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Diabetes Mellitus: HELP
Articles by Linda Garcia Mellbin
Based on 20 articles published since 2010
(Why 20 articles?)
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Between 2010 and 2020, L. Mellbin wrote the following 20 articles about Diabetes Mellitus.
 
+ Citations + Abstracts
1 Editorial New Hope For People With Dysglycemia and Cardiovascular Disease Manifestations: Reduction of Acute Coronary Events With Pioglitazone. 2017

Rydén, Lars / Mellbin, Linda. ·From Cardiology Unit, Department of Medicine K2, Karolinska Institutet, Stockholm, Sweden. lars.ryden@ki.se. · From Cardiology Unit, Department of Medicine K2, Karolinska Institutet, Stockholm, Sweden. ·Circulation · Pubmed #28507248.

ABSTRACT: -- No abstract --

2 Review Diabetes: Prevalence, prognosis and management of a potent cardiovascular risk factor. 2017

Norhammar, Anna / Mellbin, Linda / Cosentino, Francesco. ·1 Cardiology Unit, Department of Medicine Solna, Karolinska University Hospital, Stockholm, Sweden. · 2 Capio S:t Görans hospital, Sankt Göransplan, Stockholm, Sweden. ·Eur J Prev Cardiol · Pubmed #28618910.

ABSTRACT: This review highlights the increased risk of cardiovascular disease and the dismal prognosis after acute coronary events when diabetes is present. Although there have been improvements in this area, diabetes still confers an increased risk. In order to achieve successful outcomes in individuals with diabetes, extensive treatment of risk factors and the use of all available evidence-based therapies are needed. In this context, glucose-lowering therapies and antithrombotic and revascularisation strategies are detailed in this review. Emerging data indicate that novel glucose-lowering drugs may impact cardiovascular outcome with mechanisms that are beyond glucose control. In addition, this review addresses hidden diabetes and impaired glucose tolerance in patients with acute and stable coronary artery disease and how they influence future cardiovascular risk.

3 Review The clinical burden of type 2 diabetes in patients with acute coronary syndromes: prognosis and implications for short- and long-term management. 2014

Katz, Pamela / Leiter, Lawrence A / Mellbin, Linda / Rydén, Lars. ·Division of Endocrinology & Metabolism, Department of Medicine, University of Manitoba, Winnipeg, MB, Canada. · Division of Endocrinology & Metabolism, Keenan Research Centre, Li Ka Shing Knowledge Institute, St. Michael's Hospital, Toronto, ON, Canada Departments of Medicine and Nutritional Sciences, University of Toronto, Toronto, ON, Canada. · Cardiology Unit, Department of Medicine, Solna, Karolinska Institutet, Stockholm, Sweden linda.mellbin@karolinska.se. · Cardiology Unit, Department of Medicine, Solna, Karolinska Institutet, Stockholm, Sweden. ·Diab Vasc Dis Res · Pubmed #25187508.

ABSTRACT: Type 2 diabetes mellitus (T2DM) is associated with increased morbidity and mortality in patients with acute coronary syndromes (ACS). Cardiometabolic risk factors, including hyperglycaemia, insulin resistance, atherogenic dyslipidaemia, increased visceral fat and inflammation, are associated with increased risk in this population and represent potential targets for treatment. In this review, management strategies for patients with T2DM post-ACS, both in the acute-care setting and in the long-term, are discussed. Although the benefits of long-term, aggressive, multifactorial risk factor modification are well established, a significant burden of recurrent events remains and the search for novel strategies continues. Several studies are assessing the potential cardiovascular (CV) benefits and safety of various classes of newer agents. Of these, AleCardio (aleglitazar), Examination of Cardiovascular Outcomes With Alogliptin versus Standard of Care in Patients With Type 2 Diabetes Mellitus and Acute Coronary Syndrome (EXAMINE; alogliptin) and Evaluation of LIXisenatide in Acute Coronary Syndrome (ELIXA; lixisenatide) specifically address patients with type 2 diabetes post-ACS. The mechanisms of action of these new therapies and aims of the CV outcome studies are briefly reviewed. The prevalence of type 2 diabetes continues to increase worldwide highlighting the need for new strategies that address the complex underlying processes that drive atherosclerosis and CV events in this high-risk patient population.

4 Article 2019 ESC Guidelines on diabetes, pre-diabetes, and cardiovascular diseases developed in collaboration with the EASD. 2020

Cosentino, Francesco / Grant, Peter J / Aboyans, Victor / Bailey, Clifford J / Ceriello, Antonio / Delgado, Victoria / Federici, Massimo / Filippatos, Gerasimos / Grobbee, Diederick E / Hansen, Tina Birgitte / Huikuri, Heikki V / Johansson, Isabelle / Jüni, Peter / Lettino, Maddalena / Marx, Nikolaus / Mellbin, Linda G / Östgren, Carl J / Rocca, Bianca / Roffi, Marco / Sattar, Naveed / Seferović, Petar M / Sousa-Uva, Miguel / Valensi, Paul / Wheeler, David C / Anonymous20081124. · ·Eur Heart J · Pubmed #31497854.

