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| 5. |
- Kristenson, Margareta, 1950-, et al.
(author)
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Ultrasound determined carotid and femoral atherosclerosis in Lithuanian and Swedish men : The LiVicordia study
- 2000
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In: Atherosclerosis. - 0021-9150 .- 1879-1484. ; 151:2, s. 501-508
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Journal article (peer-reviewed)abstract
- Coronary heart disease mortality is four times higher in Lithuanian compared to Swedish middle-aged men. Using the same equipment (Acuson XP10 with 5 MHz linear transducer) and staff, we compared the amount of atherosclerosis in carotid and femoral arteries in 100 randomly sampled 50-year-old men in each of the cities Vilnius, Lithuania and Linköping, Sweden. Atherosclerotic plaques were more abundant in Vilnius men compared to Linköping men (53 versus 28% in the common carotid artery, 73 versus 37% in the common femoral artery, P<0.001 for both). Plaques were thicker and more extended in arteries of Vilnius men, and an ultrasound atherosclerosis score was higher in both carotid and femoral arteries (P<0.001 for all). More Vilnius men had a maximal intima-media thickness of the common femoral artery above 1 mm (P<0.005). Stiffness in the common carotid artery was higher in Vilnius men (P<0.001). In a linear regression model of the pooled material, after adjustment for city was made, smoking, systolic blood pressure, low density lipoprotein cholesterol and β-carotene (inversely) significantly contributed to a high total ultrasound score (r2=0.32). These findings show that the higher coronary mortality noted in Lithuanian men goes together with a higher prevalence of early peripheral atherosclerosis.
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| 6. |
- Assman, Gerd, et al.
(author)
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Implications of emerging risk factors for therapeutic intervention
- 2005
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In: NMCD. Nutrition Metabolism and Cardiovascular Diseases. - : Elsevier BV. - 0939-4753 .- 1590-3729. ; 15:5, s. 373-381
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Journal article (peer-reviewed)abstract
- 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.
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| 7. |
- Ballantyne, CM, et al.
(author)
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Influence of low high-density lipoprotein cholesterol and elevated triglyceride on coronary heart disease events and response to simvastatin therapy in 4S
- 2001
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In: Circulation. - 0009-7322 .- 1524-4539. ; 104:25, s. 3046-3051
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Journal article (peer-reviewed)abstract
- 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.
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| 10. |
- Blomqvist, Henrik, 1975-, et al.
(author)
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Monocyte chemoattractant protein‐1 and CC‐chemokine receptor‐2 in severe hypercholesterolaemia
- 2003
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In: Scandinavian Journal of Clinical and Laboratory Investigation. - : Informa UK Limited. - 0036-5513 .- 1502-7686. ; 63:7-8, s. 513-519
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Journal article (peer-reviewed)abstract
- 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.
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| 12. |
- Ekman, Bertil, et al.
(author)
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A dose titration model for recombinant GH substitution aiming at normal plasma concentrations of IGF-I in hypopituitary adults
- 2002
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In: European Journal of Endocrinology. - : Oxford University Press (OUP). - 0804-4643 .- 1479-683X. ; 147:1, s. 49-57
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Journal article (peer-reviewed)abstract
- 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.
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| 15. |
- Hirsch, Mark, et al.
(author)
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Rosuvastatin is cost-effective compared with atorvastatin in reaching cholesterol goals
- 2005
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In: International Journal of Cardiology. - : Elsevier BV. - 0167-5273 .- 1874-1754. ; 104:3, s. 251-256
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Journal article (peer-reviewed)abstract
- 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.
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| 16. |
- Hollman, Gunilla, 1953-, et al.
(author)
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Disease knowledge and adherence to treatment in patients with familial hypercholesterolemia
- 2006
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In: Journal of Cardiovascular Nursing. - 0889-4655 .- 1550-5049. ; 21:2, s. 103-108
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Journal article (peer-reviewed)abstract
- 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.
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| 17. |
- Hollman, Gunilla, 1953-, et al.
(author)
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Familial hypercholesterolaemia and quality of life in family members
- 2003
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In: Preventive Medicine. - 0091-7435 .- 1096-0260. ; 36:5, s. 569-574
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Journal article (peer-reviewed)abstract
- BackgroundAwareness 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.MethodsNames 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.ResultsFamily 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.ConclusionsFamily 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.
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| 21. |
- Hollman, Gunilla, 1953-, et al.
(author)
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Quality of life in patients with familial hypercholesterolaemia
- 2002
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In: Journal of Internal Medicine. - : Wiley. - 0954-6820 .- 1365-2796. ; 251:4, s. 331-337
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Journal article (peer-reviewed)abstract
- 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.
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| 22. |
- Hollman, Gunilla, 1953-, et al.
(author)
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The meaning of quality of life among patients with familial hypercholesterolemia
- 2004
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In: Journal of Cardiovascular Nursing. - 0889-4655 .- 1550-5049. ; 19:4, s. 243-250
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Journal article (peer-reviewed)abstract
- 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.
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| 23. |
- Jardine, Alan G., et al.
