivity index (QUICKI) decreased significantly. In comparison with the controls, the patients had lower fasting blood glucose, fasting insulin and Lp(a) levels at baseline, but these differences disappeared after GH substitution. The two groups had equal insulin sensitivity (QUICKI), but 2 h oral glucose tolerance test values of blood glucose and insulin were significantly higher in the patients at the end of the study.

    CONCLUSIONS: In conclusion our data suggest that the starting dose of GH substitution and the dose titration steps should be individualised according to GH sensitivity (gender) and the IGF-I level aimed for (age). The reduced insulin sensitivity induced by GH substitution could be viewed as a normalisation if compared with control subjects.

  • 11.
    Faergeman, Ole
    et al.
    Arhus University Hospital.
    Holme, Ingar
    Ullevaal University Hospital.
    Fayyad, Rana
    Pfizer Inc.
    Bhatia, Sonal
    Pfizer Inc.
    Grundy, Scott M
    University of Texas.
    Kastelein, John J P
    University of Amsterdam.
    LaRosa, John C
    SUNY Hlth Science Centre.
    Lytken Larsen, Mogens
    Arhus University Hospital.
    Lindahl, Christina
    Östergötlands Läns Landsting, Local Health Care Services in the East of Östergötland, Department of Internal Medicine VHN.
    Olsson, Anders G
    Linköping University, Department of Medicine and Health Sciences, Internal Medicine . Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Centre for Medicine, Department of Endocrinology and Gastroenterology UHL.
    Tikkanen, Matti J
    University of Helsinki.
    Waters, David D
    San Francisco General Hospital.
    Pedersen, Terje R
    Ullevaal University Hospital.
    Plasma Triglycerides and Cardiovascular Events in the Treating to New Targets and Incremental Decrease in End-Points Through Aggressive Lipid Lowering Trials of Statins in Patients With Coronary Artery Disease2009In: AMERICAN JOURNAL OF CARDIOLOGY, ISSN 0002-9149, Vol. 104, no 4, p. 459-463Article in journal (Refereed)
    Abstract [en]

    We determined the ability of in-trial measurements of triglycerides (TGs) to predict new cardiovascular events (CVEs) using data from the Incremental Decrease in End Points through Aggressive Lipid Lowering (IDEAL) and Treating to New Targets (TNT) trials. The trials compared atorvastatin 80 mg/day with moderate-dose statin therapy (simvastatin 20 to 40 mg/day in IDEAL and atorvastatin 10 mg/day in TNT) in patients with clinically evident coronary heart disease or a history of myocardial infarction. The outcome measurement in the present research was CVE occurring after the first year of the trial. After adjusting for age, gender, and study, risk of CVEs increased with increasing TGs (p andlt;0.001 for trend across quintiles of TGs). Patients in the highest quintile had a 63% higher rate of CVEs than patients in the lowest quintile (hazard ratio 1.63, 95% confidence interval 1.46 to 1.81) and the relation of TGs to risk was apparent even within the normal range of TGs. The ability of TG measurements to predict risk decreased when high-density lipoprotein cholesterol and apolipoprotein B:apolipoprotein A-I were included in the statistical analysis, and it was abolished with inclusion of further variables (diabetes, body mass index, glucose, hypertension, and smoking; (p = 0.044 and 0.621, respectively, for trend across quintiles of TGs). Similar results were obtained in patients in whom low-density lipoprotein cholesterol had been lowered to guideline-recommended levels. In conclusion, even slightly increased TG levels are associated with higher risk of recurrence of CVEs in statin-treated patients and should be considered a useful marker of risk.

  • 12. Fellstrom, B
    et al.
    Holdaas, H
    Jardine, AG
    Holme, I
    Nyberg, G
    Fauchald, P
    Gronhagen-Riska, C
    Madsen, S
    Neumayer, HH
    Cole, E
    Maes, B
    Ambuhl, P
    Olsson, Anders
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Health Sciences, Internal Medicine . Östergötlands Läns Landsting, Centre for Medicine, Department of Endocrinology and Gastroenterology UHL.
    Hartmann, A
    Logan, JO
    Pedersen, TR
    Effect of fluvastatin on renal end points in the Assessment of Lescol in Renal Transplant (ALERT) trial2004In: Kidney International, ISSN 0085-2538, E-ISSN 1523-1755, Vol. 66, no 4, p. 1549-1555Article in journal (Refereed)
    Abstract [en]

    Background. Hyperlipidemia is a risk factor for long-term renal transplant dysfunction, but no prospective clinical trials have investigated the effects of statin treatment on graft function in renal transplant recipients. The aim of the present study was to evaluate the effect of fluvastatin on long-term renal transplant function and development of chronic allograft nephropathy in the ALERT (Assessment of Lescol in Renal Transplantation) study. Methods. ALERT was a randomized, double-blind, placebo-controlled study of the effect of fluvastatin, 40 mg and 80 mg daily, in renal transplant recipients. Patients were randomized to receive either fluvastatin (N = 1050) or placebo (N = 1052) and followed for five to six years. Renal end points included graft loss or doubling of serum creatinine or death, glomerular filtration rate (GFR) was also measured during follow-up in a subset of patients (N = 439). Results. There were 283 patients (13.5%) with graft loss, mainly due to chronic rejection (82%), yielding an annual rate of 2.4%. Fluvastatin treatment significantly lowered mean low-density lipoprotein (LDL)-cholesterol levels by 32% (95% CI 33 to 30) compared with placebo, but had no significant effect on the incidence of renal graft loss or doubling of serum creatinine, or decline in GFR throughout follow-up in the whole study population. Neither was any treatment effect by fluvastatin found in any of the subgroups analyzed. Conclusion. Fluvastatin treatment significantly improves lipid values in renal transplant recipients but has no effect on graft loss or doubling of serum creatinine.

  • 13.
    Fellstrom, B.
    et al.
    Fellström, B., University Hospital, Uppsala, Sweden, Department of Medical Science, Renal Unit, University Hospital, Uppsala, Sweden.
    Holdaas, H.
    Rikshospitalet, Oslo, Norway.
    Jardine, A.G.
    University of Glasgow, Glasgow, United Kingdom.
    Nyberg, G.
    Sahlgrenska University Hospital, Göteborg, Sweden.
    Gronhagen-Riska, C.
    Grönhagen-Riska, C., University Hospital, Helsinki, Finland.
    Madsen, S.
    Skejby Hospital, Aarhus, Denmark.
    Neumayer, H.-H.
    Univ. Klin. Charité, Berlin, Germany.
    Cole, E.
    Toronto General Hospital, Toronto, Ont., Canada.
    Maes, B.
    University Hospital, Leuven, Belgium.
    Ambuhl, P.
    Ambühl, P., University Hospital, Zürich, Switzerland.
    Olsson, Anders
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Health Sciences, Internal Medicine . Östergötlands Läns Landsting, Centre for Medicine, Department of Endocrinology and Gastroenterology UHL.
    Staffler, B.
    Novartis, Basel, Switzerland.
    Pedersen, T.R.
    Preventive Medicine Clinic, Ullevaal University Hospital, Oslo, Norway.
    Risk factors for reaching renal endpoints in the Assessment of Lescol in Renal Transplantation (ALERT) trial2005In: Transplantation, ISSN 0041-1337, E-ISSN 1534-6080, Vol. 79, no 2, p. 205-212Article in journal (Refereed)
    Abstract [en]

    Background. The aim of the study was to identity risk factors for long-term renal transplant function and development of chronic allograft nephropathy (CAN) in renal transplant recipients included in the Assessment of Lescol in Renal Transplantation (ALERT) trial. Methods. The ALERT trial was a randomized, double-blind, placebo-controlled study of the effect of fluvastatin, 40 and 80 mg/day, in renal transplant recipients who were randomized to receive fluvastatin (Lescol) (n=1,050) or placebo (n=1,052) over 5 to 6 years of follow-up. Renal endpoints including graft loss or doubling of serum creatinine or death were analyzed by univariate and multivariate regression analysis in the placebo group. Results. There were 137 graft losses (13.5%) in the placebo group, mainly caused by CAN (82%). Univariate risk factors for graft loss or doubling of serum creatinine were as follows: serum creatinine, proteinuria, hypertension, pulse pressure, time since transplantation, donor age, human leukocyte antigen-DR mismatches, treatment for rejection, low high-density lipoprotein cholesterol, and smoking. Multivariate analysis revealed independent risk factors for graft loss as follows: serum creatinine (relative risk [RR], 3.12 per 100-µM increase), proteinuria (RR, 1.64 per 1-g/24 hr increase), and pulse pressure (RR, 1.12 per 10 mm Hg), whereas age was a protective factor. With patient death in the composite endpoint, diabetes mellitus, smoking, age, and number of transplantations were also risk factors. Conclusions. Independent risk factors for graft loss or doubling of serum creatinine or patient death are mainly related to renal transplant function, proteinuria, and blood pressure, which emphasizes the importance of renoprotective treatment regimens in this population.

