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1.
  • Axelsson, Magnus, et al. (author)
  • GRB110721A : AN EXTREME PEAK ENERGY AND SIGNATURES OF THE PHOTOSPHERE
  • 2012
  • In: Astrophysical Journal Letters. - 2041-8205. ; 757:2
  • Journal article (peer-reviewed)abstract
    • GRB110721A was observed by the Fermi Gamma-ray Space Telescope using its two instruments, the Large Area Telescope (LAT) and the Gamma-ray Burst Monitor (GBM). The burst consisted of one major emission episode which lasted for similar to 24.5 s (in the GBM) and had a peak flux of (5.7 +/- 0.2) x 10(-5) erg s(-1) cm(-2). The time-resolved emission spectrum is best modeled with a combination of a Band function and a blackbody spectrum. The peak energy of the Band component was initially 15 +/- 2 MeV, which is the highest value ever detected in a GRB. This measurement was made possible by combining GBM/BGO data with LAT Low Energy events to achieve continuous 10-100 MeV coverage. The peak energy later decreased as a power law in time with an index of -1.89 +/- 0.10. The temperature of the blackbody component also decreased, starting from similar to 80 keV, and the decay showed a significant break after similar to 2 s. The spectrum provides strong constraints on the standard synchrotron model, indicating that alternative mechanisms may give rise to the emission at these energies.
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  • Palmer, M. K., et al. (author)
  • Comparing a novel equation for calculating low-density lipoprotein cholesterol with the Friedewald equation: A VOYAGER analysis
  • 2019
  • In: Clinical Biochemistry. - : Elsevier BV. - 0009-9120 .- 1873-2933. ; 64, s. 24-29
  • Journal article (peer-reviewed)abstract
    • Treating elevated low-density lipoprotein cholesterol (LDL-C) to risk-stratified target levels is recommended in several guidelines. Thus, accurate estimation of LDL-C is required. LDL-C is typically calculated using the Friedewald equation: (total cholesterol) - (non-high-density lipoprotein cholesterol [non-HDL-C]) - (triglycerides [TGs]/5). As the equation uses a fixed value equal to 5 as a divisor for TGs, it does not account for inter-individual variability, often resulting in underestimation of risk and potentially undertreatment. It is specifically inapplicable in patients with fasting triglycerides >= 400 mg/dL. A novel method of LDL-C calculation was derived and validated by Martin et al.: (non-HDL-C) - (triglycerides/adjustable factor). This equation uses an adjustable factor, the median TG:very-low-density lipoprotein cholesterol ratio in strata defined by levels of TG and non-HDLC, as divisor for TGs, and the adjustable factor ranging from 3 to 12 has been shown to provide more accurate estimates of LDL-C compared with the Friedewald equation using a direct assay as the gold standard. We used 70,209 baseline and on-treatment lipid values from the VOYAGER meta-analysis database to determine the difference in calculated LDL-C values using the Friedewald and novel equations. In patients with TGs < 400 mg/dL, LDL-C values calculated using the novel equation were plotted against those calculated using the Friedewald equation. The novel equation generally resulted in LDL-C values greater than the Friedewald calculation, with differences increasing with decreasing LDL-C levels; 23% of individuals who reached a LDL-C target of 70 mg/dL with the Friedewald equation did not achieve this target when the novel equation was used to calculate LDL-C; these figures were 8% and 2% for < 100 mg/dL and < 130 mg/dL targets, respectively. In patients with triglycerides >= 400 mg/dL, in whom the Friedewald equation is not valid, lipid values calculated using the novel equation were compared with those obtained by beta-quantification. Values calculated with the novel equation did not appear to be closely related with those calculated by beta-quantification in these patients. In conclusion, the novel equation provides a higher estimation of exact LDL-C values than the Friedewald equation, particularly in patients with low LDL-C levels, which may result in undertreatment of some patients whose LDL-C was calculated using the Friedewald method. However, neither may be suitable for patients with TG >= 400 mg/dL.