(author)
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Fluvastatin prevents cardiac death and myocardial infarction in renal transplant recipients : post-hoc subgroup analyses of the ALERT Study
- 2004
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In: American Journal of Transplantation. - : Elsevier BV. - 1600-6135 .- 1600-6143. ; 4:6, s. 988-995
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Journal article (peer-reviewed)abstract
- Renal transplant recipients have a greatly increased risk of premature cardiovascular disease. The ALERT study was a multicenter, randomized, double-blind, placebo-controlled trial of fluvastatin (40-80 mg/day) in 2102 renal transplant recipients followed for 5-6 years. The main study used a composite cardiac end-point including myocardial infarction, cardiac death and cardiac interventions. Although reduced by fluvastatin, this primary end-point failed to achieve statistical significance thus precluding analysis of predefined subgroups. Therefore, in the present survival analysis, we used an alternative primary end-point of cardiac death or definite nonfatal myocardial infarction (as used in other cardiac outcome trials) which was significantly reduced by Fluvastatin therapy and permits subgroup analysis. Fluvastatin reduced LDL-cholesterol by 1 mmol/L compared with placebo, and the incidence of cardiac death or definite myocardial infarction was reduced from 104 to 70 events (RR 0.65; 95% CI 0.48, 0.88; p = 0.005). Fluvastatin use was associated with reduction in cardiac death or nonfatal myocardial infarction, which achieved statistical significance in many subgroups. The subgroups included patients at lower cardiovascular risk, who were younger, nondiabetic, nonsmokers and without pre-existing CVD. These data support the early introduction of statins following renal transplantation.
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| 24. |
- Kinlay, S, et al.
(author)
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Effect of atorvastatin on risk of recurrent cardiovascular events after an acute coronary syndrome associated with high soluble CD40 ligand in the Myocardial Ischemia Reduction with Aggressive Cholesterol Lowering (MIRACL) study
- 2004
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In: Circulation. - 0009-7322 .- 1524-4539. ; 110:4, s. 386-391
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Journal article (peer-reviewed)abstract
- Background - Patients with acute coronary syndromes have elevated plasma levels of the proinflammatory, prothrombotic cytokine CD40 ligand (sCD40L). Statins inhibit CD40L signaling in vitro, but there are no prospective studies of statins and sCD40L in acute coronary syndromes. Methods and Results - We measured sCD40L in subjects with an acute coronary syndrome enrolled in the Myocardial Ischemia Reduction with Aggressive Cholesterol Lowering (MIRACL) study. Subjects were randomized in this double-blind trial to atorvastatin 80 mg/d or placebo for 16 weeks. Plasma CD40L was measured from 2908 (94%) of 3086 subjects at baseline and 2352 (76%) at 16 weeks. Odds ratios (Ors) and 95% Cis from logistic regression models assessed the risk of recurrent cardiovascular events over 16 weeks (death, nonfatal myocardial infarction, cardiac arrest, and worsening angina requiring rehospitalization) in the placebo group from baseline sCD40L and the effect of atorvastatin on the risk associated with CD40L in all subjects. The effects of atorvastatin on plasma concentrations of CD40L were assessed by Wilcoxon tests. There was a threshold effect, with only high sCD40L (>90th centile) being a risk factor for a recurrent cardiovascular event (OR 1.86, 95% CI 1.25 to 2.77). This risk was abolished by atorvastatin (OR 1.09, 95% CI 0.69 to 1.76), which reduced the risk by 48%. Atorvastatin had only a modest effect on sCD40L (P=0-08). Conclusions - In patients with acute coronary syndromes, atorvastatin abrogated the risk of recurrent cardiovascular events associated with high sCD40L. Early statin therapy after acute coronary syndromes counters the risk associated with elevated sCD40L.
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| 25. |
- Kinlay, S, et al.
(author)
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High-dose atorvastatin enhances the decline in inflammatory markers in patients with acute coronary syndromes in the MIRACL study
- 2003
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In: Circulation. - 0009-7322 .- 1524-4539. ; 108:13, s. 1560-1566
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Journal article (peer-reviewed)abstract
- Background - Inflammation promotes acute coronary syndromes and ensuing clinical complications. Although statins reduce inflammatory markers in asymptomatic adults or in patients with stable angina, the effect of statins on the markedly heightened inflammation in patients with acute coronary syndromes is unknown. Methods and Results - We measured C-reactive protein (CRP), serum amyloid A (SAA), and interleukin 6 (IL-6) in 2402 subjects enrolled the Myocardial Ischemia Reduction with Aggressive Cholesterol Lowering (MIRACL) study. Subjects with unstable angina or non-Q-wave myocardial infarction were randomized to atorvastatin 80 mg/d or placebo within 24 to 96 hours of hospital admission and treated for 16 weeks. The effect of treatment on inflammatory markers was assessed by ANCOVA after adjustment for presenting syndrome, country, and initial level of marker. All 3 markers were markedly elevated at randomization and declined over the 16 weeks in both treatment groups. Compared with placebo, atorvastatin significantly reduced CRP, -83% (95% CI, -84%, -81%) versus -74% (95% CI, -75%, -71%) (P<0.0001) and SAA, -80% (95% CI, -82%, -78%) versus -77% (-79%, -75%) (P=0.0006) but not IL-6, -55% (95% CI, -57%, -53%) versus -53% (95% CI, -55%, -51%) (P=0.3). Reductions in CRP and SAA were observed in patients with unstable angina and non-Q-wave myocardial infarction, with initial LDL cholesterol <3.2 of =3.2 mmol/L (125 mg/dL), age =65 or <65 years, and in men and women. By 16 weeks, CRP was 34% lower with atorvastatin than with placebo. Conclusions - High-dose atorvastatin potentiated the decline in inflammation in patients with acute coronary syndromes. This supports the value of early statin therapy in these patients.