  • 14.
    Fraley, Alexander E
    et al.
    University of California.
    Schwartz, Gregory G
    University of Colorado.
    Olsson, Anders
    Linköping University, Department of Medicine and Health Sciences, Internal Medicine . Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Centre for Medicine, Department of Endocrinology and Gastroenterology UHL.
    Kinlay, Scott
    Harvard University.
    Szarek, Michael
    Pfizer Pharmaceutical Grp.
    Rifai, Nader
    Harvard University.
    Libby, Peter
    Brigham & Womens Hospital.
    Ganz, Peter
    Brigham & Womens Hospital.
    Witztum, Joseph L
    University of California.
    Tsimikas, Sotirios
    University of California.
    Relationship of Oxidized Phospholipids and Biomarkers of Oxidized Low- Density Lipoprotein With Cardiovascular Risk Factors, Inflammatory Biomarkers, and Effect of Statin Therapy in Patients With Acute Coronary Syndromes Results From the MIRACL (Myocardial Ischemia Reduction With Aggressive Cholesterol Lowering) Trial2009In: JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, ISSN 0735-1097, Vol. 53, no 23, p. 2186-2196Article in journal (Refereed)
    Abstract [en]

    Objectives This study sought to define the relationship between oxidative biomarkers, cardiovascular disease (CVD) risk factors, and inflammatory and thrombosis biomarkers. Background Elevated levels of oxidized phospholipids (OxPL) on apolipoprotein B particles (apoB) represent a novel biomarker of CVD. Previous studies suggest that an increase in OxPL/apoB reflects a positive response to statins and a low-fat diet. Methods This study measured OxPL/apoB, lipoprotein (a) [Lp(a)], and oxidized low-density lipoprotein (OxLDL) biomarkers, consisting of immunoglobulin (Ig) G and IgM autoantibodies to malondialdehyde (MDA)-low-density lipoprotein (LDL) and IgG and IgM apoB-100 immune complexes (IC/apoB), at baseline and after 16 weeks of treatment with atorvastatin 80 mg/day or placebo in 2,342 patients with acute coronary syndromes (ACS) enrolled in the MIRACL (Myocardial Ischemia Reduction With Aggressive Cholesterol Lowering) trial. Results At baseline, potentially atheroprotective IgM autoantibodies and IgM IC/apoB were lower in male patients, diabetic patients, and patients andgt;65 years of age. Patients with an LDL level greater than the median (122 mg/dl) had higher levels of OxPL/apoB, Lp(a), and OxLDL biomarkers compared with those who had an LDL level less than the median. Atorvastatin resulted in significantly larger changes in all biomarkers in female patients, patients age andlt;65 years, patients with LDL cholesterol andlt;122 mg/dl, nonsmokers, and nondiabetic patients (p andlt; 0.0001 for all). In particular, a significant increase in OxPL/apoB in response to atorvastatin was noted in all 20 subgroups evaluated. Weak or no significant correlations were noted between all OxLDL biomarkers and C-reactive protein, serum amyloid A, tissue plasminogen activator, interleukin-6, intercellular adhesion molecule, vascular cell adhesion molecule, P-selectin, and E-selectin at randomization and 16 weeks. Conclusions In patients with ACS, baseline levels of oxidative biomarkers varied according to specific CVD risk factors and were largely independent of inflammatory biomarkers. Atorvastatin uniformly increased OxPL/apoB levels in all subgroups studied. Future studies are warranted to assess whether the increase in OxPL/apoB levels reflects the benefit of effective therapeutic interventions and prediction of new CVD events.

  • 15.
    G Olsson, Anders
    Linköping University, Department of Medicine and Health Sciences, Internal Medicine . Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Centre for Medicine, Department of Endocrinology and Gastroenterology UHL.
    Lipid lowering and aortic valve disease2009In: CURRENT ATHEROSCLEROSIS REPORTS, ISSN 1523-3804, Vol. 11, no 5, p. 377-383Article in journal (Refereed)
    Abstract [en]

    Several retrospective and nonrandomized studies have indicated that lowering atherogenic lipoprotein, in particular low-density lipoprotein cholesterol, may retard the hemodynamic progression of aortic stenosis (AS). This valvular disease shares pathogenic and pathoanatomic similarities with atherosclerosis, at least in their early developments. Two randomized placebo-controlled studies researching the effect of lowering low-density lipoprotein on AS progression and its clinical consequences have been published recently-the Scottish Aortic Stenosis and Lipid Lowering Trial, Impact on Regression (SALTIRE) study and the Simvastatin and Ezetimibe in Aortic Stenosis (SEAS) study. Both of these studies had neutral outcomes. The causes for the negative outcome may be that cholesterol lowering does not influence AS development in a clinically significant way or it may be due to traits in the design of the studies or treatments. Therefore, statin treatment for prevention of AS progression cannot be ruled out as a future therapeutic option in AS. The outcome of the ongoing Aortic Stenosis Progression Observation: Measuring Effects of Rosuvastatin (ASTRONOMER) study, which is examining lipid lowering as a treatment for AS, is greatly anticipated.

  • 16.
    Gandhi, Sanya K.
    et al.
    AstraZeneca LP, Wilmington, DE, USA.
    Jensen, Marie M.
    AstraZeneca, Lund, Sweden.
    Fox, Kathleen M.
    Strategic HealthCare Solution, Monkton, MD, USA.
    Smolen, Lee
    Medical Decision Modeling Inc, Indianapolis, IN, USA.
    Olsson, Anders
    Linköping University, Department of Medical and Health Sciences, Internal Medicine. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Heart and Medicine Center, Department of Endocrinology.
    Paulsson, Thomas
    AstraZeneca, Södertälje, Sweden.
    Cost-effectiveness of resuvastatin in comparison with generic atorvastatin and simvastatin in a Swedish population at high risk of cardiovascular events2012In: ClinicoEconomics and Outcomes Research, ISSN 1178-6981, Vol. 4, p. 1-11Article in journal (Refereed)
    Abstract [en]

    Background: To assess the long-term cost-effectiveness of rosuvastatin therapy compared with generic simvastatin and generic atorvastatin in reducing the incidence of cardiovascular events and mortality in a Swedish population with Framingham risk ≥20%.

    Methods: A probabilistic Monte Carlo simulation model based on data from JUPITER (the Justification for the Use of statins in Prevention: an Intervention Trial Evaluating Rosuvastatin) was used to estimate the long-term cost-effectiveness of rosuvastatin 20 mg daily versus simvastatin or atorvastatin 40 mg for the prevention of cardiovascular death and morbidity. The three-stage model included cardiovascular event prevention simulating the 4 years of JUPITER, initial prevention beyond the trial, and subsequent cardiovascular event prevention. A Swedish health care payer perspective (direct costs only) was modeled for a lifetime horizon, with 2008/2009 as the costing period. Univariate and probabilistic sensitivity analyses were performed.

    Results: The incremental cost per quality-adjusted life-year (QALY) gained with rosuvastatin 20 mg over simvastatin or atorvastatin 40 mg ranged from SEK88,113 (rosuvastatin 20 mg versus simvastatin 40 mg; Framingham risk ≥30%; net avoidance of 34 events/1000 patients) to SEK497,542 (versus atorvastatin 40 mg: Framingham risk ≥20%; net avoidance of 11 events/1000 patients) over a lifetime horizon. Probabilistic sensitivity analyses indicated that at a willingness-to-pay threshold of SEK500,000/QALY, rosuvastatin 20 mg would be cost-effective for approximately 75%–85% of simulations relative to atorvastatin or simvastatin 40 mg. Sensitivity analyses indicated the findings to be robust.

    Conclusion: Rosuvastatin 20 mg is cost-effective over a lifetime horizon compared with generic simvastatin or atorvastatin 40 mg in patients at high cardiovascular risk in Sweden.

  • 17.
    Garvin, Peter
    et al.
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Department of Health and Society, Division of Preventive and Social Medicine and Public Health Science.
    Jonasson, Lena
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Care, Cardiology. Östergötlands Läns Landsting, Heart Centre, Department of Cardiology.
    Kristenson, Margareta
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Department of Health and Society, Division of Preventive and Social Medicine and Public Health Science. Östergötlands Läns Landsting, Centre for Public Health Sciences, Centre for Public Health Sciences.
    Nijm, Johnny
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Care, Cardiology.
    Nilsson, Lennart
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Care, Cardiology.
    Olsson, Anders
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Care, Internal Medicine. Östergötlands Läns Landsting, Centre for Medicine, Department of Endocrinology and Gastroenterology UHL.
    Psychosocial factors in atherosclerosis2006In: XIV International Symposium on Atherosclerosis,2006, 2006Conference paper (Other academic)
  • 18.
    Gotto, AM
    et al.
    Care Of Jou J, Cornell Univ, Weill Med Coll, New York, NY 10021 USA Linkoping Univ Hosp, Clin Res Ctr, S-58185 Linkoping, Sweden.
    Olsson, Anders
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Health Sciences, Internal Medicine . Östergötlands Läns Landsting, Centre for Medicine, Department of Endocrinology and Gastroenterology UHL.
    A symposium: In Search of the Ideal Lipid-Lowering Agent - Introduction2001In: American Journal of Cardiology, ISSN 0002-9149, E-ISSN 1879-1913, Vol. 87, no 5A, p. 1B-1BOther (Other academic)
  • 19.
    Hellerström, S
    et al.
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Care, Clinical Physiology. Östergötlands Läns Landsting, Heart Centre, Department of Clinical Physiology.
    Malmgren, M
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Care, Clinical Physiology. Östergötlands Läns Landsting, Heart Centre, Department of Clinical Physiology.
    Olsson, Anders
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Care, Clinical Physiology. Östergötlands Läns Landsting, Heart Centre, Department of Clinical Physiology.
    Gustafsson, A
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Care, Clinical Physiology. Östergötlands Läns Landsting, Heart Centre, Department of Clinical Physiology.
    Granerus, Göran
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Care, Clinical Physiology. Östergötlands Läns Landsting, Heart Centre, Department of Clinical Physiology.
    Evaluation of radiation doses to medical staff working with 18 F-FDG gamma camera PET studies.2002In: World J Nucl Med,2002, 2002, p. 288-288Conference paper (Refereed)
  • 20. Hirsch, Mark
    et al.
    O´Donnell, John
    Olsson, Anders
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Care, Internal Medicine. Östergötlands Läns Landsting, Centre for Medicine, Department of Endocrinology and Gastroenterology UHL.
    Rosuvastatin is cost-effective compared with atorvastatin in reaching cholesterol goals2005In: International Journal of Cardiology, ISSN 0167-5273, E-ISSN 1874-1754, Vol. 104, no 3, p. 251-256Article in journal (Refereed)
    Abstract [en]

    Background: Lowering low-density lipoprotein cholesterol (LDL-C) levels reduces the risk of coronary heart disease. The introduction of a highly efficacious new statin, rosuvastatin, may enable more patients to be treated to LDL-C goal within a fixed budget. Objectives: To compare the cost-effectiveness of rosuvastatin 10 mg and atorvastatin 10 mg in lowering LDL-C and achieving guideline goals after 12 weeks of treatment. The LDL-C goals were those recommended by the National Cholesterol Education Program Adult Treatment Panel (NCEP ATP) III and the Third Joint European Task Force. Methods: The analysis was performed on pooled data from three clinical trials. Efficacy was measured as the percent reduction in LDL-C and the proportion of patients who reached guideline LDL-C goals following the first 12 weeks of treatment, prior to dose titration. Costs comprised drug acquisition costs only. The cost-effectiveness measures were cost per 1% reduction in LDL-C and cost per patient treated to their LDL-C goal. Results: Treatment with rosuvastatin 10 mg costs €1.85 per 1% reduction in LDL-C, compared with €2.37 per 1% reduction with atorvastatin 10 mg. The average costs per patient treated to the European LDL-C goals were €130.18 for rosuvastatin 10 mg and €242.44 for atorvastatin 10 mg. Treating to NCEP ATP III goals costs €115 per patient treated with rosuvastatin 10 mg vs. €163 per patient treated with atorvastatin 10 mg. Conclusions: Rosuvastatin has the same acquisition costs as and is more efficacious than atorvastatin in lowering LDL-C and treating patients to target LDL-C levels. © 2005 Elsevier Ireland Ltd. All rights reserved.