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  • Cederstrom, S., et al. (author)
  • New candidate genes for ST-elevation myocardial infarction
  • 2020
  • In: Journal of Internal Medicine. - : Wiley. - 0954-6820 .- 1365-2796. ; 287:1, s. 66-77
  • Journal article (peer-reviewed)abstract
    • Background Despite extensive research in atherosclerosis, the mechanisms of coronary atherothrombosis in ST-elevation myocardial infarction (STEMI) patients are undetermined. Objectives Our aim was to find candidate genes involved in STEMI by analysing leucocyte gene expression in STEMI patients, without the influence of secondary inflammation from innate immunity, which was assumed to be a consequence rather than the cause of coronary atherothrombosis. Methods Fifty-one patients were included at coronary angiography because of STEMI. Arterial blood was sampled in the acute phase (P1), at 24-48 h (P2) and at 3 months (P3). Leucocyte RNA was isolated and gene expression analysis was performed by Affymetrix Human Transcriptome Array 2.0. By omission of up- or downregulated genes at P2, secondary changes from innate immunity were excluded. Genes differentially expressed in P1 when compared to the convalescent sample in P3 were determined as genes involved in STEMI. Results Three genes were upregulated at P1 compared to P3; ABCG1 (P = 5.81 x 10(-5)), RAB20 (P = 3.69 x 10(-5)) and TMEM2 (P = 7.75 x 10(-6)) whilst four were downregulated; ACVR1 (P = 9.01 x 10(-5)), NFATC2IP (P = 8.86 x 10(-5)), SUN1 (P = 3.87 x 10(-5)) and TTC9C (P = 7.18 x 10(-6)). These genes were also highly expressed in carotid atherosclerotic plaques. Conclusions We found seven genes involved in STEMI. The study is unique regarding the blood sampling in the acute phase and omission of secondary expressed genes from innate immunity. However, the results need to be replicated by future studies.
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  • Edfors, R., et al. (author)
  • Use of proteomics to identify biomarkers associated with chronic kidney disease and long-term outcomes in patients with myocardial infarction
  • 2020
  • In: Journal of Internal Medicine. - : Wiley. - 0954-6820 .- 1365-2796. ; 288:5, s. 581-592
  • Journal article (peer-reviewed)abstract
    • Background Patients with chronic kidney disease (CKD) have poor outcomes following myocardial infarction (MI). We performed an untargeted examination of 175 biomarkers to identify those with the strongest association with CKD and to examine the association of those biomarkers with long-term outcomes. Methods A total of 175 different biomarkers from MI patients enrolled in the Swedish Web-System for Enhancement and Development of Evidence-Based Care in Heart Disease Evaluated According to Recommended Therapies (SWEDEHEART) registry were analysed either by a multiple reaction monitoring mass spectrometry assay or by a multiplex assay (proximity extension assay). Random forests statistical models were used to assess the predictor importance of biomarkers, CKD and outcomes. Results A total of 1098 MI patients with a median estimated glomerular filtration rate of 85 mL min(-1)/1.73 m(2)were followed for a median of 3.2 years. The random forests analyses, without and with adjustment for differences in demography, comorbidities and severity of disease, identified six biomarkers (adrenomedullin, TNF receptor-1, adipocyte fatty acid-binding protein-4, TNF-related apoptosis-inducing ligand receptor 2, growth differentiation factor-15 and TNF receptor-2) to be strongly associated with CKD. All six biomarkers were also amongst the 15 strongest predictors for death, and four of them were amongst the strongest predictors of subsequent MI and heart failure hospitalization. Conclusion In patients with MI, a proteomic approach could identify six biomarkers that best predicted CKD. These biomarkers were also amongst the most important predictors of long-term outcomes. Thus, these biomarkers indicate underlying mechanisms that may contribute to the poor prognosis seen in patients with MI and CKD.