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| 26. |
- Kristenson, Margareta, 1950-, et al.
(author)
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Good self-rated health is related to psychosocial resources and a strong cortisol response to acute stress : The LiVicordia study of middle-aged men
- 2005
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In: International Journal of Behavioral Medicine. - : Springer Science and Business Media LLC. - 1070-5503 .- 1532-7558. ; 12:3, s. 153-160
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Journal article (peer-reviewed)abstract
- Self-rated health (SRH) is a strong predictor for disease and death. The relations among SRH, psychosocial factors, and cortisol dynamics were tested using pooled data from the LiVicordia study of 50-year-old men in Lithuania (n = 94) and Sweden (n = 89), controlling for effect of residence. SRH was assessed by " How would you assess your own health?" A standardized laboratory stress test included measures of cortisol in serum and saliva. Good SRH related to high scale scores of decision latitude, social support at work, coping, self-esteem, and sense of coherence, to low scores of overcommitment (all p < .01) and vital exhaustion (r = -0.40, p < 0.001), to low concentrations of saliva baseline cortisol (r = -.26, p = .001), and to a strong cortisol response to stress (r = .27, p = .001). Findings that good SRH related to favorable psychosocial characteristics and to a dynamic cortisol stress response indicate a possible explanation for observed lower risk for disease and death in this state. Copyright © 2005 by Lawrence Erlbaum Associates, Inc.
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| 27. |
- Li, Wei, 1962-, et al.
(author)
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Alpha-tocopherol and astaxanthin decrease macrophage infiltration, apoptosis and vulnerability in atheroma of hyperlipidaemic rabbits
- 2004
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In: Journal of Molecular and Cellular Cardiology. - : Elsevier BV. - 0022-2828 .- 1095-8584. ; 37:5, s. 969-978
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Journal article (peer-reviewed)abstract
- The composition of atherosclerotic plaques, not just macroscopical lesion size, has been implicated in their susceptibility to rupture and the risk of thrombus formation. By focusing on the quality of lipids, macrophages, apoptosis, collagen, metalloproteinase expression and plaque integrity, we evaluated the possible anti-atherosclerotic effect of the antioxidants α-tocopherol and astaxanthin in Watanabe heritable hyperlipidemic (WHHL) rabbits. Thirty-one WHHL rabbits were divided into three groups and were fed a standard diet, as controls (N =10), or a standard diet with the addition of 500 mg α-tocopherol per kg feed (N =11) or 100 mg astaxanthin per kg feed (N =10) for 24 weeks. We found that both antioxidants, particularly astaxanthin, significantly decreased macrophage infiltration in the plaques although they did not affect lipid accumulation. All lesions in the astaxanthin-treated rabbits were classified as early plaques according to the distribution of collagen and smooth muscle cells. Both antioxidants also improved plaque stability and significantly diminished apoptosis, which mainly occurred in macrophages, matrix metalloproteinase three expressions and plaque ruptures. Although neither antioxidant altered the positive correlations between the lesion size and lipid accumulation, the lesion size and apoptosis were only positively correlated in the control group. Astaxanthin and α-tocopherol may improve plaque stability by decreasing macrophage infiltration and apoptosis in this atherosclerotic setting. Apoptosis reduction by α-tocopherol and astaxanthin may be a new anti-atherogenic property of these antioxidants. © 2004 Elsevier Ltd. All rights reserved.
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| 28. |
- Lind, S, et al.
(author)
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Autosomal recessive hypercholesterolaemia : Normalization of plasma LDL cholesterol by ezetimibe in combination with statin treatment
- 2004
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In: Journal of Internal Medicine. - : Wiley. - 0954-6820 .- 1365-2796. ; 256:5, s. 406-412
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Journal article (peer-reviewed)abstract
- Background. Severe hereditary hypercholesterolaemia is most frequently due to familial hypercholesterolaemia (FH), caused by mutations in the LDL receptor (LDLR) gene. However, a phenotype very similar to FH may also be caused by defects in other genes like the genes for apolipoprotein (apo) B-100 or autosomal recessive hypercholesterolaemia (ARH). Subject. An 8-year-old male of Lebanese origin was diagnosed with severe hypercholesterolaemia and extensive cutaneous and tendon xanthomas. Plasma LDL cholesterol before treatment was 17 mmol L-1, whilst parents and both siblings had normal levels. Diagnosis. Degradation of 125I-labelled LDL in blood lymphocytes was reduced, but not abolished. Sequencing analysis of the LDLR and apoB-100 genes were negative, whilst a splice acceptor mutation in intron 1 (IVS 1 - 1G>C) was detected in the ARH gene. The patient was homozygous for the mutation, whilst the parents were heterozygous. These findings were in agreement with a diagnosis of ARH. Treatment and clinical course. Monthly LDL apheresis and atorvastatin 120 mg daily reduced LDL cholesterol preapheresis level to 4.8 mmol L-1. When ezetimibe was given 10 mg day-1 in combination with rosuvastatin 80 mg day-1, LDL cholesterol was further lowered to 1.6 mmol L-1, which made apheresis unnecessary. Cutaneous and tendon xanthomas disappeared completely and the intima-media thickness of the common carotid arteries decreased. At age 23 he developed a small myocardial infarction. Conclusion. ARH should be considered in cases of severe hypercholesterolaemia with a pattern of recessive inheritance. Combination therapy with high-dose statin and ezetimibe seems to be the treatment of choice in ARH and may reduce or eliminate the need for LDL apheresis treatment.