  • 21.
    Holdaas, H.
    et al.
    Rikshospitalet, Oslo, Norway.
    Fellstrom, B.
    Fellström, B., University Hospital, Uppsala, Sweden.
    Cole, E.
    University Health Network, Toronto, Canada.
    Nyberg, G.
    Sahlgrenska Academy, Göteborg, Sweden.
    Olsson, Anders G.
    Linköping University, Department of Medical and Health Sciences, Internal Medicine. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Heart and Medicine Centre, Department of Endocrinology and Gastroenterology UHL.
    Pedersen, T.R.
    Ulleval University Hospital, Oslo, Norway.
    Madsen, S.
    Skejby Hospital, Aarhus, Denmark.
    Gronhagen-Riska, C.
    Grönhagen-Riska, C., Helsinki University Central Hospital, Helsinki, Finland.
    Neumayer, H.-H.
    Charité, Universitätsmedizin, Berlin, Germany.
    Maes, B.
    University Hospital, Leuven, Belgium.
    Ambuhl, P.
    Ambühl, P., University Hospital, Zürich, Switzerland.
    Hartmann, A.
    Rikshospitalet, Oslo, Norway.
    Staffler, B.
    Novartis Pharma AG, Basel, Switzerland.
    Jardine, A.G.
    University of Glasgow, Glasgow, United Kingdom.
    Long-term cardiac outcomes in renal transplant recipients receiving fluvastatin: The ALERT extension study2005In: American Journal of Transplantation, ISSN 1600-6135, E-ISSN 1600-6143, Vol. 5, no 12, p. 2929-2936Article in journal (Refereed)
    Abstract [en]

    Renal transplant recipients (RTR) have an increased risk of premature cardiovascular disease. The ALERT study is the first trial to evaluate the effect of statin therapy on cardiac outcomes following renal transplantation. Patients initially randomized to fluvastatin or placebo in the 5-6 year ALERT study were offered open-label fluvastatin XL 80 mg/day in a 2-year extension to the original study. The primary endpoint was time to first major adverse cardiac event (MACE). Of 1787 patients who completed ALERT, 1652 (92%) were followed in the extension. Mean total follow-up was 6.7 years. Mean LDL-cholesterol was 98 mg/dL (2.5 mmol/L) at last follow-up compared to a pre-study level of 159 mg/dL (4.1 mmol/L). Patients randomized to fluvastatin had a reduced risk of MACE (hazards ratio [HR] 0.79, 95% CI 0.63-0.99, p = 0.036), and a 29% reduction in cardiac death or definite non-fatal MI (HR 0.71, 95% CI 0.55-0.93, p = 0.014). Total mortality and graft loss did not differ significantly between groups. Fluvastatin produces a safe and effective reduction in LDL-cholesterol associated with reduced risk of MACE in RTR. The lipid-lowering and cardiovascular benefits of fluvastatin are comparable to those of statins in other patient groups, and support use of fluvastatin in RTR. Copyright © Blackwell Munksgaard 2005.

  • 22.
    Holdaas, H.
    et al.
    Rikshospitalet, Sognsvannsvn 20, Oslo 0072, Norway.
    Fellstrom, B.
    Fellström, B., University Hospital, Uppsala, Sweden.
    Jardine, A.G.
    University of Glasgow, Glasgow, United Kingdom.
    Holme, I.
    Preventive Medicine Clinic, Ullevaal University Hospital, Oslo, Norway.
    Nyberg, G.
    Sahlgrenska University Hospital, Göteborg, Sweden.
    Fauchald, P.
    Rikshospitalet, Sognsvannsvn 20, Oslo 0072, Norway.
    Gronhagen-Riska, C.
    Grönhagen-Riska, C., University Hospital, Helsinki, Finland.
    Madsen, S.
    Skejby Hospital, Aarhus, Denmark.
    Neumayer, H.-H.
    Univ. Klin. Charité, Berlin, Germany.
    Cole, E.
    Toronto General Hospital, Toronto, Ont., Canada.
    Maes, B.
    University Hospital, Leuven, Belgium.
    Ambuhl, P.
    Ambühl, P., University Hospital, Zürich, Switzerland.
    Olsson, Anders
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Health Sciences, Internal Medicine . Östergötlands Läns Landsting, Centre for Medicine, Department of Endocrinology and Gastroenterology UHL.
    Hartmann, A.
    Rikshospitalet, Sognsvannsvn 20, Oslo 0072, Norway.
    Solbu, D.O.
    Novartis Norge AS, Oslo, Norway.
    Pedersen, T.R.
    Preventive Medicine Clinic, Ullevaal University Hospital, Oslo, Norway.
    Effect of fluvastatin on cardiac outcomes in renal transplant recipients: A multicentre, randomised, placebo-controlled trial2003In: The Lancet, ISSN 0140-6736, E-ISSN 1474-547X, Vol. 361, no 9374, p. 2024-2031Article in journal (Refereed)
    Abstract [en]

    Background: Renal transplant recipients are at increased risk of premature cardiovascular disease. Although statins reduce cardiovascular risk in the general population, their efficacy and safety in renal transplant recipients have not been established. We investigated the effects of fluvastatin on cardiac and renal endpoints in this population. Methods: We did a multicentre, randomised, double-blind, placebo-controlled trial in 2102 renal transplant recipients with total cholesterol 4·0-9·0 mmol/L. We randomly assigned patients fluvastatin (n=1050) or placebo (n=1052) and follow up was for 5-6 years. The primary endpoint was the occurrence of a major adverse cardiac event, defined as cardiac death, non-fatal myocardial infarction (MI), or coronary intervention procedure. Secondary endpoints were individual cardiac events, combined cardiac death or non-fatal MI, cerebrovascular events, non-cardiovascular death, all-cause mortality, and graft loss or doubling of serum creatinine. Analysis was by intention to treat. Findings: After a mean follow-up of 5·1 years, fluvastatin lowered LDL cholesterol concentrations by 32%. Risk reduction with fluvastatin for the primary endpoint (risk ratio 0·83 [95% CI 0·64-1·06], p=0·139) was not significant, although there were fewer cardiac deaths or non-fatal MI (70 vs 104, 0·65 [0·48-0·88] p=0·005) in the fluvastatin group than in the placebo group. Coronary intervention procedures and other secondary endpoints did not differ significantly between groups. Interpretation: Although cardiac deaths and non-fatal MI seemed to be reduced, fluvastatin did not generally reduce rates of coronary intervention procedures or mortality. Overall effects of fluvastatin were similar to those of statins in other populations.

  • 23. Holdaas, Hallvard
    et al.
    Fellström, Bengt
    Holme, Ingar
    Nyberg, Gudrun
    Fauchald, Per
    Jardine, Alan
    Grönhagen-Riska, Carola
    Madsen, Sören
    Neymayer, Hans-Hellmut
    Cole, Edward
    Meas, Bart
    Thomas, Weinreich
    Olsson, Anders
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Care, Internal Medicine. Östergötlands Läns Landsting, MKC-2, GE: endomed.
    Pedersen, Terje
    Benghozi, Renée
    Hartmann, Anders
    Effects of fluvastatin on cardiac events in renal transplant patients: ALERT (assessment of Lescol in renal tranplantion) study design and baseline data2001In: Journal of Cardiovascular Risk, ISSN 1350-6277, E-ISSN 1473-5652, Vol. 8, p. 63-71Article in journal (Refereed)
  • 24.
    Hollman, Gunilla
    et al.
    Linköping University, Department of Medicine and Care, Internal Medicine. Linköping University, Faculty of Health Sciences.
    Ek, Anna-Christina
    Linköping University, Department of Medicine and Care, Nursing Science. Linköping University, Faculty of Health Sciences.
    Eriksson, Mats
    Huddinge University Hospital, Stockholm, Sweden.
    Olsson, Anders
    Linköping University, Department of Medicine and Care, Internal Medicine. Linköping University, Faculty of Health Sciences.
    Quality of life in familial hypercholesterolaemia families2001Conference paper (Other academic)
  • 25.
    Hollman, Gunilla
    et al.
    Linköping University, Department of Medicine and Care, Internal Medicine. Linköping University, Faculty of Health Sciences.
    Ek, Anna-Christina
    Linköping University, Department of Medicine and Care, Nursing Science. Linköping University, Faculty of Health Sciences.
    Eriksson, Mats
    Huddinge University Hospital, Stockholm, Sweden.
    Olsson, Anders G.
    Linköping University, Department of Medicine and Care, Internal Medicine. Linköping University, Faculty of Health Sciences.
    Quality of life in genetic disease: The example of familial hypercholesterolaemia2000In: Atherosclerosis XII, 2000Conference paper (Other academic)
  • 26.
    Hollman, Gunilla
    et al.
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Care, Internal Medicine.
    Ek, Anna-Christina
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Care, Nursing Science.
    Olsson, Anders
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Care, Internal Medicine. Östergötlands Läns Landsting, Centre for Medicine, Department of Endocrinology and Gastroenterology UHL.
    Only one of four patients with familial hypercholesterolaemia reach cholesterol treatment goals in primary prevention2004In: Journal of Internal Medicine, ISSN 0954-6820, E-ISSN 1365-2796, Vol. 256, no 2, p. 176-177Article in journal (Other academic)
  • 27.
    Hollman, Gunilla
    et al.
    Linköping University, Department of Medicine and Care, Internal Medicine. Linköping University, Faculty of Health Sciences.
    Ek, Anna-Christina
    Linköping University, Department of Medicine and Care, Nursing Science. Linköping University, Faculty of Health Sciences.
    Olsson, Anders
    Linköping University, Department of Medicine and Care, Internal Medicine. Linköping University, Faculty of Health Sciences.
    Berterö, Carina
    Linköping University, Department of Medicine and Care, Nursing Science. Linköping University, Faculty of Health Sciences.
    The meaning of quality of life among patients with familial hypercholesterolemia2004In: Journal of Cardiovascular Nursing, ISSN 0889-4655, E-ISSN 1550-5049, Vol. 19, no 4, p. 243-250Article in journal (Refereed)
    Abstract [en]

    Background: Living with a genetic predisposition to disease may influence quality of life. The presence of premature disease can lead to an increased focus on family history and genetic predisposition.