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  • Karlson, Björn W., 1953, et al. (author)
  • A VOYAGER Meta-Analysis of the Impact of Statin Therapy on Low-Density Lipoprotein Cholesterol and Triglyceride Levels in Patients With Hypertriglyceridemia
  • 2016
  • In: American Journal of Cardiology. - : Elsevier BV. - 0002-9149 .- 1879-1913. ; 117:9, s. 1444-1448
  • Journal article (peer-reviewed)abstract
    • Elevated triglyceride (TG) levels are associated with increased cardiovascular disease risk. In patients with mild-to-moderate hypertriglyceridemia, defined by the European Atherosclerosis Society Consensus Panel as a TG level of 177 to 885 mg/dl (2.0 to 10.0 mmol/L), low-density lipoprotein cholesterol (LDL-C) reduction remains the primary treatment goal. Using data from the indiVidual patient meta-analysis Of statin therapY in At risk Groups: Effects of Rosuvastatin, atorvastatin and simvastatin (VOYAGER) meta-analysis, we analyzed LDL-C and TG reductions in patients with baseline TG 2177 mg/dl (>= 2.0 mmol/L). Least squares mean percentage change from baseline in LDL-C and TG was compared using 15,800 patient exposures to rosuvastatin 5 to 40 mg, atorvastatin 10 to 80 mg, and simvastatin 10 to 80 mg in patients with baseline TG >= 177 mg/dl (>= 2.0 mmol/L). Comparisons were made using mixed-effects models with data only from studies directly comparing treatments by randomized design. Mean LDL-C reductions ranged from -26.9% to -55.5%. Rosuvastatin 10 to 40 mg resulted in significantly greater LDL-C reductions than equal or double doses of atorvastatin and simvastatin (p <0.05). Mean TG reductions ranged from -15.1% to -31.3%. Rosuvastatin 10 mg resulted in significantly greater TG reductions than atorvastatin 10 mg (p <0.05). Rosuvastatin 20 and 40 mg resulted in TG reductions similar to those with equal doses of atorvastatin. Rosuvastatin 10 to 40 mg resulted in significantly greater TG reductions than equal or double doses of simvastatin (p <0.05). In conclusion, in patients with hypertriglyceridemia, LDL-C reduction was substantial and dependent on the choice and dose of statin. TG reduction was numerically less than for LDL-C, and additional TG-lowering therapy may be considered to further reduce residual cardiovascular risk. (C) 2016 Elsevier Inc. All rights reserved.
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  • Karlson, Björn W., 1953, et al. (author)
  • Achievement of 2011 European low-density lipoprotein cholesterol (LDL-C) goals of either < 70 mg/dl or >= 50% reduction in high-risk patients: Results from VOYAGER
  • 2013
  • In: Atherosclerosis. - : Elsevier BV. - 0021-9150 .- 1879-1484. ; 228:1, s. 265-269
  • Journal article (peer-reviewed)abstract
    • Objective Guidelines published in 2011 by the European Atherosclerosis Society and the European Society of Cardiology recommend a goal of either low-density lipoprotein cholesterol (LDL-C) <70 mg/dl (∼1.8 mmol/l) or ≥50% reduction in LDL-C for patients at very high cardiovascular risk. The aim of this study was to determine the percentage of high-risk patients from the VOYAGER individual patient data meta-analysis treated with rosuvastatin 10–40 mg, atorvastatin 10–80 mg or simvastatin 10–80 mg who achieved this goal. Methods We analysed 25,075 patient exposures from high-risk patients. Paired comparisons were made between each rosuvastatin dose and an equal or higher dose of either atorvastatin or simvastatin, with a series of meta-analyses that included only randomised studies that directly compared rosuvastatin and its comparator treatments. Results As statin dose increased, higher percentages of patients achieved LDL-C <70 mg/dl or ≥50% LDL-C reduction. A greater percentage achieved this goal with rosuvastatin 10–40 mg (43.8–79.0%) than with equal or double milligram doses of atorvastatin (16.1–65.2%) or simvastatin (0–39.7%). Paired comparisons showed statistically significant differences for: rosuvastatin 10 mg vs. atorvastatin 10–20 mg and simvastatin 10–20 mg; rosuvastatin 20 mg vs. atorvastatin 20–40 mg and simvastatin 20–80 mg; and rosuvastatin 40 mg vs. atorvastatin 40–80 mg and simvastatin 40–80 mg (all p < 0.001). Conclusion These data from VOYAGER highlight the importance of an effective statin at an appropriate dose to achieve treatment goals for LDL-C in patients with very high cardiovascular risk.