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| 29. |
- Lindgren, Peter, et al.
(author)
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Cost-effectiveness of high-dose atorvastatin compared with regular dose simvastatin
- 2007
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In: European Heart Journal. - : Oxford University Press (OUP). - 0195-668X .- 1522-9645. ; 28:12, s. 1448-1453
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Journal article (peer-reviewed)abstract
- Aims: The aim of the study was to evaluate the long-term cost-effectiveness of high-dose atorvastatin when compared with generic simvastatin for secondary prevention in Denmark, Finland, Norway, and Sweden based on the recently completed IDEAL trial. Methods and results: The IDEAL trial showed that high-dose treatment with atorvastatin was associated with fewer non-fatal myocardial infarctions (MI) or coronary heart disease death (RR 0.89, 95% CI 0.78-1.01) and major cardiovascular events by (RR 0.87, 95% CI 0.77-0.98) or any coronary event (RR 0.84, 95% CI 0.76-0.91) than simvastatin with no significant difference in the number of serious adverse events. Costs during the trial period was estimated based on the trial data and a Markov model was constructed where the risk of MIs and revascularization procedures and the long-term costs, quality of life, and mortality associated with these events was simulated. Costs were based on resource consumptions recorded in the trial multiplied with recent unit costs from each country. Both direct health care costs and indirect costs (costs from lost production due to work absence) were included. Intervention lasted for the duration of the trial (4.8 years) while health-effects and costs are predicted for the lifespan of the patient. The main outcome was quality adjusted life-years (QALY) gained. High-dose treatment was predicted to lead to a mean increase in survival of 0.049 years per patient and 0.033 QALYs gained. The cost to gain one QALY was predicted to 47 197€ (Denmark), 62 639€ (Finland), 35 210€ (Norway), and 43 667€ (Sweden), with cost-effectiveness ratio decreasing with higher risk. Conclusion: In the prevention of cardiovascular events among patients with a previous MI, high-dose atorvastatin appears to be a cost-effective strategy when compared with generic simvastatin 20-40 mg in Denmark, Norway, and Sweden. In Finland, it is cost-effective in high-risk patients. The key driver of the cost-effectiveness is the price-difference between 80 mg atorvastatin and generic simvastatin. © The European Society of Cardiology 2007. All rights reserved.
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| 30. |
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| 31. |
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| 32. |
- Nielsen, Niels Erik, et al.
(author)
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Plasma lipoprotein particle concentrations in postmenopausal women with unstable coronary artery disease : Analysis of diagnostic accuracy using receiver operating characteristics
- 2000
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In: Journal of Internal Medicine. - : Wiley. - 0954-6820 .- 1365-2796. ; 247:1, s. 43-52
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Journal article (peer-reviewed)abstract
- Background.The contribution of plasma lipids to cardiovascular risk is usually evaluated by measuring plasma concentrations of total cholesterol, triglycerides and HDL cholesterol, and calculating LDL cholesterol concentration. We investigated plasma concentrations of apolipoproteins and lipoprotein particles in women with unstable coronary artery disease (CAD) to evaluate whether these, better than the routine lipid status, could differentiate women with and without coronary atherosclerosis.Methods. Blood samples for lipid analyses were collected from 119 angiographically examined postmenopausal 49–79-year-old women with unstable CAD, and from 101 age-matched controls. Mean plasma concentrations were compared and the discriminatory ability of the different variables were tested using receiver operating characteristics (ROC).Results. At coronary angiography 19% had normal vessels and 81% had coronary atherosclerosis. A disturbed triglyceride metabolism was the most pronounced lipid abnormality in women with unstable CAD and coronary atherosclerosis. ROC showed that none of the evaluated variables had a particularly high discriminatory power regarding unstable CAD or coronary atherosclerosis. The ratio cholesterol/HDL cholesterol was best with an ROC area of 0.79. Furthermore, the newer lipid variables, i.e. lipoprotein particles and apolipoproteins, were no better than the traditional variables.Conclusion. Lipoprotein changes reflecting a disturbed triglyceride metabolism are most pronounced in women with unstable CAD and coronary atherosclerosis. Lipoprotein particles and apolipoproteins alone were no better than lipids and lipoproteins in separating women with from those without coronary atherosclerosis. Our study does not support the measurement of apolipoproteins and lipoprotein particles on the basis of diagnostic accuracy alone.
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| 33. |
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| 34. |
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| 35. |
- Olsson, Anders, 1940-, et al.