    Objective: The purpose of this study was to describe quality of life in patients with the genetic disease, familial hypercholesterolemia, who are at an increased risk of premature coronary heart disease.

    Methods: Interviews from 12 adult patients with FH were analyzed using constant comparative analysis. The findings of this qualitative study revealed that for patients, quality of life was equated with harmony in life, the core category. Attaining harmony in life presumes satisfaction and togetherness. Cognizance of the threat of coronary heart disease and impending mortality is balanced by the support of togetherness and satisfaction that builds harmony in life.

    Conclusion: When caring for patients with familial hypercholesterolemia, it is important to meet each patient on his or her own level, and to support balance and their choices for maintaining or regaining harmony in life.

  • 28.
    Hollman, Gunilla
    et al.
    Linköping University, Department of Medicine and Care, Internal Medicine. Linköping University, Faculty of Health Sciences.
    Ek, Anna-Christina
    Linköping University, Department of Medicine and Care, Nursing Science. Linköping University, Faculty of Health Sciences.
    Olsson, Anders G.
    Linköping University, Department of Medicine and Care, Internal Medicine. Linköping University, Faculty of Health Sciences.
    Achievement of treatment goals2004Conference paper (Other academic)
  • 29.
    Hollman, Gunilla
    et al.
    Linköping University, Department of Medicine and Care, Internal Medicine. Linköping University, Faculty of Health Sciences.
    Ek, Anna-Christina
    Linköping University, Department of Medicine and Care, Nursing Science. Linköping University, Faculty of Health Sciences.
    Olsson, Anders G.
    Linköping University, Department of Medicine and Care, Internal Medicine. Linköping University, Faculty of Health Sciences.
    Achievement of treatment goals, adherence and disease knowledge in patients with familial hypercholesterolaemiaManuscript (preprint) (Other academic)
    Abstract [en]

    Background: Effective treatment is available for patients with familial hypercholesterolaemia (FH). Nevertheless the treatment goal seems hard to reach in all patients. We investigated to what extent recommended international treatment goals were achieved for total cholesterol and low-density lipoprotein (LDL) cholesterol, adherence to drug treatment and if achievement of treatment goals was influenced by knowledge.

    Design: Cross-sectional design.

    Methods: Patients with FH, above 18 years of age, n=74, were asked to participate. Drug treatment, laboratory results, blood pressure and smoking were documented, a questionnaire on adherence and knowledge about FH was sent to the patients. Response rate for the questionnaire was 92 % (n=68).

    Results: The treatment goals for LDL cholesterol (< 3.0 mmol/L) and total cholesterol (<5.0 mmol/L) were reached in 23% and 22% of the patients, respectively. Patients with LDL cholesterol < 3.0 mmol/L who were on treatment followed the prescription to a significantly higher degree than patients with LDL cholesterol ≥ 3.0 mmol/L, (p=0.001). For patient knowledge, the mean was 6.8±2.2 out of 11 possible. The patients had knowledge about cholesterol, self-care prevention and the reason for drug treatment. Patients were less informed about the chance of getting FH and family history.

    Conclusion: Intensified drug treatment is motivated since 23 % of the patients with FH reached treatment goals. In spite of the absence of relation between LDL cholesterol level and knowledge in the present study, we believe that increased disease lmowledge would facilitate for patients to face the difficulties of the condition.

  • 30.
    Hollman, Gunilla
    et al.
    Linköping University, Department of Medicine and Care, Internal Medicine. Linköping University, Faculty of Health Sciences.
    Ek, Anna-Christina
    Linköping University, Department of Medicine and Care, Nursing Science. Linköping University, Faculty of Health Sciences.
    Olsson, Anders G.
    Linköping University, Department of Medicine and Care, Internal Medicine. Linköping University, Faculty of Health Sciences.
    Quality of life in family members in families with familial hypercholesterolemia2002Conference paper (Other academic)
  • 31.
    Hollman, Gunilla
    et al.
    Linköping University, Department of Medicine and Care, Internal Medicine. Linköping University, Faculty of Health Sciences.
    Gullberg, Mats
    Linköping University, Department of Medicine and Care, Nursing Science. Linköping University, Faculty of Health Sciences.
    Ek, Anna-Christina
    Linköping University, Department of Medicine and Care, Nursing Science. Linköping University, Faculty of Health Sciences.
    Eriksson, Mats
    Centre for Metabolism Endocrinology, Huddinge University Hospital, Stockholm, Sweden.
    Olsson, Anders G.
    Linköping University, Department of Medicine and Care, Internal Medicine. Linköping University, Faculty of Health Sciences.
    Quality of life in patients with familial hypercholesterolaemia2002In: Journal of Internal Medicine, ISSN 0954-6820, E-ISSN 1365-2796, Vol. 251, no 4, p. 331-337Article in journal (Refereed)
    Abstract [en]

    Objectives.  The primary aim of this study was to analyse quality of life in adult patients with familial hypercholesterolaemia (FH), a genetic disorder with increased risk of coronary heart disease (CHD). Secondary aims were to find explanatory factors for quality of life and anxiety.

    Design. A descriptive cross-sectional design was used.

    Setting.  Outpatients from lipid clinics at two university hospitals in Sweden were included. Patients with heterozygous FH and a randomly selected control group participated by filling out questionnaires.

    Subjects.  Two hundred and eighty patients with heterozygous FH above 18 years of age were asked, and 212 of whom 185 were free of overt CHD, participated. Of a control group of 2980 persons 1485 were included for comparison.

    Methods. We used Likert-type questionnaires: the Quality of Life Index (QLI) consisting of four subscales, the Hospital Anxiety and Depression Scale (HAD), the Mastery Scale measuring coping and a questionnaire on health and lipids constructed for FH patients.

    Results.  Patients with FH were significantly more satisfied with overall quality of life 21.8 ± 0.3 (SEM) vs. controls 21.1 ± 0.1 and this was also the case in three of four subscales, all differences P < 0.05. Anxiety about getting CHD was expressed amongst 86% of the patients with FH.

    Conclusions. Quality of life amongst patients with FH was at least as good as in controls but they were worried about getting CHD.

  • 32.
    Hollman, Gunilla
    et al.
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Care, Nursing Science.
    Olsson, Anders
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Care, Internal Medicine. Östergötlands Läns Landsting, Centre for Medicine, Department of Endocrinology and Gastroenterology UHL.
    Ek, Anna-Christina
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Care, Nursing Science. Östergötlands Läns Landsting, Local Health Care Services in Central Östergötland, Department of Acute Internal Medicine.
    Disease knowledge and adherence to treatment in patients with familial hypercholesterolemia2006In: Journal of Cardiovascular Nursing, ISSN 0889-4655, E-ISSN 1550-5049, Vol. 21, no 2, p. 103-108Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Familial hypercholesterolemia (FH) is one of the most common genetic metabolic disorders and is associated with a high risk of premature coronary heart disease. Primary prevention directed at lifestyle changes, combined with preventive medical treatment, is the most important way to reduce the risk of coronary heart disease in individuals with FH. Knowledge about the condition and adherence to drug treatment may facilitate reaching treatment goals. OBJECTIVE: The purpose of this study was to describe disease knowledge and adherence to treatment in patients with FH. SUBJECTS AND METHODS: Seventy-four patients, more than 18 years of age, with FH were asked to participate. A questionnaire on disease knowledge about FH and adherence to drug treatment was sent to the patients. Response rate was 92% (n = 68). Drug treatment, laboratory results, blood pressure, and smoking were also documented. RESULTS: Most patients knew about cholesterol, prevention, and the reason for drug treatment but were less informed about the risk of genetic transmission and family history. No significant correlation was found between knowledge and low-density lipoprotein cholesterol level. A significant, negative correlation between adherence and low-density lipoprotein cholesterol level was found (r = -.354, P < .01). CONCLUSIONS: Patients with FH had scant understanding about the risk of genetic transmission and family history. High adherence to drug prescription has significant correlation to low-density lipoprotein cholesterol level. © 2006 Lippincott Williams & Wilkins, Inc.

  • 33.
    Hollman, Gunilla
    et al.
    Linköping University, Department of Medicine and Care, Internal Medicine. Linköping University, Faculty of Health Sciences.
    Olsson, Anders
    Linköping University, Department of Medicine and Care, Internal Medicine. Linköping University, Faculty of Health Sciences.
    Ek, Anna-Christina
    Linköping University, Department of Medicine and Care, Nursing Science. Linköping University, Faculty of Health Sciences.
    Familial hypercholesterolaemia and quality of life in family members2003In: Preventive Medicine, ISSN 0091-7435, E-ISSN 1096-0260, Vol. 36, no 5, p. 569-574Article in journal (Refereed)
    Abstract [en]

    Background

    Awareness of genetic disease in the family may influence quality of life. The purpose of this study was to describe quality of life among nonaffected members of families with familial hypercholesterolaemia. All were aware of the risk for coronary heart disease. Their quality of life was compared with a reference group and with the patients with familial hypercholesterolesterolaemia themselves.

    Methods

    Names of family members (n = 129) were given by the patients with familial hypercholesterolaemia. A randomly selected reference group (n = 1485) and patients with familial hypercholesterolaemia (n = 185) were included for comparison. They all completed the questionnaire Quality of Life Index, the Hospital Anxiety and Depression Scale, and the Mastery Scale measuring coping. Family members and patients with familial hypercholesterolaemia also completed a questionnaire on health and lipids.

    Results

    Family members were more satisfied with family life, mean 22.1 ± 3.5 (SD), and psychological/spiritual life, 22.9 ± 4.0, than the reference group, 21.4 ± 4.3 and 21.1 ± 4.8, respectively; this was particularly expressed among partners, P < 0.05. Of family members, 91% were anxious about the patient with familial hypercholesterolaemia developing coronary heart disease.

    Conclusions

    Family members have as good a quality of life as members of the reference group, but they were anxious about the patient with familial hypercholesterolaemia developing coronary heart disease.