ABSTRACT: -- No abstract --

5 Article Clinical implications of cardiovascular outcome trials in type 2 diabetes. 2019

Mellbin, L G / Wang, A / Rydén, L. ·Cardiology Unit, Department of Medicine K2, Karolinska Institutet, Stockholm, Sweden. linda.mellbin@ki.se. · Heart and Vascular Theme, Karolinska University Hospital, 17176, Stockholm, Sweden. linda.mellbin@ki.se. · Cardiology Unit, Department of Medicine K2, Karolinska Institutet, Stockholm, Sweden. ·Herz · Pubmed #30805659.

ABSTRACT: Cardiovascular disease (CVD) is the main reason for premature death in patients with type 2 diabetes. Hyperglycemia, the hallmark of diabetes, has long been considered the link between diabetes and CVD, and many trials focused on preventing CVD manifestations by means of tight glucose control. However, diabetes is a multifactorial disease in which, e. g., insulin resistance, endothelial dysfunction, and factors such as hypertension and dyslipidemia contribute. Thus, treatment needs to be multifactorial and take cardiovascular aspects into account. Newer classes of drugs, originally launched for glucose lowering, among them dipeptidyl-peptidase (DPP)-4 inhibitors, sodium-glucose cotransporter (SGLT)-2 inhibitors, and glucagon-like peptide (GLP)-1 receptor agonists, have been studied in large cardiovascular outcome trials (CVOT). Several SGLT-2 inhibitors and GLP-1 receptor agonists are associated with a reduction of cardiovascular events (cardiovascular death, nonfatal myocardial infarction, and nonfatal stroke). Although the mechanisms behind the effects are not fully understood, an important reason for the benefits of SGLT-2 inhibitors seems be a reduction in heart failure, while GLP-1 receptor agonists may retard the development of the atherosclerotic vascular disease or may be effective by stabilizing plaques. The outcomes of these studies have been taken into account in recently issued guidelines and an important task for diabetologists, cardiologists, and general practitioners is to incorporate the findings of these trials into clinical practice.

6 Article Copeptin and insulin-like growth factor binding protein-1 during follow-up after an acute myocardial infarction in patients with type 2 diabetes: A report from the Diabetes Mellitus Insulin-Glucose Infusion in Acute Myocardial Infarction 2 cohort. 2019

Smáradóttir, Maria Isabel / Catrina, Sergiu-Bogdan / Brismar, Kerstin / Norhammar, Anna / Gyberg, Viveca / Mellbin, Linda G. ·1 Division of Cardiology, Department of Medicine, Solna, Karolinska Institutet, Stockholm, Sweden. · 2 Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden. ·Diab Vasc Dis Res · Pubmed #30309264.

ABSTRACT: PURPOSE: Copeptin and insulin-like growth factor binding protein-1 analysed at admission for a myocardial infarction in patients with type 2 diabetes mellitus predicts cardiovascular events. The present aim was to study the association between copeptin and insulin-like growth factor binding protein-1, the development of the levels over time, and if the predictive value remained when measured at hospital discharge and 3 months thereafter. METHODS: Copeptin and insulin-like growth factor binding protein-1 were analysed in patients (median age = 70, male = 68%) with type 2 diabetes mellitus + myocardial infarction at admission (n = 393), discharge (n = 309) and 3 months later (n = 288). The primary endpoint was cardiovascular event (cardiovascular death/non-fatal myocardial infarction/stroke) with the three time points as separate baselines. RESULTS: The median copeptin levels were 21.8 pmol/L at admission, 8.5 pmol/L at discharge and 8.4 pmol/L after 3 months, while insulin-like growth factor binding protein-1 levels continued to increase. There were significant correlations between the biomarkers at all occasions. During an average follow-up of 2.5 years, copeptin, but not insulin-like growth factor binding protein-1, predicted cardiovascular event at all occasions in unadjusted analyses. Copeptin remained as a predictor at discharge and after 3 months in the final multiple model (including: heart failure/age/creatinine clearance). CONCLUSION: The relationship between copeptin and insulin-like growth factor binding protein-1 during the initial phase of a myocardial infarction persisted in a less-stressful situation, and copeptin remained as a prognostic indicator at discharge and 3 months later.

7 Article Effectiveness of different outreach strategies to identify individuals at high risk of diabetes in a heterogeneous population: a study in the Swedish municipality of Södertälje. 2018

Shahim, Bahira / Hasselberg, Sofia / Boldt-Christmas, Oscar / Gyberg, Viveca / Mellbin, Linda / Rydén, Lars. ·1 Department of Medicine Solna, Karolinska Institutet, Sweden. · 2 McKinsey & Company, Stockholm, Sweden. · 3 Getinge AB, Gothenburg, Sweden. · 4 Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, Sweden. ·Eur J Prev Cardiol · Pubmed #30289273.