(author)
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A 52-week, multicenter, randomized, parallel-group, double-blind, double-dummy study to assess the efficacy of atorvastatin and simvastatin in reaching low-density lipoprotein cholesterol and triglyceride targets: The treat-to-target (3T) study
- 2003
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In: Clinical Therapeutics. - 0149-2918 .- 1879-114X. ; 25:1, s. 119-138
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Journal article (peer-reviewed)abstract
- Background: Guidelines for the prevention of coronary heart disease call for low-density lipoprotein cholesterol (LDL-C) reduction as the primary target of treatment and reduction of triglycerides (TG) as an additional target. Objective: The purpose of this study was to investigate the ability of atorvastatin and simvastatin to reduce LDL-C and TG concentrations and to meet 3 target lipid levels: LDL-C less than or equal to2.6 mmol/L; TG less than or equal to1.5 mmol/L; and both LDL-C less than or equal to2.6 mmol/L and TG less than or equal to1.5 mmol/L. Methods: The Treat-to-Target (3T) Study was a 52-week, multicenter, randomized, parallel-group study. Using the double-blind, double-dummy technique, adult patients aged 35 to 75 years with cardiovascular disease and dyslipidemia, defined as LDL-C concentration less than or equal to4.0 mmol/L (greater than or equal to155 mg/dL), were randomised in a 1:1 ratio to receive once-daily oral treatment with 20 mg atorvastatin or 20 mg simvastatin. Fasting (12-hour) blood samples for the estimation of lipid levels and clinical laboratory values were collected after 4, 8, 12, 26, and 52 weeks. The dose was doubled after 12 weeks if the target National Cholesterol Education Program level of LDL-C (less than or equal to2.6 mmol/L [100 mg/dL]) was not reached at 8 weeks. Results: The intent-to-treat analysis included 552 patients (418 men, 134 women) randomized to receive atorvastatin and 535 (404 men, 131 women) randomized to receive simvastatin. The number of patients enrolled in the study allowed the evaluation of the drugs' effects on TG. Patient demographic characteristics were similar for the 2 treatment groups, and there were no differences in baseline lipid values. Compared with simvastatin, atorvastatin produced significantly greater reductions in LDL-C (8 weeks: -46% vs -40%, P < 0.001; 52 weeks: -49% vs -44%, P < 0.001) and in TG (8 weeks: -23% vs -14%, P < 0.001; 52 weeks: -24% vs -16%, P < 0.001). Compared with simvastatin-treated patients, a significantly greater number of atorvastatin-treated patients reached the LDL-C target after 8 weeks (45% vs 24%; P < 0.001). Fewer atorvastatin patients needed to have their dose doubled; nevertheless more atorvastatin patients reached the LDL-C target after 52 weeks (61% vs 41%; P < 0.001). Both statins were well tolerated. Muscular symptoms occurred in 12 patients (2.2%) in the atorvastatin group and in 13 patients (2.4%) in the simvastatin group. Conclusions: Atorvastatin 20 or 40 mg/d for up to 1 year of treatment was significantly more effective than simvastatin 20 or 40 mg/d in reducing LDL-C and TG levels and at achieving recommended lipid targets in this selected patient population with cardiovascular disease and dyslipidemia. Both statins were well tolerated.
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| 36. |
- Olsson, Anders, 1940-
(author)
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A new statin : A new standard
- 2001
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In: American Journal of Managed Care. - 1096-1860. ; 7, s. 152-154
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Journal article (peer-reviewed)
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| 37. |
- Olsson, Anders, 1940-, et al.
(author)
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A pharmacoeconomic evaluation of aggressive cholesterol lowering in Sweden
- 2004
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In: International Journal of Cardiology. - : Elsevier BV. - 0167-5273 .- 1874-1754. ; 96:1, s. 51-57
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Journal article (peer-reviewed)abstract
- Objective: To estimate the short-term healthcare costs and incremental cost per event avoided, associated with aggressive atorvastatin treatment in patients with acute coronary syndrome in Sweden. Methods: The total expected 16-week healthcare costs per patient on atorvastatin 80 mg per day and placebo were compared using clinical outcomes data from The Myocardial Ischemia Reduction with Aggressive Cholesterol Lowering (MIRACL) study and Swedish cost data sources. The incremental cost per event avoided was also assessed for. The clinical outcomes measured in this pharmacoeconomic analysis included: death, cardiac arrest, non-fatal myocardial infarction, fatal myocardial infarction, angina pectoris, non-fatal stroke, congestive heart failure, and surgical or percutaneous coronary revascularizations. All direct medical costs were taken into account. Results: The probability of the occurrence of an event was 40.4% per patient in the placebo cohort and 36.6% per patient in the atorvastatin cohort. The total expected cost per patient was SEK 17,887 (1950. 21€11 EUR=9.17231 SEK.) in the placebo group and SEK 18,465 (2013.06€) in the atorvastatin group, resulting in an incremental cost of SEK 578 (63.0137€) per patient. The cost per event avoided was SEK 15,076 (1643.64€). Sixty six percent of the cost of atorvastatin treatment was offset by the cost savings obtained through the reduction in the number of events in the atorvastatin group compared to the placebo group. Conclusions: In Sweden, the clinical benefits of aggressive short-term atorvastatin treatment administered within a few days after acute coronary syndrome is associated with a substantial hospitalization cost offset secondary to the clinical benefits of atorvastatin. © 2003 Elsevier Ireland Ltd. All rights reserved.