  • 34.
    Hollman, Gunilla
    et al.
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Care, Internal Medicine.
    Olsson, Anders
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Care, Internal Medicine. Östergötlands Läns Landsting, MKC - Medicin och kirurgicentrum, EMK-endokrin.
    Ek, Anna-Christina
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Care, Nursing Science. Östergötlands Läns Landsting, Local Health Care Services in Central Östergötland, Department of Acute Internal Medicine.
    Quality of life in non affected family members of familial hypercholesterolemia families2002In: Konferens Familjefokuserad omvårdnad, Kalmar,2002, 2002Conference paper (Refereed)
  • 35.
    Hollman, Gunilla
    et al.
    Linköping University, Department of Medicine and Care, Internal Medicine. Linköping University, Faculty of Health Sciences.
    Olsson, Anders G.
    Linköping University, Department of Medicine and Care, Internal Medicine. Linköping University, Faculty of Health Sciences.
    Ek, Anna-Christina
    Linköping University, Department of Medicine and Care, Nursing Science. Linköping University, Faculty of Health Sciences.
    The meaning of quality of life among patients with familial hypercholesterolaemia2003Conference paper (Other academic)
  • 36.
    Holme, I.
    et al.
    Center of Preventive Medicine, Ullevål University Hospital, Oslo, Norway, Department of Biostatistics, Centre for Preventive Medicine, Ullevål University Hospital, Kirkeveien 166, N-0407 Oslo, Norway.
    Cater, N.B.
    Pfizer, Pfizer Inc., New York, NY, United States.
    Faergeman, O.
    Department of Medicine-Cardiology A, Århus University Hospital, Århus, Denmark.
    Kastelein, J.J.P.
    Department of Vascular Medicine, Academic Hospital Amsterdam, Amsterdam, Netherlands.
    Olsson, Anders G.
    Linköping University, Department of Medical and Health Sciences, Internal Medicine. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Heart and Medicine Centre, Department of Endocrinology and Gastroenterology UHL.
    Tikkanen, M.J.
    Department of Medicine, Division of Cardiology, Helsinki University Central Hospital, Helsinki, Finland.
    Lytken, Larsen M.
    Lytken Larsen, M., Department of Medicine-Cardiology A, Århus University Hospital, Århus, Denmark.
    Lindahl, C.
    Pfizer Sweden, Sollentuna, Sweden.
    Pedersen, T.R.
    Center of Preventive Medicine, Ullevål University Hospital, Oslo, Norway.
    Lipoprotein predictors of cardiovascular events in statin-treated patients with coronary heart disease. Insights from the Incremental Decrease in End-points through Aggressive Lipid-lowering Trial (IDEAL)2008In: Annals of Medicine, ISSN 0785-3890, E-ISSN 1365-2060, Vol. 40, no 6, p. 456-464Article in journal (Refereed)
    Abstract [en]

    Background. Few studies have looked into the ability of measurements of apolipoprotein B (apoB) and apolipoprotein A-1 (apoA-1) or apoB/apoA-1 to predict new coronary heart disease (CHD) events in patients with CHD on statin treatment. Aims. In the IDEAL trial, to compare lipoprotein components to predict CHD events and to what degree differences in those parameters could explain the observed outcome. Methods. We compared the ability of treatment with atorvastatin 80 mg/day to that of simvastatin 20-40 mg/day to prevent CHD events in patients with CHD and used Cox regression models to study the relationships between on-treatment levels of lipoprotein components to subsequent major coronary events (MCE). Findings. Variables related to low-density lipoprotein cholesterol (LDL-C) carried more predictive information than those related to high-density lipoprotein cholesterol (HDL-C), but LDL-C was less predictive than both non-HDL-C and apoB. The ratio of apoB to apoA-1 was most strongly related to MCE. However, for estimating differences in relative risk reduction between the treatment groups, apoB and non-HDL-C were the strongest predictors. Interpretation. The on-treatment level of apoB/apoA-1 was the strongest predictor of MCE in the pooled patient population, whereas apoB and non-HDL-C were best able to explain the difference in outcome between treatment groups. Measurements of apoB and apoA-1 should be more widely available for routine clinical assessments. © 2008 Informa UK Ltd. (Informa Healthcare, Taylor & Francis AS).

  • 37.
    Holme, I
    et al.
    Oslo University Hospital.
    Fayyad, R
    Pfizer Inc.
    Faergeman, O
    Arhus University Hospital.
    Kastelein, J J P
    Acad Hospital.
    Olsson, Anders
    Linköping University, Department of Medicine and Health Sciences, Internal Medicine . Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Centre for Medicine, Department of Endocrinology and Gastroenterology UHL.
    Tikkanen, M J
    University Helsinki.
    Larsen, M L
    Arhus University Hospital.
    Lindahl, C
    Pfizer Sweden.
    Holdaas, H
    University of Oslo.
    Pedersen, T R
    Oslo University Hospital.
    Cardiovascular outcomes and their relationships to lipoprotein components in patients with and without chronic kidney disease: results from the IDEAL trial2010In: JOURNAL OF INTERNAL MEDICINE, ISSN 0954-6820, Vol. 267, no 6, p. 567-575Article in journal (Refereed)
    Abstract [en]

    Cardiovascular outcomes and their relationships to lipoprotein components in patients with and without chronic kidney disease: Results from the IDEAL trial. J Intern Med 2010; 267:567-575. Objectives. In Incremental Decrease in Endpoints through Aggressive Lipid-lowering (IDEAL), we compared cardiovascular outcomes in patients with and without chronic kidney disease (CKD) (estimated glomerular filtration rate andlt; 60 mL min-1 1.73 m-2) and analysed relationships between lipoprotein components (LC) and major coronary events (MCE) and other cardiovascular (CV) events. Design. Exploratory analysis of CV endpoints in a randomized trial comparing high dose of atorvastatin to usual dose of simvastatin on MCE. Settings. Patients with CKD were compared with the non-CKD patients. Cox regression models were used to study the relationships between on-treatment levels of LC and incident MCE. Findings. Chronic kidney disease was strongly associated with cardiovascular end-points including total mortality. In patients with CKD, a significant benefit of high dose atorvastatin treatment was found for any CV events, stroke and peripheral artery disease, but not for MCE. However, all cardiovascular end-points except stroke and CV mortality were reduced in the non-CKD group. Differential changes in LC or relationships to LC could not explain the different treatment outcomes in MCE in the two groups. Interpretation. Chronic kidney disease was a powerful risk factor for all cardiovascular end-points. The reason why the significant reductions achieved by high-dose statin treatment in most CV end-points in the non-CKD group were only in part matched by similar reductions in the CKD patients is not apparent. This difference did not result from differential changes in or relations to LC, but limited power may have increased the possibility of chance findings.

  • 38.
    Holme, Ingar
    et al.
    Ullevaal University Hospital.
    E Strandberg, Timo
    University of Oulu.
    Faergeman, Ole
    Arhus University Hospital.
    Kastelein, John J P
    University of Amsterdam.
    Olsson, Anders
    Linköping University, Department of Medicine and Health Sciences, Internal Medicine . Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Centre for Medicine, Department of Endocrinology and Gastroenterology UHL.
    Tikkanen, Matti J
    University of Helsinki.
    Lytken Larsen, Mogens
    Arhus University Hospital.
    Lindahl, Christina
    Pfizer Sweden.
    Pedersen, Terje R
    Ullevaal University Hospital.
    Congestive heart failure is associated with lipoprotein components in statin-treated patients with coronary heart disease Insights from the Incremental Decrease in End points Through Aggressive Lipid Lowering Trial (IDEAL)2009In: ATHEROSCLEROSIS, ISSN 0021-9150, Vol. 205, no 2, p. 522-527Article in journal (Refereed)
    Abstract [en]

    Background: Very few, if any, studies have assessed the ability of apolipoproteins to predict new-onset of congestive heart failure (HF) in statin-treated patients with coronary heart disease (CHD). Aims: To employ the Incremental Decrease in End points Through Aggressive Lipid Lowering Trial (IDEAL) study database to assess the association of on-treatment lipoprotein components with prediction of HF events and to compare their predictive value with that of established risk factors such as hypertension and diabetes. Methods: We used Cox regression models to study the relationships between on-treatment levels of apolipoproteins A1 and B to subsequent HE Chi square information value from the log likelihood was used to compare the predictive value of lipoprotein components with established risk factors of HF. Findings: In the IDEAL study, on-treatment apolipoproteins proved to be associated with the occurrence of new-onset HE Variables related to low-density lipoprotein cholesterol (LDL-C) carried less predictive information than those related to high-density lipoprotein cholesterol (HDL-C), and apoA-1 was the single variable most strongly associated with HF. LDL-C was less predictive than both non-HDL-C (total cholesterol minus HDL-C) and apoB. The ratio of apoB to apoA-1 was most strongly related to HF after adjustment for potential confounders, among which diabetes had a stronger correlation with HF than did hypertension. ApoB/apoA-1 carried approximately 2.2 times more of the statistical information value than that of diabetes. Calculation of the net reclassification improvement index revealed that about 3.7% of the patients had to be reclassified into more correct categories of risk once apoB/apoA-1 was added to the adjustment factors. The reduction in risk by intensive lipid-lowering treatment as compared to usual-dose simvastatin was well predicted by the difference in apoB/apoA-1 on-treatment levels. Interpretation: The on-treatment ratio of apoB/apoA-1 was the strongest predictor of HF in CHD patients of both IDEAL treatment arms combined, mostly driven by the strong association with apoA-1, whereas LDL-C and non-HDL-C were less able to predict HF outcome. The predictive information value contained within apoB/apoA-1 was about 2.2 times more than that of diabetes. Between-treatment group differences in HF were to a significant extent explained by on-treatment differences in apoB/apoA-1, mostly through the changes in apoB. We argue therefore, on-treatment lipoprotein components contribute to the overall future risk of HF in statin-treated patients with CHD.