ABSTRACT: BACKGROUND: Identifying type 2 diabetes mellitus (T2DM) is a prerequisite for the institution of preventive measures to reduce future micro and macrovascular complications. Approximately 50% of people with T2DM are undiagnosed, challenging the assumption that a traditional primary healthcare setting is the most efficient way to reach people at risk of T2DM. A setting of this kind may be even more suboptimal when it comes to reaching immigrants, who often appear to have inferior access to healthcare and/or are less likely to attend routine health checks at primary healthcare centres. OBJECTIVES: The objective of this study was to identify the best strategy to reach individuals at high risk of T2DM and thereby cardiovascular disease in a heterogeneous population. METHODS: All 18-65-year-old inhabitants in the Swedish municipality of Södertälje ( n∼51,000) without known T2DM and cardiovascular disease were encouraged to complete the Finnish Diabetes Risk Score (FINDRISC: score > 15 indicating a high and > 20 a very high risk of future T2DM and cardiovascular disease) through the following communication channels: primary care centres, workplaces, Syrian orthodox churches, pharmacies, crowded public places, mass media, social media and mail. Data collection lasted for six weeks. RESULTS: The highest response rate was obtained through workplaces (27%) and the largest proportion of respondents at high/very high risk through the Syrian orthodox churches (18%). The proportion reached through primary care centres was 4%, of whom 5% were at elevated risk. The cost of identifying a person at elevated risk through the Syrian orthodox church was €104 compared with €8 through workplaces and €112 through primary care centres. CONCLUSIONS: The choice of communication channels was important to reach high/very high-risk individuals for T2DM and for screening costs. In this immigrant-dense community, primary care centres were inferior to strategies using workplaces and churches in terms of both the proportion of identified at-risk individuals and costs.

8 Article Dynamics of testosterone levels in patients with newly detected glucose abnormalities and acute myocardial infarction. 2018

Wang, Anne / Arver, Stefan / Flanagan, John / Gyberg, Viveca / Näsman, Per / Ritsinger, Viveca / Mellbin, Linda G. ·1 Division of Cardiology, Department of Medicine, Solna, Karolinska Institutet, Stockholm, Sweden. · 2 Department of Medicine, Center for Andrology and Sexual Medicine, Karolinska Institutet, Huddinge, Sweden. · 3 Department of Neurobiology, Centre for Family Medicine, Care Sciences and Society, Karolinska Institutet, Huddinge, Sweden. · 4 Center for Safety Research, KTH Royal Institute of Technology, Stockholm, Sweden. · 5 Department of Research and Development, Region Kronoberg, Växjö, Sweden. · 6 Heart & Vascular Theme, Karolinska University Hospital, Stockholm, Sweden. ·Diab Vasc Dis Res · Pubmed #30280926.

ABSTRACT: OBJECTIVE: Low testosterone has been associated with increased cardiovascular risk and glucose abnormalities. This study explored the prevalence of low testosterone, dynamics over time and prognostic implications in acute myocardial infarction patients with or without glucose abnormalities. METHODS: Male acute myocardial infarction patients (n = 123) and healthy controls (n = 124) were categorised as having normal or abnormal glucose tolerance (impaired glucose tolerance or diabetes) by oral glucose tolerance testing. Testosterone was measured at hospital admission, discharge, 3 and 12 months thereafter in patients. Patients and controls were followed for 11 years for major cardiovascular events (cardiovascular death/acute myocardial infarction/stroke/severe heart failure). RESULTS: At hospital admission, more patients had low testosterone (⩽300 ng/dl) and lower median levels than controls (64 vs 28%; p < 0.001 and 243 vs 380 ng/dl; p < 0.01). At the subsequent time points, testosterone had increased to 311, 345 and 357 ng/dl. Patients with abnormal glucose tolerance had the highest prevalence (75%) of low levels. In adjusted Cox regression models, neither total nor free testosterone predicted major cardiovascular events. CONCLUSION: Low testosterone levels were common in male acute myocardial infarction patients in the acute phase, especially in the presence of abnormal glucose tolerance, but increased over time indicating that testosterone measured in close proximity to acute myocardial infarction should be interpreted with caution.

9 Article Adiponectin, Free Fatty Acids, and Cardiovascular Outcomes in Patients With Type 2 Diabetes and Acute Coronary Syndrome. 2018