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  • Karlson, Björn W., 1953, et al. (author)
  • Comparison of the effects of different statins and doses on lipid levels in patients with diabetes: Results from VOYAGER
  • 2012
  • In: Nutrition Metabolism and Cardiovascular Diseases. - : Elsevier BV. - 0939-4753 .- 1590-3729. ; 22:9, s. 697-703
  • Journal article (peer-reviewed)abstract
    • Background and aims: Diabetes mellitus is a well-known risk factor for cardiovascular disease, and brings an increased risk of vascular events and a higher mortality rate. Treatment guidelines recommend statins in patients with diabetes, with low-density lipoprotein cholesterol (LDL-C) targets of 100 mg dl(-1) (similar to 2.5 mmol l(-1)), and 80 (similar to 2.0 mmol l(-1)) or 70 mg dl(-1) (similar to 1.8 mmol l(-1)) in especially high-risk patients. The current study used the VOYAGER (an indiVidual patient data-meta-analysis Of statin therapY in At risk Groups: Effects of Rosuvastatin, atorvastatin, and simvastatin) database to characterise effects of rosuvastatin, atorvastatin and simvastatin in different doses on lipid levels in diabetes patients. Methods and results: The VOYAGER database included individual patient data from 37 studies involving comparisons of rosuvastatin with either atorvastatin or simvastatin. Of the 32 258 patients included, 8859 (27.5%) had diabetes. Rosuvastatin appeared to be the most efficacious of the three statins, both for lowering LDL-C and for reaching a target level of <70 mg dl(-1) for LDL-C. It was also more effective than atorvastatin at raising high-density lipoprotein cholesterol in the diabetes population. These results are consistent with the overall VOYAGER results. Conclusions: This meta-analysis of 8859 patients with diabetes mellitus shows favourable effects on lipids with the three statins studied, in line with results for the overall VOYAGER population. The importance of using an effective statin at an effective dose to reach treatment goals for such high-risk patients is evident. (c) 2012 Elsevier B.V. All rights reserved.
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  • Karlson, Björn W., 1953, et al. (author)
  • Effects of age, gender and statin dose on lipid levels: Results from the VOYAGER meta-analysis database
  • 2017
  • In: Atherosclerosis. - : Elsevier BV. - 0021-9150 .- 1879-1484. ; 265, s. 54-59
  • Journal article (peer-reviewed)abstract
    • Background and aims The effectiveness of statins in the treatment of dyslipidaemia and reduction of cardiovascular risk is well established. However, the association of statin-mediated lipid effects with age and gender is unclear. This study aimed to determine whether age and gender are associated with statin-mediated changes in low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C) and non-HDL-C. Methods Individual patient data (n = 32,258) were obtained from VOYAGER. Least-squares mean percentage change from baseline in LDL-C, non-HDL-C and HDL-C with atorvastatin 10–80 mg, rosuvastatin 5–40 mg or simvastatin 10–80 mg was estimated in women aged <70 years, women aged ≥70 years, men aged <70 years and men aged ≥70 years. Results All statins and doses gave significant dose-dependent reductions in LDL-C and non-HDL-C, and increases in HDL-C, in all four patient groups. A 2.1% greater reduction in LDL-C was observed in women, compared with men (p < 0.0001). Patients aged ≥70 years experienced a 2.7% greater reduction in LDL-C compared with younger patients (p < 0.0001). Similar results were also observed for statin-mediated changes in non-HDL-C. Men experienced a significantly greater increase in HDL-C than women, and patients aged ≥70 years achieved a significantly greater increase than younger patients (both p = 0.001). Conclusions While statins improve the lipid profile in all gender and age groups analysed, the improvements are greater in women than in men and in those aged ≥70 years compared with those aged <70 years. © 2017 Elsevier B.V.
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  • Karlson, Björn W., 1953, et al. (author)
  • Modeling Statin-Induced Reductions of Cardiovascular Events in Primary Prevention: A VOYAGER Meta-Analysis
  • 2018
  • In: Cardiology. - : S. Karger AG. - 0008-6312 .- 1421-9751. ; 140:1, s. 30-34
  • Journal article (peer-reviewed)abstract