  • 39.
    Holme, Ingar
    et al.
    Oslo University Hospital.
    Szarek, Michael
    Cater, Nilo B
    Pfizer Inc.
    Faergeman, Ole
    Pfizer Inc.
    Kastelein, John J P
    University of Amsterdam.
    Olsson, Anders
    Linköping University, Department of Medicine and Health Sciences, Internal Medicine . Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Centre for Medicine, Department of Endocrinology and Gastroenterology UHL.
    Tikkanen, Matti J
    Helsinki University Hospital.
    Lytken Larsen, Mogens
    Arhus University Hospital.
    Lindahl, Christina
    Pfizer Sweden.
    Pedersen, Terje R
    Oslo University Hospital.
    Adherence-adjusted efficacy with intensive versus standard statin therapy in patients with acute myocardial infarction in the IDEAL study2009In: EUROPEAN JOURNAL OF CARDIOVASCULAR PREVENTION and REHABILITATION, ISSN 1741-8267, Vol. 16, no 3, p. 315-320Article in journal (Refereed)
    Abstract [en]

    Background The Incremental Decrease in End Points through Aggressive Lipid Lowering trial showed that the primary endpoint major coronary event was reduced by 11% (0.78-1.01) using atorvastatin 80 mg versus simvastatin 20-40 mg in patients with coronary heart disease (P=0.07). Adherence was high in both treatment groups but significantly higher in patients treated with simvastatin. Design The Incremental Decrease in End Points through Aggressive Lipid Lowering was a prescription trial with a prospective randomized open label endpoint evaluation. Methods and results Adherence was calculated as exposure time on prescribed drugs divided by total follow-up time until death or end of follow-up and was a potential confounder. Adjusting for categorical adherence below or above 80% by two methods revealed that the relative risk reduction of the primary endpoint was more in the region of 15% (P=0.02) than 11% as found unadjusted. Censoring at the first occurrence of a cardiovascular event rather than at death increased this estimate to 17% (P=0.02). Noncardiovascular mortality was reduced on atorvastatin treatment by 21% (1-37%) after adjustment for adherence, whereas such reduction was not observed for cardiovascular mortality. Conclusion This study found that the difference in adherence between treatment groups may have underestimated the true effect of the treatment differential. Usage of prospective randomized open label endpoint evaluation design should be carefully considered when well-known treatments are compared with rather new ones and especially in segments where patients could be more vulnerable, as in the elderly. Nonadherers in a clinical trial may be at especially high risk of fatal and nonfatal endpoints from various diseases and should be carefully monitored.

  • 40.
    Holmes, Michael V.
    et al.
    UCL, England .
    Simon, Tabassome
    Hop St Antoine, France .
    J Exeter, Holly
    UCL, England .
    Folkersen, Lasse
    Karolinska Institute, Sweden .
    Asselbergs, Folkert W.
    University of Medical Centre Utrecht, Netherlands .
    Guardiola, Montse
    University of Rovira and Virgili, Spain .
    Cooper, Jackie A.
    UCL, England .
    Palmen, Jutta
    UCL, England .
    Hubacek, Jaroslav A.
    Institute Clin and Expt Med, Czech Republic .
    Carruthers, Kathryn F.
    University of Edinburgh, Scotland .
    Horne, Benjamin D.
    Intermt Medical Centre, UT USA .
    Brunisholz, Kimberly D.
    Intermt Medical Centre, UT USA .
    Mega, Jessica L.
    Brigham and Womens Hospital, MA USA .
    Van Iperen, Erik P A
    Durrer Centre Cardiogenet Research, Netherlands .
    Li, Mingyao
    University of Penn School Med, PA USA .
    Leusink, Maarten
    University of Utrecht, Netherlands .
    Trompet, Stella
    Leiden University of Medical Centre, Netherlands .
    Verschuren, Jeffrey J W.
    Leiden University of Medical Centre, Netherlands .
    Kees Hovingh, G
    University of Amsterdam, Netherlands .
    Dehghan, Abbas
    Erasmus MC, Netherlands .
    Nelson, Christopher P.
    University of Leicester, England .
    Kotti, Salma
    Hop St Antoine, France .
    Danchin, Nicolas
    University of Ulm, Germany .
    Scholz, Markus
    University of Leipzig, Germany .
    Haase L., Christiane
    Copenhagen University Hospital, Denmark .
    Rothenbacher, Dietrich
    University of Ulm, Germany .
    Swerdlow, Daniel I.
    UCL, England .
    Kuchenbaecker, Karoline B.
    University of Cambridge, England .
    Staines-Urias, Eleonora
    London School Hyg and Trop Med, England .
    Goel, Anuj
    University of Oxford, England .
    van t Hooft, Ferdinand
    Karolinska Institute, Sweden .
    Gertow, Karl
    Karolinska Institute, Sweden .
    de Faire, Ulf
    Karolinska Institute, Sweden .
    Panayiotou, Andrie G.
    Cyprus Cardiovasc Educ and Research Trust, Cyprus .
    Tremoli, Elena
    University of Milan, Italy .
    Baldassarre, Damiano
    University of Milan, Italy .
    Veglia, Fabrizio
    IRCCS, Italy .
    Holdt, Lesca M.
    University of Leipzig, Germany .
    Beutner, Frank
    University of Leipzig, Germany .
    Gansevoort, Ron T.
    University of Groningen, Netherlands .
    Navis, Gerjan J.
    University of Groningen, Netherlands .
    Mateo Leach, Irene
    University of Groningen, Netherlands .
    Breitling, Lutz P.
    German Cancer Research Centre, Germany .
    Brenner, Hermann
    German Cancer Research Centre, Germany .
    Thiery, Joachim
    University of Leipzig, Germany .
    Dallmeier, Dhayana
    University of Ulm Medical Centre, Germany .
    Franco-Cereceda, Anders
    Karolinska Institute, Sweden .
    Boer, Jolanda M A.
    National Institute Public Health and Environm, Netherlands .
    Stephens, Jeffrey W.
    Swansea University, Wales .
    Hofker, Marten H.
    University of Groningen, Netherlands .
    Tedgui, Alain
    INSERM, France .
    Hofman, Albert
    Erasmus MC, Netherlands .
    Uitterlinden, Andre G.
    Erasmus MC, Netherlands .
    Adamkova, Vera
    Institute Clin and Expt Med, Czech Republic .
    Pitha, Jan
    Institute Clin and Expt Med, Czech Republic .
    Onland-Moret, Charlotte N.
    University of Medical Centre Utrecht, Netherlands .
    Cramer, Maarten J.
    University of Medical Centre Utrecht, Netherlands .
    Nathoe, Hendrik M.
    University of Medical Centre Utrecht, Netherlands .
    Spiering, Wilko
    University of Medical Centre Utrecht, Netherlands .
    Klungel, Olaf H.
    University of Utrecht, Netherlands .
    Kumari, Meena
    UCL, England .
    Whincup, Peter H.
    University of London, England .
    Morrow, David A.
    Brigham and Womens Hospital, MA USA .
    Braund, Peter S.
    University of Leicester, England .
    Hall, Alistair S.
    University of Leeds, England .
    Olsson, Anders G.
    Linköping University, Department of Medical and Health Sciences, Division of Cardiovascular Medicine. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Heart and Medicine Center, Department of Endocrinology. Stockholm Heart Centre, Sweden .
    Doevendans, Pieter A.
    University of Medical Centre Utrecht, Netherlands .
    Trip, Mieke D.
    University of Amsterdam, Netherlands .
    Tobin, Martin D.
    University of Leicester, England .
    Hamsten, Anders
    Karolinska Institute, Sweden .
    Watkins, Hugh
    University of Oxford, England .
    Koenig, Wolfgang
    University of Ulm Medical Centre, Germany .
    Nicolaides, Andrew N.
    University of London Imperial Coll Science Technology and Med, England .
    Teupser, Daniel
    University of Leipzig, Germany .
    Day, Ian N M
    Hop St Antoine, France .
    F Carlquist, John
    Intermt Medical Centre, UT USA .
    Gaunt, Tom R.
    University of Bristol, England .
    Ford, Ian
    University of Glasgow, Scotland .
    Sattar, Naveed
    University of Glasgow, Scotland .
    Tsimikas, Sotirios
    University of Calif San Diego, CA USA .
    Schwartz, Gregory G.
    VA Medical Centre, CO USA .
    Lawlor, Debbie A.
    University of Bristol, England .
    Morris, Richard W.
    UCL, England .
    Sandhu, Manjinder S.
    VA Medical Centre, CO USA .
    Poledne, Rudolf
    Institute Clin and Expt Med, Czech Republic .
    Maitland-van der Zee, Anke H.
    University of Utrecht, Netherlands .
    Khaw, Kay-Tee
    University of Cambridge, England .
    Keating, Brendan J.
    Childrens Hospital Philadelphia, PA USA .
    van der Harst, Pim
    University of Groningen, Netherlands .
    Price, Jackie F.
    University of Edinburgh, Scotland .
    Mehta, Shamir R.
    McMaster University, Canada .
    Yusuf, Salim
    McMaster University, Canada .
    Witteman, Jaqueline C M
    Erasmus MC, Netherlands .
    Franco, Oscar H.
    Erasmus MC, Netherlands .
    Jukema, Wouter J.
    Durrer Centre Cardiogenet Research, Netherlands .
    de Knijff, Peter
    Leiden University of Medical Centre, Netherlands .
    Tybjaerg-Hansen, Anne
    Copenhagen University Hospital, Denmark .
    Rader, Daniel J.
    Penn Heart and Vasc Centre, PA USA .
    Farrall, Martin
    University of Oxford, England .
    Samani, Nilesh J.
    University of Leicester, England .
    Kivimaki, Mika
    UCL, England .
    Fox, Keith A A.
    University of Edinburgh, Scotland .
    Humphries, Steve E.
    UCL, England .
    Anderson, Jeffrey L.
    Intermt Medical Centre, UT USA .
    Boekholdt, Matthijs S.
    University of Amsterdam, Netherlands .
    Palmer, Tom M.
    University of Warwick, England .
    Eriksson, Per
    Karolinska Institute, Sweden .
    Pare, Guillaume
    McMaster University, Canada .
    Hingorani, Aroon D.
    UCL, England .
    Sabatine, Marc S.
    Brigham and Womens Hospital, MA USA .
    Mallat, Ziad
    INSERM, France .
    Casas, Juan P.
    UCL, England .
    Talmud, Philippa J.
    UCL, England .
    Secretory Phospholipase A(2)-IIA and Cardiovascular Disease2013In: Journal of the American College of Cardiology, ISSN 0735-1097, E-ISSN 1558-3597, Vol. 62, no 21, p. 1966-1976Article in journal (Refereed)
    Abstract [en]

    Objectives This study sought to investigate the role of secretory phospholipase A(2) (sPLA(2))-IIA in cardiovascular disease. less thanbrgreater than less thanbrgreater thanBackground Higher circulating levels of sPLA(2)-IIA mass or sPLA(2) enzyme activity have been associated with increased risk of cardiovascular events. However, it is not clear if this association is causal. A recent phase III clinical trial of an sPLA(2) inhibitor (varespladib) was stopped prematurely for lack of efficacy. less thanbrgreater than less thanbrgreater thanMethods We conducted a Mendelian randomization meta-analysis of 19 general population studies (8,021 incident, 7,513 prevalent major vascular events [MVE] in 74,683 individuals) and 10 acute coronary syndrome (ACS) cohorts (2,520 recurrent MVE in 18,355 individuals) using rs11573156, a variant in PLA2G2A encoding the sPLA(2)-IIA isoenzyme, as an instrumental variable. less thanbrgreater than less thanbrgreater thanResults PLA2G2A rs11573156 C allele associated with lower circulating sPLA(2)-IIA mass (38% to 44%) and sPLA(2) enzyme activity (3% to 23%) per C allele. The odds ratio (OR) for MVE per rs11573156 C allele was 1.02 (95% confidence interval [CI]: 0.98 to 1.06) in general populations and 0.96 (95% CI: 0.90 to 1.03) in ACS cohorts. In the general population studies, the OR derived from the genetic instrumental variable analysis for MVE for a 1-log unit lower sPLA(2)-IIA mass was 1.04 (95% CI: 0.96 to 1.13), and differed from the non-genetic observational estimate (OR: 0.69; 95% CI: 0.61 to 0.79). In the ACS cohorts, both the genetic instrumental variable and observational ORs showed a null association with MVE. Instrumental variable analysis failed to show associations between sPLA2 enzyme activity and MVE. less thanbrgreater than less thanbrgreater thanConclusions Reducing sPLA(2)-IIA mass is unlikely to be a useful therapeutic goal for preventing cardiovascular events.