Schrieks, Ilse C / Nozza, Anna / Stähli, Barbara E / Buse, John B / Henry, Robert R / Malmberg, Klas / Neal, Bruce / Nicholls, Stephen J / Rydén, Lars / Mellbin, Linda / Svensson, Anders / Wedel, Hans / Weichert, Arlette / Lincoff, A Michael / Tardif, Jean-Claude / Grobbee, Diederick E / Schwartz, Gregory G. ·Julius Clinical and Julius Center for Health Sciences and Primary Care, University Medical Center Utrecht, Utrecht, the Netherlands ilse.schrieks@juliusclinical.com. · Montreal Health Innovations Coordinating Center, Montreal Heart Institute, Montreal, Canada. · Department of Cardiology, Charité Berlin-University Medicine, Campus Benjamin Franklin, Berlin, Germany. · University of North Carolina School of Medicine, Chapel Hill, NC. · University of California San Diego, San Diego, CA. · Karolinska Institutet and Vicore Pharma, Stockholm, Sweden. · The George Institute for Global Health, University of Sydney, Sydney, Australia. · South Australian Health and Medical Research Institute, The University of Adelaide, Adelaide, Australia. · Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden. · F. Hoffmann-La Roche Ltd., Basel, Switzerland. · Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden. · Department of Cardiovascular Medicine, Cleveland Clinic Coordinating Center for Clinical Research (C5Research), Cleveland, OH. · Montreal Heart Institute, Université de Montréal, Montreal, Canada. · Julius Clinical and Julius Center for Health Sciences and Primary Care, University Medical Center Utrecht, Utrecht, the Netherlands. · Division of Cardiology, VA Medical Center and University of Colorado School of Medicine, Denver, CO. ·Diabetes Care · Pubmed #29903845.

ABSTRACT: OBJECTIVE: In observational cohorts, adiponectin is inversely associated and free fatty acids (FFAs) are directly associated with incident coronary heart disease (CHD). Adiponectin tends to be reduced and FFAs elevated in type 2 diabetes. We investigated relationships of adiponectin and FFA and major adverse cardiovascular events (MACEs) and death in patients with acute coronary syndrome (ACS) and type 2 diabetes using data from the AleCardio (Effect of Aleglitazar on Cardiovascular Outcomes After Acute Coronary Syndrome in Patients With Type 2 Diabetes Mellitus) trial, which compared the PPAR-α/γ agonist aleglitazar with placebo. RESEARCH DESIGN AND METHODS: Using Cox regression adjusted for demographic, laboratory, and treatment variables, we determined associations of baseline adiponectin and FFAs, or the change in adiponectin and FFAs from baseline, with MACEs (cardiovascular death, myocardial infarction, or stroke) and death. RESULTS: A twofold higher baseline adiponectin ( CONCLUSIONS: In contrast to prior observational data for incident CHD, adiponectin is prospectively associated with MACEs and death in patients with type 2 diabetes and ACS, and an increase in adiponectin from baseline is directly related to death. These findings raise the possibility that adiponectin has different effects in patients with type 2 diabetes and ACS than in populations without prevalent cardiovascular disease. Consistent with prior data, FFAs are directly associated with adverse outcomes.

10 Article Homeostasis Model Assessment of Insulin Resistance and Survival in Patients With Diabetes and Acute Coronary Syndrome. 2018

Stähli, Barbara E / Nozza, Anna / Schrieks, Ilse C / Buse, John B / Malmberg, Klas / Mellbin, Linda / Neal, Bruce / Nicholls, Stephen J / Rydén, Lars / Svensson, Anders / Wedel, Hans / Weichert, Arlette / Lincoff, A Michael / Grobbee, Diederick E / Tardif, Jean-Claude / Schwartz, Gregory G. ·Department of Cardiology, Charité Berlin - University Medicine, Campus Benjamin Franklin, Berlin, Germany. · Montreal Heart Institute and Université de Montréal, Montreal, Canada. · Montreal Health Innovations Coordinating Center, Montreal QC, Canada. · Julius Clinical and Julius Center for Health Sciences and Primary Care, University Medical Center Utrecht, Utrecht, CD Zeist, Netherlands. · University of North Carolina School of Medicine, Chapel Hill, North Carolina. · Karolinska Institutet, Stockholm, Sweden. · Vicore Pharma, Mölndal, Sweden. · Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden. · George Institute for Global Health and University of Sydney, Newtown, New South Wales, Australia. · South Australian Health and Medical Research Institute, University of Adelaide, Adelaide, South Australia, Australia. · F. Hoffmann-La Roche Ltd, Basel, Switzerland. · Health Metrics, Sahlgrenska Academy at University of Gothenburg, Gothenburg, Sweden. · Department of Cardiovascular Medicine, Cleveland Clinic Coordinating Center for Clinical Research, Cleveland, Ohio. · VA Medical Center and University of Colorado School of Medicine, Denver, Colorado. ·J Clin Endocrinol Metab · Pubmed #29659887.