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| 38. |
- Olsson, Anders, 1940-
(author)
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A to Z
- 2005
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In: Information från Läkemedelsverket. - 1101-7104. ; 1, s. 16-17
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Journal article (pop. science, debate, etc.)
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| 39. |
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| 40. |
- Olsson, Anders, 1940-, et al.
(author)
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Are early clinical effects of cholesterol lowering mediated through effects on inflammation?
- 2002
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In: Acta Physiologica Scandinavica. - 0001-6772 .- 1365-201X. ; 176:2, s. 147-150
-
Journal article (peer-reviewed)abstract
- In a randomized, double-blind trial in 3086 patients with unstable angina pectoris or non-Q wave myocardial infarction we investigated if 80 mg of atorvastatin daily could improve outcome of cardiovascular events during a short period of time (16 weeks) compared with placebo. Baseline LDL cholesterol was 3.2 mmol L-1 (124 mg dL-1) and decreased by 40% to 1.9 mmol L-1 (72 mg dL-1) during atorvastatin treatment. The primary endpoint, which was a composite of death, non-fatal acute myocardial infarction, cardiac arrest with resuscitation or recurrent symptomatic myocardial ischaemia with objective evidence and requiring emergency rehospitalization occurred in 228 patients (14.8%) in the atorvastatin group and 269 patients (17.4%) in the placebo group. The relative risk was 0.84 and 95% confidence interval was 0.70-1.00 (P = 0.048). Thus for patients with acute coronary syndromes, lipid-lowering therapy with high dose atorvastatin reduces recurrent ischaemic events in the short-term. A possible mechanism behind this rapid clinical effect induced by statin treatment is on inflammatory processes. Recent studies strongly suggest that acute T-cell activation is involved in the pathogenesis of unstable angina. In another study we investigated whether circulating T cells showed signs of activation in patients with stable angina pectoris (SA). Systemic venous blood samples were taken from 38 men with SA and 42 healthy controls. The T-cell receptor expression was assessed by three-colour flow cytometry using monoclonal antibodies against CD3, CD4, CD8, CD25 and human leucocyte antigen (HLA)-DR. Soluble interleukin-2 receptor (sIL-2R) was measured as the circulating form in serum. Levels of circulating CD3+ and CD4+ T cells tended to be higher in patients compared with controls. Patients were also shown to have a significant increase in CD4+ T cells expressing the activation markers CD25 (P < 0.05) and HLA-DR (P < 0.01). Furthermore, serum levels of sIL-2R were significantly higher (P < 0.001) in patients than in controls. We also observed that the T-cell response was more pronounced in patients without simvastatin treatment (n = 18) compared with simvastatin-treated patients (n = 20). In conclusion, our findings indicate that a continuous immune system activation takes place in patients with chronic angina pectoris, predominantly involving proliferation of CD4+ T cells. Statin treatment seems to be able to decrease this inflammatory response.
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| 41. |
- Olsson, Anders, 1940-
(author)
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Are lower levels of low-density lipoprotein cholesterol beneficial? A review of recent data
- 2006
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In: Current Atherosclerosis Reports. - : Springer Science and Business Media LLC. - 1523-3804 .- 1534-6242. ; 8:5, s. 382-389
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Journal article (peer-reviewed)abstract
- In the 1960s, epidemiologic studies established a link between elevated serum cholesterol and increased risk of cardiovascular events. Extensive clinical trial data subsequently highlighted 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (ie, statins) as the most effective pharmacotherapy for lowering low-density lipoprotein (LDL) cholesterol, and showed that statin-mediated LDL cholesterol reductions were associated with significant improvements in cardiovascular outcomes. Such findings are reflected in current cardiovascular disease management guidelines, which focus on LDL cholesterol as the primary therapeutic target. These guidelines recommend target LDL cholesterol levels. However, a number of clinical trials have failed to identify an LDL cholesterol threshold level below which no further cardiovascular risk reduction occurs. Such findings suggest that optimal risk reduction may require greater reductions in LDL cholesterol than are currently being achieved. This review examines recent data highlighting the benefits of more pronounced LDL cholesterol reductions and considers how this could be achieved in clinical practice when many patients are not even reaching current targets. Copyright © 2006 by Current Science Inc.
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| 42. |
- Olsson, Anders, 1940-, et al.
(author)
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Can LDL cholesterol be too low? Possible risks of extremely low levels
- 2017
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In: Journal of Internal Medicine. - : WILEY. - 0954-6820 .- 1365-2796. ; 281:6, s. 534-553
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Research review (peer-reviewed)abstract
- Following the continuous accumulation of evidence supporting the beneficial role of reducing low-density lipoprotein cholesterol (LDL-C) levels in the treatment and prevention of atherosclerotic cardiovascular disease and its complications, therapeutic possibilities now exist to lower LDL-C to very low levels, similar to or even lower than those seen in newborns and nonhuman species. In addition to the important task of evaluating potential side effects of such treatments, the question arises whether extremely low LDL-C levels per se may provoke adverse effects in humans. In this review, we summarize information from studies of human cellular and organ physiology, phenotypic characterization of rare genetic diseases of lipid metabolism, and experience from clinical trials. Specifically, we emphasize the importance of the robustness of the regulatory systems that maintain balanced fluxes and levels of cholesterol at both cellular and organismal levels. Even at extremely low LDL-C levels, critical capacities of steroid hormone and bile acid production are preserved, and the presence of a cholesterol blood-brain barrier protects cells in the central nervous system. Apparent relationships sometimes reported between less pronounced low LDL-C levels and disease states such as cancer, depression, infectious disease and others can generally be explained as secondary phenomena. Drug-related side effects including an increased propensity for development of type 2 diabetes occur during statin treatment, whilst further evaluation of more potent LDL-lowering treatments such as PCSK9 inhibitors is needed. Experience from the recently reported and ongoing large event-driven trials are of great interest, and further evaluation including careful analysis of cognitive functions will be important. This is an article from the symposium: Risks and benefits of Extremely Low LDL Cholesterol.