  • 41.
    Jacobsson, Leif S.
    et al.
    Linköping University, Department of Medical and Health Sciences, Pharmacology. Linköping University, Faculty of Health Sciences.
    Persson, Karin
    Linköping University, Department of Medical and Health Sciences, Pharmacology. Linköping University, Faculty of Health Sciences.
    Aberg, Gunnar
    Linköping University, Department of Medical and Health Sciences, Pharmacology. Linköping University, Faculty of Health Sciences.
    Andersson, Rolf G. G.
    Linköping University, Department of Medical and Health Sciences, Pharmacology. Linköping University, Faculty of Health Sciences.
    Karlberg, Bengt E.
    Linköping University, Department of Medicine and Care, Internal Medicine. Linköping University, Faculty of Health Sciences.
    Olsson, Anders G.
    Linköping University, Department of Medicine and Care, Internal Medicine. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Local Health Care Services in Central Östergötland, Department of Endocrinology and Gastroenterology.
    Antiatherosclerotic Effects of the Angiotensin-Converting Enzyme Inhibitors Captopril and Fosinopril in Hypercholesterolemic Minipigs1994In: Journal of Cardiovascular Pharmacology, ISSN 0160-2446, E-ISSN 1533-4023, Vol. 24, no 4, p. 670-677Article in journal (Refereed)
    Abstract [en]

    We evaluated the two angiotensin-converting enzyme (ACE) inhibitors captopril and fosinopril with regard to possible antiatherosclerotic effects in minipigs. Experimental hypercholesterolemia and atherosclerosis was produced in 33 minipigs of the Gottingen strain by an egg yolk/cholesterol-enriched diet for 1 year. One group (n = 11) was fed the atherogenic diet alone and served as a control. A second group (n = 11) received captopril (80 mg/kg/day) added to the atherogenic diet, and a third group (n = 11) was treated in the same manner but with fosinopril (8 mg/kglday). The drug treatments produced significant reduction in serum ACE activity associated with a reactive increase in plasma renin activity (PRA), but had only minor effects on plasma lipids and lipoproteins. At the end of the treatment period, all animals were killed and examined for degree of atherosclerosis. The percentage of atherosclerotic area in the abdominal aorta was significantly lower in both drug-treated groups as compared with controls. Furthermore, accumulation of cholesterol in the thoracic and abdominal aorta was inhibited by drug treatment. Finally, the percentage of intimal thickening in abdominal aorta was significantly reduced in the drug-treated groups. In conclusion, the ACE inhibitors captopril and fosinopril inhibited development of atherosclerosis in hypercholesterolemic minipigs.

  • 42. Jardine, AG
    et al.
    Fellstrom, B
    Logan, JO
    Cole, E
    Nyberg, G
    Gronhagen-Riska, C
    Madsen, S
    Neumayer, HH
    Maes, B
    Ambuhl, P
    Olsson, Anders
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Health Sciences, Internal Medicine . Östergötlands Läns Landsting, Centre for Medicine, Department of Endocrinology and Gastroenterology UHL.
    Pedersen, T
    Holdaas, H
    Cardiovascular risk and renal transplantation: Post hoc analyses of the Assessment of Lescol in Renal Transplantation (ALERT) study2005In: American Journal of Kidney Diseases, ISSN 0272-6386, E-ISSN 1523-6838, Vol. 46, no 3, p. 529-536Article in journal (Refereed)
    Abstract [en]

    Background Renal transplantation is associated with an increased risk for premature cardiovascular disease. We analyzed the data in the placebo arm of Assessment of Lescol in Renal Transplantation (ALERT) to improve our understanding of the relationship between cardiovascular risk factors and outcomes in this unique population. Methods: We performed Cox survival analysis for myocardial infarction, cardiac death, and noncardiac death in 1,052 patients recruited to the placebo arm of ALERT. These subjects were aged 30 to 75 years, had stable graft function at least 6 months after transplantation, had a serum total cholesterol level between 155 and 348 mg/dL (4 and 9 mmol/L), and were receiving cyclosporine-based immunosuppression. Results: The results confirm previous studies. In multivarlate analysis, preexisting coronary heart disease (hazard ratio [HR], 3.69, P < 0.001), total cholesterol level (HR, 1.55 per 50 mg/dL, P = 0.0045), and prior acute rejection (HR, 2.36, P = 0.0023) were independent risk factors. Conversely, independent risk factors for cardiac death were age (HR, 1.58 per decade, P = 0.0033), diabetes (HR, 3.35, P = 0.0002), ST-T changes on the ECG (HR, 3.17, P = 0.0004), and serum creatinine level (HR, 2.65 per milligram per deciliter, P < 0.0001). Conclusion: This analysis confirms that renal transplant recipients share risk factors for myocardial infarction and cardiac death with the general population. However, the pattern of risk factors and their relationship with outcomes is atypical, highlighting the unique nature of cardiovascular risk in transplant recipients.

  • 43. Jonasson, L
    et al.
    Linderfalk, C
    Olsson, J
    Wikby, A
    Olsson, Anders
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Care, Internal Medicine. Östergötlands Läns Landsting, MKC-2, GE: endomed.
    Systemic T-cell activation in stable angina pectoris2002In: American Journal of Cardiology, ISSN 0002-9149, E-ISSN 1879-1913, Vol. 89, no 6, p. 754-756Article in journal (Refereed)
  • 44. Jonasson, L
    et al.
    Linderfalk, C
    Hoeglandssjukhuset, Eksjoe, Sweden Univ Coll Hlth Sci, Jonkoping, Sweden Linkoping Univ Hosp, S-58185 Linkoping, Sweden.
    Wikby, A
    Hoeglandssjukhuset, Eksjoe, Sweden Univ Coll Hlth Sci, Jonkoping, Sweden Linkoping Univ Hosp, S-58185 Linkoping, Sweden.
    Olsson, Anders
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Health Sciences, Internal Medicine . Östergötlands Läns Landsting, Centre for Medicine, Department of Endocrinology and Gastroenterology UHL.
    T lymphocyte activation in stable angina pectoris: The influence of statin treatment.2000In: Circulation, ISSN 0009-7322, E-ISSN 1524-4539, Vol. 102, no 18, p. 1990-Conference paper (Other academic)
  • 45.
    Jonasson, Lena
    et al.
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Health Sciences, Cardiology . Östergötlands Läns Landsting, Heart Centre, Department of Cardiology.
    Wikby, A.
    Dept. of Nat. Sci. and Biomedicine, School of Health Sciences, Jönköping University, Jönköping, Sweden.
    Olsson, Anders
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Health Sciences, Internal Medicine . Östergötlands Läns Landsting, Centre for Medicine, Department of Endocrinology and Gastroenterology UHL.
    Low serum ß-carotene reflects immune activation in patients with coronary artery disease2003In: NMCD. Nutrition Metabolism and Cardiovascular Diseases, ISSN 0939-4753, E-ISSN 1590-3729, Vol. 13, no 3, p. 120-125Article in journal (Refereed)
    Abstract [en]

    Background and Aim: Low serum levels of antioxidant vitamins are associated with coronary artery disease (CAD). An immunomodulatory effect of antioxidants has been proposed. The aim of the study was to investigate whether an increased immune response in CAD patients was associated with suppressed circulating levels of antioxidant vitamins. Methods and Results: Forty-four men with stable angina and angiographically verified CAD were included as well as 69 healthy controls. T cell subsets in peripheral blood were quantified by 3-colour flow cytometry. C-reactive protein (CRP), soluble interleukin-2 receptor (sIL-2R) and the lipophilic antioxidants a-tocopherol, ß-carotene and lycopene were determined in serum. Compared with controls, patients had signs of an enhanced inflammatory activity assessed by significantly increased levels of CRP, sIL-2R and CD4+CD25+T cell subsets. Patients also had significantly lower ß-carotene and lycopene levels whereas a-tocopherol levels did not differ. The increased inflammatory/immune parameters in patients showed a significant inverse relationship to serum ß-carotene but not to lycopene or a-tocopherol. Conclusions: Low serum ß-carotene in CAD patients reflects activation of the immune system. Inflammation should be considered as an important confounding factor when analysing data on ß-carotene and CAD. © 2003, Medikal Press.