ABSTRACT: Objective: Insulin resistance has been linked to development and progression of atherosclerosis and is present in most patients with type 2 diabetes. Whether the degree of insulin resistance predicts adverse outcomes in patients with type 2 diabetes and acute coronary syndrome (ACS) is uncertain. Design: The Effect of Aleglitazar on Cardiovascular Outcomes after Acute Coronary Syndrome in Patients with Type 2 Diabetes Mellitus trial compared the peroxisome proliferator-activated receptor-α/γ agonist aleglitazar with placebo in patients with type 2 diabetes and recent ACS. In participants not treated with insulin, we determined whether baseline homeostasis model assessment of insulin resistance (HOMA-IR; n = 4303) or the change in HOMA-IR on assigned study treatment (n = 3568) was related to the risk of death or major adverse cardiovascular events (cardiovascular death, myocardial infarction, and stroke) in unadjusted and adjusted models. Because an inverse association of HOMA-IR with N-terminal pro-B-type natriuretic peptide (NT-proBNP) has been described, we specifically examined effects of adjustment for the latter. Results: In unadjusted analysis, twofold higher baseline HOMA-IR was associated with lower risk of death [hazard ratio (HR): 0.79, 95% CI: 0.68 to 0.91, P = 0.002]. Adjustment for 24 standard demographic and clinical variables had minimal effect on this association. However, after further adjustment for NT-proBNP, the association of HOMA-IR with death was no longer present (adjusted HR: 0.99, 95% CI: 0.83 to 1.19, P = 0.94). Baseline HOMA-IR was not associated with major adverse cardiovascular events, nor was the change in HOMA-IR on study treatment associated with death or major adverse cardiovascular events. Conclusions: After accounting for levels of NT-proBNP, insulin resistance assessed by HOMA-IR is not related to the risk of death or major adverse cardiovascular events in patients with type 2 diabetes and ACS.

11 Article The Prognostic Value of Fasting Plasma Glucose, Two-Hour Postload Glucose, and HbA 2017

Shahim, Bahira / De Bacquer, Dirk / De Backer, Guy / Gyberg, Viveca / Kotseva, Kornelia / Mellbin, Linda / Schnell, Oliver / Tuomilehto, Jaakko / Wood, David / Rydén, Lars. ·Cardiology Unit, Department of Medicine, Karolinska Institutet, Stockholm, Sweden bahirashahim@gmail.com. · Department of Public Health, Ghent University, Ghent, Belgium. · Cardiology Unit, Department of Medicine, Karolinska Institutet, Stockholm, Sweden. · Department of Cardiovascular Medicine, National Heart and Lung Institute, Imperial College London, London, U.K. · Forschergruppe Diabetes e.V., Munich, Germany. · Disease Risk Unit, National Institute for Health and Welfare, Helsinki, Finland. · Diabetes Research Group, King Abdulaziz University, Jeddah, Saudi Arabia. ·Diabetes Care · Pubmed #28637653.

ABSTRACT: OBJECTIVE: Three tests are recommended for identifying dysglycemia: fasting glucose (FPG), 2-h postload glucose (2h-PG) from an oral glucose tolerance test (OGTT), and glycated hemoglobin A RESEARCH DESIGN AND METHODS: FPG, 2h-PG, and HbA RESULTS: Complete information including all three glycemic parameters was available in 3,775 patients (94.3%), of whom 246 (6.5%) experienced the primary end point. Neither FPG nor HbA CONCLUSIONS: The 2h-PG, in contrast to FPG and HbA

12 Article The effect of basal insulin glargine on the fibrinolytic system and von Willebrand factor in people with dysglycaemia and high risk for cardiovascular events: Swedish substudy of the Outcome Reduction with an Initial Glargine Intervention trial. 2017

Rautio, Aslak / Boman, Kurt / Gerstein, Hertzel C / Hernestål-Boman, Jenny / Lee, Shun Fu / Olofsson, Mona / Mellbin, Linda Garcia. ·1 Department of Public Health and Clinical Medicine, Umeå University, Umeå, Sweden. · 2 Department of Medicine, Sunderby Hospital, Luleå, Sweden. · 3 Research Unit, Skellefteå Hospital, Skellefteå, Sweden. · 4 Population Health Research Institute, Hamilton Health Sciences and McMaster University, Hamilton, ON, Canada. · 5 Unit of Cardiology, Department of Medicine, Solna, Karolinska Institutet, Stockholm, Sweden. ·Diab Vasc Dis Res · Pubmed #28403644.

ABSTRACT: INTRODUCTION: Fibrinolytic factors, plasminogen activator inhibitor-1, tissue plasminogen activator, tissue plasminogen activator/plasminogen activator-complex and the haemostatic factor von Willebrand factor are known markers of cardiovascular disease. Their plasma levels are adversely affected in patients with dysglycaemia, and glucose normalization with insulin glargine might improve the levels of these factors. METHODS: Prespecified Swedish substudy of the Outcome Reduction with an Initial Glargine Intervention trial (ClinicalTrials.gov number, NCT00069784). Tissue plasminogen activator activity, tissue plasminogen activator antigen, plasminogen activator inhibitor-1 antigen, tissue plasminogen activator/plasminogen activator inhibitor-1 complex and von Willebrand factor were analysed at study start, after 2 years and at the end of the study (median follow-up of 6.2 years). RESULTS: Of 129 patients (mean age of 64 ± 7 years, females: 19%), 68 (53%) and 61 (47%) were randomized to the insulin glargine and standard care group, respectively. Allocation to insulin glargine did not significantly affect the studied fibrinolytic markers or von Willebrand factor compared to standard care. Likewise, there were no significant differences in plasminogen activator inhibitor-1, tissue plasminogen activator antigen and von Willebrand factor. During the whole study period, the within-group analysis revealed a curvilinear pattern and significant changes for tissue plasminogen activator/plasminogen activator inhibitor-1 complex, tissue plasminogen activator antigen and von Willebrand factor in the insulin glargine but not in the standard care group. CONCLUSION: In people with dysglycaemia and other cardiovascular risk factors, basal insulin does not improve the levels of markers of fibrinolysis or von Willebrand factor compared to standard glucose-lowering treatments.