    • Objective: We used individual patient data from the VOYAGER database to estimate cardiovascular (CV) risk reduction with commonly used high-intensity statins. Methods: In patients with known atherosclerotic CV disease (ASCVD) treated with high-intensity statin therapy (n = 6,735), the predicted risk reduction was estimated using the Cholesterol Treatment Trialists' Collaboration meta-analysis, which determined risk reduction per 38.7 mg/dL statin-mediated reduction in low-density lipoprotein cholesterol. Results: The greatest reductions in risk were seen in major vascular events (estimated rate ratios ranged from 0.55 with rosuvastatin [RSV] 40 mg to 0.60 with atorvastatin [ATV] 40 mg) and coronary heart disease death (estimated rate ratios ranged from 0.58 with RSV 40 mg to 0.64 with ATV 40 mg). Conclusions: Our results show that, in individuals without clinical ASCVD, statin therapy has the potential to reduce the frequency of CV events. (C) 2018 S. Karger AG, Basel
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  • Karlson, Björn W., 1953, et al. (author)
  • To what extent do high-intensity statins reduce low-density lipoprotein cholesterol in each of the four statin benefit groups identified by the 2013 American College of Cardiology/American Heart Association guidelines? A VOYAGER meta-analysis
  • 2015
  • In: Atherosclerosis. - : Elsevier BV. - 0021-9150 .- 1879-1484. ; 241:2, s. 450-454
  • Journal article (peer-reviewed)abstract
    • Background: The 2013 American College of Cardiology and American Heart Association (ACC/AHA) guidelines identify four patient groups who benefit from moderate-or high-intensity statin treatment; those with: 1) atherosclerotic cardiovascular disease (ASCVD); 2) low-density lipoprotein cholesterol (LDL-C) >= 190 mg/dl; 3) diabetes; or 4) a 10-year ASCVD risk >= 7.5%. High-intensity statins, anticipated to reduce LDL-C by >= 50%, were identified as rosuvastatin 20-40 mg and atorvastatin 40-80 mg. Methods and Results: Individual patient data (32,258) from the VOYAGER database of 37 studies were used to calculate least-squares mean (LSM) percentage change in LDL-C during 8496 patient exposures to rosuvastatin 20-40 mg, and atorvastatin 40-80 mg in the four patient benefit groups. LSM percentage reductions in LDL-C with rosuvastatin 20 and 40 mg were greater than with atorvastatin 40 mg, overall and in each statin benefit group, and with rosuvastatin 40 mg were greater than with atorvastatin 80 mg overall and in three of the four benefit groups (all p < 0.05). For example, in the ASCVD group, 40%, 59%, 57% and 71% of patients treated with atorvastatin 40 mg, atorvastatin 80 mg, rosuvastatin 20 mg and rosuvastatin 40 mg, respectively, had a >= 50% reduction in LDL-C. Conclusions: The choice and dose of statin have an impact both on the percentage LDL-C reduction and achievement of >= 50% reduction in LDL-C, overall and within each of the four statin benefit groups outlined by the 2013 ACC/AHA guidelines. This may be of importance for clinicians in their choice of treatment for individual patients. (C) 2015 Elsevier Ireland Ltd. All rights reserved.
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  • Palmer, M. K., et al. (author)
  • Achievement of LDL-C goals depends on baseline LDL-C and choice and dose of statin: An analysis from the VOYAGER database
  • 2013
  • In: European Journal of Preventive Cardiology. - : Oxford University Press (OUP). - 2047-4873 .- 2047-4881. ; 20:6, s. 1080-1087
  • Journal article (peer-reviewed)abstract
    • Background Reducing low-density lipoprotein cholesterol (LDL-C) levels decreases cardiovascular risk in direct proportion to the decrease in LDL-C. Design The aim of this study was to assess the importance of baseline LDL-C and choice and dose of statin in achievement of LDL-C goals of 100 and 70mg/dl, using a novel statistical model. The analysis included 30,102 patient exposures to rosuvastatin 10-40mg or atorvastatin 10-80mg from 31 direct comparative trials in the VOYAGER database. Methods For each statin dose, percentage goal achievement was plotted for 20 equally large subgroups defined by baseline LDL-C. Logistic regression analysis was then performed for each statin dose to estimate the percentage of patients reaching target. Best-fit logistic regression curves were plotted pair-wise', comparing each rosuvastatin dose with equal or higher doses of atorvastatin. Results LDL-C <100mg/dl was achieved by 53.7-85.5% of patients on rosuvastatin 10-40mg and 43.3-80.0% of those on atorvastatin 10-80mg, whereas LDL-C <70mg/dl was achieved by 4.5-44.0% of rosuvastatin-treated patients and 6.5-41.4% of those on atorvastatin. Similar differences in efficacy favouring rosuvastatin over equal or double doses of atorvastatin were observed across the range of baseline LDL-C levels for both LDL-C goals, being more pronounced at higher baseline values. Conclusions Baseline LDL-C and choice and dose of statin are important for LDL-C goal achievement. The present analysis may allow prediction of individual patient response to different statins at different doses.