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| 43. |
- Olsson, Anders, 1940-, et al.
(author)
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Comparison of the efficacy and tolerability of fluvastatin extended-release and immediate-release formulations in the treatment of primary hypercholesterolemia : A randomized trial
- 2001
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In: Clinical Therapeutics. - 0149-2918 .- 1879-114X. ; 23:1, s. 45-61
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Journal article (peer-reviewed)abstract
- Background: A new extended-release (ER) formulation of fluvastatin 80 mg has been developed for once-daily treatment of primary hypercholesterolemia. Objective: The purpose of this study was to compare the lipid-lowering efficacy and tolerability of fluvastatin ER (80 mg once daily) versus fluvastatin immediate-release (IR) (40 mg once or twice daily). Methods: Following a 4-week placebo/dietary run-in period, patients with primary hypercholesterolemia type IIa or IIb (low-density lipoprotein cholesterol [LDL-C] =160 mg/dL and triglycerides [TG] =400 mg/dL) were randomized (2:1:1) to receive fluvastatin ER 80 mg once daily at bedtime (QPM), fluvastatin IR 40 mg QPM, or fluvastatin IR 40 mg BID for 24 weeks. Patients who had homozygous familial hypercholesterolemia, type I, III, IV, V, or secondary hyperlipoproteinemia, diabetes, or evidence of liver or renal impairment were excluded. At weeks 0, 2, 4, 8, 12, 16, 20, and 24 of the active-treatment period, levels of LDL-C, high-density lipoprotein cholesterol (HDL-C), TG, and total cholesterol (TC) were measured. Results: Of the 1183 patients enrolled, 695 were randomly assigned to treatment, 346 to fluvastatin ER 80 mg QPM, 174 to fluvastatin IR 40 mg QPM, and 175 to fluvastatin IR 40 mg BID. Patients were well matched between groups, with a mean age of-56 years and body mass index of 27 kg/m2, 56.0% of patients (389/695) were female and 97.7% (679/695) were white. Fluvastatin ER 80 mg QPM lowered LDL-C levels significantly more than did fluvastatin IR 40 mg QPM (33.7% vs 24.4%, P < 0.001) and as effectively as fluvastatin IR 40 mg BID (33.9%). More than half of the patients administered fluvastatin ER 80 mg QPM and IR 40 mg BID achieved reductions in LDL-C levels of =35%, more than half of those administered fluvastatin IR 40 mg QPM experienced reductions in LDL-C levels of =25%. The mean reductions in LDL:HDL ratio, TC, and apolipoprotein B levels in the fluvastatin ER 80 mg QPM group were significantly greater than the reductions in the IR 40 mg QPM group (P < 0.001). In patients with mixed dyslipidemia, fluvastatin ER 80 mg reduced triglycerides by 21.8% (median 28%) and increased HDL-C by 14.5%. Fluvastatin ER 80 mg QPM was well tolerated, with incidences of clinically notable elevations in alanine aminotransferase, aspartate aminotransferase, and creatine kinase levels and musculoskeletal adverse events comparable to those in the IR 40 mg QPM group. Conclusion: The ER 80-mg formulation of fluvastatin is effective and well tolerated as a once-daily starting and maintenance treatment for primary hypercholesterolemia.
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| 44. |
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| 45. |
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| 46. |
- Olsson, Anders, 1940-, et al.
(author)
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Early initiation of treatment with statins in acute coronary syndromes
- 2002
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In: Annals of Medicine. - : Informa UK Limited. - 0785-3890 .- 1365-2060. ; 34:1, s. 37-41
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Journal article (peer-reviewed)abstract
- Statins may act rapidly to reverse abnormalities of the arterial wall that may predispose to recurrent ischemic events after acute coronary syndromes. Such abnormalities are endothelial dysfunction, a local inflammatory response, and an exaggerated thrombogenic tendency. In one study almost 20 000 patients with first myocardial infarction were studied with regard to statin treatment (28%) or not. Baseline characteristics were adjusted using multivariate regression analysis including propensity analysis. One year mortality was 3.7/5.0% in statin/not statin groups, respectively, P = 0.001, relative risk 0.75. In another study of more than 20 000 patients, 18% were prescribed statin after an acute coronary syndrome and followed for six months. Propensity analysis was performed in this study as well. Deaths in statin/not statin groups were 1.7/3.5%, P < 0.0001, relative risk 0.48. In the Myocardial Ischemia Reduction with Aggressive Cholesterol Lowering (MIRACL), a double-blind randomized, placebo-controlled intervention study, 3086 patient with acute non-Q-wave coronary syndromes were allocated immediately in hospital to receive atorvastatin 80 mg daily or placebo for four months. No lower limit for plasma LDL cholesterol was used. Primary endpoint was time to first occurrence of death, non-fatal myocardial infarction, cardiac arrest, and worsening angina with objective evidence of ischemia. This was significantly reduced compared to the placebo group by 2.4% (14.8 versus 17.2%, relative risk 0.84, P = 0.048). Atorvastatin also reduced significantly fatal or non-fatal strokes. Possible mechanisms behind these acute beneficial effects are discussed. The studies highlight the importance of treatment with a statin in the early management of acute coronary syndromes and the need to incorporate this therapeutic strategy in national guidelines and treatment recommendations.