13 Article Post-Discharge Worsening Renal Function in Patients with Type 2 Diabetes and Recent Acute Coronary Syndrome. 2017

Morici, Nuccia / Savonitto, Stefano / Ponticelli, Claudio / Schrieks, Ilse C / Nozza, Anna / Cosentino, Francesco / Stähli, Barbara E / Perrone Filardi, Pasquale / Schwartz, Gregory G / Mellbin, Linda / Lincoff, A Michael / Tardif, Jean-Claude / Grobbee, Diederick E. ·Unità di Terapia Intensiva Cardiologica, ASST Grande Ospedale Metropolitano Niguarda Ca' Granda, Milano, Italy. Electronic address: nuccia.morici@ospedaleniguarda.it. · Dipartimento Cardiovascolare, Ospedale A. Manzoni, Lecco, Italy. · Division of Nephrology, Humanitas Clinical Research Center, Rozzano (Milano), Italy. · Julius Center for Health Sciences and Primary Care and Julius Clinical, Utrecht, the Netherlands. · Montreal Health Innovations Coordinating Center, Quebec, Canada. · Cardiology Unit, Department of Medicine, Karolinska University Hospital, Stockholm, Sweden. · Montreal Heart Institute, Université de Montréal, Quebec, Canada. · Department of Advanced Biomedical Sciences, Federico II University, Naples, Italy. · Veterans Affairs Medical Center and University of Colorado School of Medicine, Denver. · Department of Cardiovascular Medicine, Cleveland Clinic Foundation, Ohio. · Montreal Health Innovations Coordinating Center, Quebec, Canada; Montreal Heart Institute, Université de Montréal, Quebec, Canada. ·Am J Med · Pubmed #28344139.

ABSTRACT: BACKGROUND: Worsening renal function during hospitalization for an acute coronary syndrome is strongly predictive of in-hospital and long-term outcome. However, the role of post-discharge worsening renal function has never been investigated in this setting. METHODS: We considered the placebo cohort of the AleCardio trial comparing aleglitazar with standard medical therapy among patients with type 2 diabetes mellitus and a recent acute coronary syndrome. Patients who had died or had been admitted to hospital for heart failure before the 6-month follow-up, as well as patients without complete renal function data, were excluded, leaving 2776 patients for the analysis. Worsening renal function was defined as a >20% reduction in estimated glomerular filtration rate from discharge to 6 months, or progression to macroalbuminuria. The Cox regression analysis was used to determine the prognostic impact of 6-month renal deterioration on the composite of all-cause death and hospitalization for heart failure. RESULTS: Worsening renal function occurred in 204 patients (7.34%). At a median follow-up of 2 years the estimated rates of death and hospitalization for heart failure per 100 person-years were 3.45 (95% confidence interval [CI], 2.46-6.36) for those with worsening renal function, versus 1.43 (95% CI, 1.14-1.79) for patients with stable renal function. At the adjusted analysis worsening renal function was associated with the composite endpoint (hazard ratio 2.65; 95% CI, 1.57-4.49; P <.001). CONCLUSIONS: Post-discharge worsening renal function is not infrequent among patients with type 2 diabetes and acute coronary syndromes with normal or mildly depressed renal function, and is a strong predictor of adverse cardiovascular events.

14 Article The haemoglobin glycation index as predictor of diabetes-related complications in the AleCardio trial. 2017

van Steen, Sigrid Cj / Schrieks, Ilse C / Hoekstra, Joost Bl / Lincoff, A Michael / Tardif, Jean-Claude / Mellbin, Linda G / Rydén, Lars / Grobbee, Diederick E / DeVries, J Hans / Anonymous2790896. ·1 Department of Endocrinology, Academic Medical Centre, University of Amsterdam, The Netherlands. · 2 Julius Clinical, Zeist, The Netherlands. · 3 Julius Centre for Health Sciences and Primary Care, University Medical Centre Utrecht, The Netherlands. · 4 Department of Cardiovascular Medicine, Cleveland Clinic Coordinating Center for Clinical Research, USA. · 5 Montreal Heart Institute Coordinating Center, Université de Montréal, Canada. · 6 Department of Medicine, Cardiology Unit, Karolinska Institutet, Sweden. ·Eur J Prev Cardiol · Pubmed #28186441.