  • 46. Kaminskas, A
    et al.
    Ziedén, Bo
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Care, Internal Medicine. Östergötlands Läns Landsting, MKC-2, GE: endomed.
    Elving, B
    Linköping University, Faculty of Health Sciences. Linköping University, Department of health and environment. Östergötlands Läns Landsting, FHVC - Folkhälsovetenskapligt centrum, Förebygg.med.
    Kristenson, Margareta
    Linköping University, Faculty of Health Sciences. Linköping University, Department of health and environment. Östergötlands Läns Landsting, FHVC - Folkhälsovetenskapligt centrum, Förebygg.med.
    Abaravicius, A
    Bergdahl, Björn
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Care, Cardiology. Östergötlands Läns Landsting, Heart Centre, Department of Cardiology.
    Olsson, Anders
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Care, Internal Medicine. Östergötlands Läns Landsting, MKC-2, GE: endomed.
    Kucinskiene, Z
    Adipose tissue fatty acids in men from two populations with different cardiovascular risk - the LiVicordia study.1999In: Scandinavian Journal of Clinical and Laboratory Investigation, ISSN 0036-5513, E-ISSN 1502-7686, Vol. 59, p. 227-232Article in journal (Refereed)
  • 47.
    Karppi, J.
    et al.
    Research Institute of Public Health, University of Kuopio, P.O. Box 1627, FI-70211 Kuopio, Finland.
    Rissanen, T.H.
    Research Institute of Public Health, University of Kuopio, P.O. Box 1627, FI-70211 Kuopio, Finland, Department of Public Health and Clinical Nutrition, University of Kuopio, P.O. Box 1627, FI-70211 Kuopio, Finland.
    Nyyssonen, K.
    Nyyssönen, K., Research Institute of Public Health, University of Kuopio, P.O. Box 1627, FI-70211 Kuopio, Finland, Research Institute of Public Health, University of Kuopio, P.O. Box 1627, FI-70210 Kuopio, Finland.
    Kaikkonen, J.
    Oy Jurilab Ltd., Microkatu 1, FI-70210 Kuopio, Finland.
    Olsson, Anders G.
    Linköping University, Department of Medical and Health Sciences, Internal Medicine. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Local Health Care Services in Central Östergötland, Department of Endocrinology and Gastroenterology.
    Voutilainen, S.
    Research Institute of Public Health, University of Kuopio, P.O. Box 1627, FI-70211 Kuopio, Finland.
    Salonen, J.T.
    Research Institute of Public Health, University of Kuopio, P.O. Box 1627, FI-70211 Kuopio, Finland, Oy Jurilab Ltd., Microkatu 1, FI-70210 Kuopio, Finland.
    Effects of astaxanthin supplementation on lipid peroxidation2007In: International Journal for Vitamin and Nutrition Research, ISSN 0300-9831, E-ISSN 1664-2821, Vol. 77, no 1Article in journal (Refereed)
    Abstract [en]

    Astaxanthin, the main carotenoid pigment in aquatic animals, has greater antioxidant activity in vitro (protecting against lipid peroxidation) and a more polar configuration than other carotenoids. We investigated the effect of three-month astaxanthin supplementation on lipid peroxidation in healthy non-smoking Finnish men, aged 19-33 years by using a randomized double-blind study design. Also absorption of astaxanthin from capsules into bloodstream and its safety were evaluated. The intervention group received two 4-mg astaxanthin (Astaxin®) capsules daily, and the control group two identical-looking placebo capsules. Astaxanthin supplementation elevated plasma astaxanthin levels to 0.032 µmol/L (p < 0.001 for the change compared with the placebo group). We observed that levels of plasma 12- and 15-hydroxy fatty acids were reduced statistically significantly in the astaxanthin group (p = 0.048 and p = 0.047 respectively) during supplementation, but not in the placebo group and the change of 15-hydroxy fatty acid was almost significantly greater (p = 0.056) in the astaxanthin group, as compared with the placebo group. The present study suggests that intestinal absorption of astaxanthin delivered as capsules is adequate, and well tolerated. Supplementation with astaxanthin may decrease in vivo oxidation of fatty acids in healthy men. © Hogrefe & Huber Publishers.

  • 48.
    Kastelein, John J. P.
    et al.
    Univ Amsterdam, Acad Med Ctr, Dept Vasc Med, NL-1100 DD Amsterdam, Netherlands.
    van der Steeg, Wim A.
    Univ Amsterdam, Acad Med Ctr, Dept Vasc Med, NL-1100 DD Amsterdam, Netherlands.
    Holme, Ingar
    Ullevaal Univ Hosp, Ctr Prevent Med, Oslo, Norway.
    Gaffney, Michael
    Pfizer Inc, New York, NY USA.
    Cater, Nilo B.
    Pfizer Inc, New York, NY USA.
    Barter, Philip
    Heart Res Inst, Sydney, NSW, Australia.
    Deedwania, Prakash
    Vet Affairs Cent Calif Healthcare Syst, San Francisco, CA USA.
    Olsson, Anders
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Health Sciences, Internal Medicine . Östergötlands Läns Landsting, Centre for Medicine, Department of Endocrinology and Gastroenterology UHL.
    Boekholdt, S. Matthijs
    Univ Amsterdam, Acad Med Ctr, Dept Vasc Med, NL-1100 DD Amsterdam, Netherlands.
    Demicco, David A.
    Pfizer Inc, New York, NY USA.
    Szarek, Michael
    Pfizer Inc, New York, NY USA.
    LaRosa, John C.
    SUNY Hlth Sci Ctr, Brooklyn, NY 11203 USA.
    Pedersen, Terje R.
    Ullevaal Univ Hosp, Ctr Prevent Med, Oslo, Norway.
    Grundy, S
    Univ Texas SW Med Ctr Dallas, Dallas, TX 75390 USA.
    Lipids, apolipoproteins, and their ratios in relation to cardiovascular events with statin treatment2008In: Circulation, ISSN 0009-7322, E-ISSN 1524-4539, Vol. 117, no 23, p. 3002-3009Article in journal (Refereed)
    Abstract [en]

    Background - Low-density lipoprotein (LDL)cholesterol is the principal target of lipid-lowering therapy, but recent evidence has suggested more appropriate targets. We compared the relationships of on-treatment levels of LDL cholesterol, non-high-density lipoprotein (HDL) cholesterol, and apolipoprotein B, as well as ratios of total/HDL cholesterol, LDL/HDL cholesterol, and apolipoprotein B/A-I, with the occurrence of cardiovascular events in patients receiving statin therapy. Methods and Results - A post hoc analysis was performed that combined data from 2 prospective, randomized clinical trials in which 10 001 ("Treating to New Targets") and 8888 ("Incremental Decrease in End Points through Aggressive Lipid Lowering") patients with established coronary heart disease were assigned to usual-dose or high-dose statin treatment. In models with LDL cholesterol, non-HDL cholesterol and apolipoprotein B were positively associated with cardiovascular outcome, whereas a positive relationship with LDL cholesterol was lost. In a model that contained non-HDL cholesterol and apolipoprotein B, neither was significant owing to collinearity. Total/HDL cholesterol ratio and the apolipoprotein B/A-I ratio in particular were each more closely associated with outcome than any of the individual proatherogenic lipoprotein parameters. Conclusions - In patients receiving statin therapy, on-treatment levels of non-HDL cholesterol and apolipoprotein B were more closely associated with cardiovascular outcome than levels of LDL cholesterol. Inclusion of measurements of the antiatherogenic lipoprotein fraction further strengthened the relationships. These data support the use of non-HDL cholesterol or apolipoprotein B as novel treatment targets for statin therapy. Given the absence of interventions that have been proven to consistently reduce cardiovascular disease risk through raising plasma levels of HDL cholesterol or apolipoprotein A-I, it seems premature to consider the ratio variables as clinically useful.

  • 49.
    Kee Ryu, Sung
    et al.
    Eulji University.
    Mallat, Ziad
    University of Cambridge.
    Benessiano, Joelle
    Paris Descartes University.
    Tedgui, Alain
    Paris Descartes University.
    Olsson, Anders
    Linköping University, Department of Medical and Health Sciences, Internal Medicine. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Heart and Medicine Centre, Department of Endocrinology and Gastroenterology UHL.
    Bao, Weihang
    Pfizer Inc.
    Schwartz, Gregory G
    University of Colorado.
    Tsimikas, Sotirios
    University of Calif San Diego.
    Phospholipase A(2) Enzymes, High-Dose Atorvastatin, and Prediction of Ischemic Events After Acute Coronary Syndromes2012In: Circulation, ISSN 0009-7322, E-ISSN 1524-4539, Vol. 125, no 6, p. 757-U71Article in journal (Refereed)
    Abstract [en]

    Background-Secretory phospholipase A2 (sPLA(2)) and lipoprotein-associated phospholipase A2 (Lp-PLA(2)) are enzyme biomarkers of increased cardiovascular risk and targets of emerging therapeutic agents. Their relationship to cardiovascular events in the setting of high-dose statin therapy compared with placebo in patients with acute coronary syndrome is not known. less thanbrgreater than less thanbrgreater thanMethods and Results-sPLA(2) and Lp-PLA(2) mass and activity were measured in 2587 patients in the Myocardial Ischemia Reduction With Acute Cholesterol Lowering (MIRACL) trial at baseline and after 16 weeks of treatment with atorvastatin 80 mg/d or placebo. Baseline levels of sPLA(2) and Lp-PLA(2) mass and activity were not associated with the primary efficacy measure of the trial of death, myocardial infarction, or unstable angina. However, in the overall cohort, baseline sPLA(2) mass predicted risk of death after multivariable adjustment (hazard ratio for 2-fold increase, 1.30; 95% confidence interval, 1.09 -1.56; P = 0.004). This association remained significant when examined separately in the placebo group but not in the atorvastatin group. Compared with placebo, atorvastatin reduced median sPLA(2) mass (-32.1% versus -23.1%), sPLA(2) activity (-29.5% versus -19.2%), Lp-PLA(2) mass (-35.8% versus -6.2%), and Lp-PLA(2) activity (-24.3% versus 5.4%; P andlt; 0.001 for all). Atorvastatin reduced the hazard of death associated with elevated sPLA(2) mass and activity by approximate to 50%. less thanbrgreater than less thanbrgreater thanConclusions-sPLA(2) mass independently predicts death during a 16-week period after acute coronary syndrome. High-dose atorvastatin significantly reduces sPLA(2) and Lp-PLA(2) mass and activity after acute coronary syndrome and mitigates the risk of death associated with sPLA(2) mass. Atorvastatin may exert antiinflammatory effects on phospholipases that contribute to its therapeutic benefit after acute coronary syndrome.

  • 50. Kinlay, S
    et al.
    Libby, P
    Ganz, P
    Schwartz, GG
    Olsson, Anders
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Health Sciences, Internal Medicine . Östergötlands Läns Landsting, Centre for Medicine, Department of Endocrinology and Gastroenterology UHL.
    Leslie, SJ
    Sasiela, WJ
    Szarek, M
    Early intervention with atorvastatin modulates Th1/Th2 imbalance in patients with acute coronary syndrome: From bedside to bench - Response2004In: Circulation, ISSN 0009-7322, E-ISSN 1524-4539, Vol. 109, no 18, p. E213-E214Other (Other academic)
1234 1 - 50 of 185
CiteExportLink to result list
Permanent link
Cite
Citation style
  • apa
  • harvard1
  • ieee
  • modern-language-association-8th-edition
  • vancouver
  • oxford
  • Other style
More styles
Language
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Other locale
More languages
Output format
  • html
  • text
  • asciidoc
  • rtf