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| 47. |
- Olsson, Anders, 1940-, et al.
(author)
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Effects of rosuvastatin and atorvastatin compared over 52 weeks of treatment in patients with hypercholesterolemia
- 2002
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In: American Heart Journal. - : Elsevier BV. - 0002-8703 .- 1097-6744. ; 144:6, s. 1044-1051
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Journal article (peer-reviewed)abstract
- Background: Despite the demonstrated benefits of low-density lipoprotein cholesterol (LDL-C) reduction in reducing the risk of coronary heart disease, many patients receiving lipid-lowering therapy fail to achieve LDL-C goals. We compared the effects of rosuvastatin and atorvastatin in reducing LDL-C and achieving LDL-C goals in patients with primary hypercholesterolemia. Methods and Results: In this 52-week, randomized, double-blind, multicenter trial (4522IL/0026), 412 patients with LDL-C 160 to <250 mg/dL received a 5-mg dose of rosuvastatin (n = 138), a 10-mg dose of rosuvastatin (n = 134), or a 10-mg dose of atorvastatin (n = 140) for 12 weeks, during the following 40 weeks, dosages could be sequentially doubled up to 80 mg if National Cholesterol Education Program Adult Treatment Panel II (ATP-II) LDL-C goals were not achieved. At 12 weeks, 5- and 10-mg doses of rosuvastatin were associated with significantly greater LDL-C reductions than 10-mg doses of atorvastatin (46% and 50% vs 39%, both P < .001). At 12 weeks, both rosuvastatin dosages brought more patients to within ATP-II and European LDL-C goals than atorvastatin (86% and 89% vs 73% and 75%, and 86% vs 55%, respectively). At 52 weeks, compared with atorvastatin, both initial rosuvastatin treatment groups significantly reduced LDL-C (47% and 53% vs 44%, P < .05 and P < .001). Overall, more patients in the initial rosuvastatin 10-mg group achieved their ATP-II LDL-C goal than those in the initial atorvastatin 10-mg group (98% vs 87%), with 82% of patients treated with rosuvastatin achieving their goal at the 10-mg starting dosage without the need for titration, compared with 59% of patients treated with atorvastatin. Both treatments were well tolerated over 52 weeks. Conclusion: Compared with atorvastatin, rosuvastatin produced greater reductions in LDL-C, which may offer advantages in LDL-C goal attainment over existing lipid-lowering therapies.
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| 48. |
- Olsson, Anders, 1940-
(author)
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En ny sorts studie behövs.
- 1999
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In: Läkartidningen. - 0023-7205 .- 1652-7518. ; 96, s. 1949-1949
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Journal article (pop. science, debate, etc.)
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| 49. |
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| 50. |
- Olsson, Anders, 1940-, et al.
(author)
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High-density lipoprotein, but not low-density lipoprotein cholesterol levels influence short-term prognosis after acute coronary syndrome : Results from the MIRACL trial
- 2005
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In: European Heart Journal. - : Oxford University Press (OUP). - 0195-668X .- 1522-9645. ; 26:9, s. 890-896
-
Journal article (peer-reviewed)abstract
- Aims: Patients with acute coronary syndrome (ACS) in the Myocardial lschaemia Reduction with Aggressive Cholesterol Lowering (MIRACL) study had diminished cardiovascular events after 16 weeks of treatment of atorvastatin 80 mg daily. We determined whether plasma lipoproteins at baseline and then at 6 weeks after randomization predicted clinical outcome. Methods and results: Cox proportional hazards models were constructed to determine relations between lipoproteins and clinical endpoint events. Baseline LDL cholesterol (LDL-C) did not predict outcome. In contrast, baseline HDL-C predicted outcome with a hazard ratio of 0.986 per mg/dL increment in HDL-C, P < 0.001, indicating 1.4% reduction in risk for each 1 mg/dL increase in HDL-C. Atorvastatin treatment profoundly lowered LDL-C, but had minimal effect on HDL-C. Neither Week 6 LDL-C nor absolute change of LDL-C from baseline by Week 6 had any significant impact on clinical endpoints occurring between Week 6 and Week 16 after randomization. Conclusion Plasma HDL-C, but not LDL-C, measured in the initial stage of ACS predicts the risk of recurrent cardiovascular events over the ensuing 16 weeks. LDL-C reduction does not account for the clinical risk reduction with atorvastatin treatment after ACS. This finding may suggest that the clinical benefit of atorvastatin after ACS is mediated by qualitative changes in the LDL particle and/or by non-lipid (pleiotropic) effects of the drug.
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