ABSTRACT: The haemoglobin glycation index (HGI) quantifies the interindividual variation in the propensity for glycation and is a predictor of diabetes complications and adverse effects of intensive glucose lowering. We investigated the relevance of HGI as independent predictor of complications by using data of the AleCardio trial. The AleCardio trial randomized 7226 type 2 diabetes patients with an acute coronary syndrome to aleglitazar or placebo. From 6458 patients with baseline glycated haemoglobin (HbA

15 Article Copeptin in patients with acute myocardial infarction and newly detected glucose abnormalities - A marker of increased stress susceptibility? A report from the Glucose in Acute Myocardial Infarction cohort. 2017

Smaradottir, Maria Isabel / Ritsinger, Viveca / Gyberg, Viveca / Norhammar, Anna / Näsman, Per / Mellbin, Linda G. ·1 Cardiology Unit, Department of Medicine, Solna, Karolinska Institutet, Stockholm, Sweden. · 2 Department of Research and Development, Region Kronoberg, Växjö, Sweden. · 3 Centre for Family Medicine, Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, Huddinge, Sweden. · 4 Center for Safety Research, KTH Royal Institute of Technology, Stockholm, Sweden. ·Diab Vasc Dis Res · Pubmed #28118730.

ABSTRACT: OBJECTIVE: To characterize copeptin levels and to explore its prognostic importance in patients with acute myocardial infarction with newly detected glucose abnormalities. METHODS: Copeptin was measured in 166 patients with acute myocardial infarction without known diabetes and in 168 age- and gender-matched controls. Participants were classified as having normal glucose tolerance or abnormal glucose tolerance (impaired glucose tolerance + type 2 diabetes mellitus) by oral glucose tolerance test. Study participants were followed over a decade for major cardiovascular event (acute myocardial infarction/stroke/congestive heart failure/cardiovascular death), cardiovascular and total death. RESULTS: Median copeptin level was higher in patients (10.5 pmol/L) than controls (5.9 pmol/L; p < 0.01). Patients with abnormal glucose tolerance had higher copeptin (12.2 pmol/L) than those with normal glucose tolerance (7.9 pmol/L; p < 0.01) but levels of copeptin did not differ in controls with abnormal glucose tolerance or normal glucose tolerance. Copeptin predicted major cardiovascular events [ n = 64; hazard ratio = 1.15 (1.01-1.32; p = 0.04)], cardiovascular mortality [ n = 29; hazard ratio = 1.24 (1.06-1.46; p = 0.01)] and total death [ n = 51; hazard ratio = 1.21 (1.05-1.40; p = 0.01)] in unadjusted Cox regression analyses in the patient cohort. In controls, copeptin predicted major cardiovascular events [ n = 26; hazard ratio = 1.17 (1.01-1.36; p = 0.03)]. CONCLUSION: Copeptin levels are highest among acute myocardial infarction patients with glucose disturbances and predict an adverse prognosis in unadjusted analyses. These findings imply that raised copeptin reflects stress rather than acting as a pathogenic factor for glucose abnormalities.

16 Article 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

Arnetz, Lisa / Hage, Camilla / Brismar, Kerstin / Catrina, Sergiu-Bogdan / Norhammar, Anna / Lundman, Pia / Wallander, Märit / Ryden, Lars / Mellbin, Linda. ·Department of Molecular Medicine and Surgery, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden lisa.arnetz@karolinska.se. · Department of Medicine, Cardiology Unit, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden. · Department of Molecular Medicine and Surgery, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden. · Division of Cardiovascular Medicine, Department of Clinical Sciences, Karolinska Institutet, Danderyd Hospital, Stockholm, Sweden. · Department of Medicine, Karolinska University Hospital Huddinge, Stockholm, Sweden. · Department of Cardiology, Karolinska University Hospital, Stockholm, Sweden. ·Diab Vasc Dis Res · Pubmed #27190088.

ABSTRACT: PURPOSE: 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.

17 Article Clinical Implications of Cardiovascular Outcome Trials in Type 2 Diabetes: From DCCT to EMPA-REG. 2016

Rydén, Lars / Shahim, Bahira / Mellbin, Linda. ·Cardiology Unit, Department of Medicine K2, Karolinska Institutet, Stockholm, Sweden. Electronic address: lars.ryden@ki.se. · Cardiology Unit, Department of Medicine K2, Karolinska Institutet, Stockholm, Sweden. ·Clin Ther · Pubmed #27107734.