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  • Arnetz, L, et al. (author)
  • Copeptin, insulin-like growth factor binding protein-1 and sitagliptin: A report from the BEta-cell function in Glucose abnormalities and Acute Myocardial Infarction study
  • 2016
  • In: Diabetes & vascular disease research. - : SAGE Publications. - 1752-8984 .- 1479-1641. ; 13:4, s. 307-311
  • Journal article (peer-reviewed)abstract
    • To investigate whether sitagliptin affects copeptin and osmolality, suggesting arginine vasopressin activation and a potential for fluid retention, compared with placebo, in patients with a recent acute coronary syndrome and newly discovered type 2 diabetes or impaired glucose tolerance. A second aim was to confirm whether copeptin correlated with insulin-like growth factor binding protein-1. Methods: Fasting blood samples were used from the BEta-cell function in Glucose abnormalities and Acute Myocardial Infarction trial, in which patients recently hospitalized due to acute coronary syndrome and with newly detected abnormal glucose tolerance were randomized to sitagliptin 100 mg once daily ( n = 34) or placebo ( n = 37). Copeptin, osmolality and insulin-like growth factor binding protein-1 were analysed at baseline and after 12 weeks. Results: Copeptin and osmolality were unaffected by sitagliptin. There was no correlation between copeptin and insulin-like growth factor binding protein-1. Conclusion: Sitagliptin therapy does not appear to be related to activation of the arginine vasopressin system.
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  • Djupsjo, C, et al. (author)
  • Preoperative disturbances of glucose metabolism and mortality after coronary artery bypass grafting
  • 2020
  • In: Open heart. - : BMJ. - 2053-3624. ; 7:1
  • Journal article (peer-reviewed)abstract
    • Disturbances of glucose metabolism are important risk factors for coronary artery disease and are associated with an increased mortality risk. The aim was to investigate the association between preoperative disturbances of glucose metabolism and long-term all-cause mortality after coronary artery bypass grafting (CABG).MethodsPatients undergoing a first isolated CABG in 2005–2013 were included. All patients without previously known diabetes underwent an oral glucose tolerance test (OGTT) before surgery. They were categorised as having normal glucose tolerance (NGT), pre-diabetes (impaired glucose tolerance and/or impaired fasting glucose) or newly discovered diabetes. Data were collected from nationwide healthcare registers. Cox regression was used to calculate adjusted HR with 95% CI for death in patients with pre-diabetes and diabetes, using NGT as reference.ResultsIn total, 497 patients aged 40–86 years were included. According to OGTT, 170 (34%) patients had NGT, 219 (44%) patients with pre-diabetes and 108 (22%) patients had newly discovered diabetes. Baseline characteristics were similar between the groups except for slightly higher age among patients with newly discovered diabetes. There were 133 (27%) deaths during a mean follow-up time of 10 years. The cumulative 10-year survival was 77% (69%–83%), 83% (77%–87%) and 71% (61%–79%) in patients with NGT, pre-diabetes and newly discovered diabetes, respectively. There was no significant difference in all-cause mortality between the groups after multivariable adjustment.ConclusionIn this study, patients with pre-diabetes or newly discovered diabetes prior to CABG had similar long-term survival compared with patients with NGT.
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  • Hage, C, et al. (author)
  • The DPP-4 inhibitor sitagliptin and endothelial function in patients with acute coronary syndromes and newly detected glucose perturbations: A report from the BEGAMI study
  • 2014
  • In: Diabetes & vascular disease research. - : SAGE Publications. - 1752-8984 .- 1479-1641. ; 11:4, s. 290-293
  • Journal article (peer-reviewed)abstract
    • Compromised endothelial function contributes to poor prognosis in patients with coronary artery disease and type 2 diabetes. Incretin-based therapy may exert beneficial cardiovascular effects beyond glucose lowering. We tested whether sitagliptin improves endothelial function. Research design and methods: In the double-blind BEta-cell function in patients with Glucose Abnormalities and Acute Myocardial Infarction (BEGAMI) trial, acute coronary syndrome (ACS)-patients with newly detected impaired glucose tolerance (IGT) or type 2 diabetes mellitus (T2DM) were randomised to sitagliptin 100 mg (n = 31) or placebo (n = 33) during 12 weeks. Endothelial function was studied as reactive hyperaemia index (RHI). Results: At baseline, the RHI was slightly compromised in both groups (sitagliptin 1.67; Q1;Q3: 1.46;2.17 vs placebo 1.61; 1.44;1.96; ns). The RHI did not change during the study period and was 1.57 (1.40;2.36) in the sitagliptin and 1.60 (1.46;1.81; ns) in the placebo group after treatment. Conclusion: Sitagliptin did not improve endothelial function in patients with ACS and newly detected glucose perturbations.
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