ABSTRACT: Cardiovascular disease is a major threat to people with diabetes. Attempts have long been made to lower cardiovascular risk by means of glucose-lowering treatment. Initially, it seemed that was an option, but subsequent trials could not verify the original observations and there was concern that some glucose-lowering drugs can actually cause cardiovascular harm. This led medical product agencies in the United States and Europe to require major outcomes trials before accepting new glucose-lowering drugs. The least requirement was noninferiority compared with existing treatment modalities. A large number of such trials have been performed or are ongoing, including >100,000 patients. The drug classes investigated are basal insulin, glucagon-like peptide-1 agonists, dipeptidyl peptidase 4 inhibitors, and sodium-glucose cotransporter-2 (SGLT2) inhibitors. This commentary discusses these trials and their outcomes, the reasons why several of them ended with neutral results (noninferiority), and that the likelihood for showing cardiovascular benefit was minor or even nonexistent. The surprising and highly rewarding impact of the SGLT2 inhibitor empagliflozin is described and potential mechanisms for cardiovascular benefits are discussed.

18 Article Patients with coronary artery disease and diabetes need improved management: a report from the EUROASPIRE IV survey: a registry from the EuroObservational Research Programme of the European Society of Cardiology. 2015

Gyberg, Viveca / De Bacquer, Dirk / De Backer, Guy / Jennings, Catriona / Kotseva, Kornelia / Mellbin, Linda / Schnell, Oliver / Tuomilehto, Jaakko / Wood, David / Rydén, Lars / Amouyel, Philippe / Bruthans, Jan / Conde, Almudena Castro / Cifkova, Renata / Deckers, Jaap W / De Sutter, Johan / Dilic, Mirza / Dolzhenko, Maryna / Erglis, Andrejs / Fras, Zlatko / Gaita, Dan / Gotcheva, Nina / Goudevenos, John / Heuschmann, Peter / Laucevicius, Aleksandras / Lehto, Seppo / Lovic, Dragan / Miličić, Davor / Moore, David / Nicolaides, Evagoras / Oganov, Raphael / Pająk, Andrzej / Pogosova, Nana / Reiner, Zeljko / Stagmo, Martin / Störk, Stefan / Tokgözoğlu, Lale / Vulic, Dusko / Anonymous4140844. ·Cardiology Unit, Department of Medicine, Karolinska Institutet, Karolinska University Hospital Solna, 171 76, Stockholm, Sweden. vivecagyberg@gmail.com. · Centre for Family Medicine, Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, Huddinge, Sweden. vivecagyberg@gmail.com. · European Society of Cardiology, Les Templiers, 2035 route des Colles, CS 80179 BIOT, 06903, Sophia Antipolis Cedex, France. Dirk.DeBacquer@UGent.be. · Department of Public Health, Ghent University, Ghent, Belgium. Dirk.DeBacquer@UGent.be. · European Society of Cardiology, Les Templiers, 2035 route des Colles, CS 80179 BIOT, 06903, Sophia Antipolis Cedex, France. guy.debacker@ugent.be. · Department of Public Health, Ghent University, Ghent, Belgium. guy.debacker@ugent.be. · European Society of Cardiology, Les Templiers, 2035 route des Colles, CS 80179 BIOT, 06903, Sophia Antipolis Cedex, France. c.jennings@imperial.ac.uk. · Department of Cardiovascular Medicine, National Heart and Lung Institute, Imperial College London, London, UK. c.jennings@imperial.ac.uk. · European Society of Cardiology, Les Templiers, 2035 route des Colles, CS 80179 BIOT, 06903, Sophia Antipolis Cedex, France. k.kotseva@imperial.ac.uk. · Department of Cardiovascular Medicine, National Heart and Lung Institute, Imperial College London, London, UK. k.kotseva@imperial.ac.uk. · Cardiology Unit, Department of Medicine, Karolinska Institutet, Karolinska University Hospital Solna, 171 76, Stockholm, Sweden. linda.mellbin@ki.se. · European Society of Cardiology, Les Templiers, 2035 route des Colles, CS 80179 BIOT, 06903, Sophia Antipolis Cedex, France. linda.mellbin@ki.se. · Forschergruppe Diabetes e.V. at the Helmholtz Center, Munich, Germany. Oliver.Schnell@lrz.uni-muenchen.de. · European Society of Cardiology, Les Templiers, 2035 route des Colles, CS 80179 BIOT, 06903, Sophia Antipolis Cedex, France. jaakko.tuomilehto@thl.fi. · Centre for Vascular Prevention, Danube-University Krems, Krems, Austria. jaakko.tuomilehto@thl.fi. · Department of Chronic Disease Prevention, National Institute for Health and Welfare, Helsinki, Finland. jaakko.tuomilehto@thl.fi. · Instituto de Investigacion Sanitaria del Hospital Universario LaPaz (IdiPAZ), Madrid, Spain. jaakko.tuomilehto@thl.fi. · Diabetes Research Group, King Abdulaziz University, Jeddah, Saudi Arabia. jaakko.tuomilehto@thl.fi. · European Society of Cardiology, Les Templiers, 2035 route des Colles, CS 80179 BIOT, 06903, Sophia Antipolis Cedex, France. d.wood@imperial.ac.uk. · Department of Cardiovascular Medicine, National Heart and Lung Institute, Imperial College London, London, UK. d.wood@imperial.ac.uk. · Cardiology Unit, Department of Medicine, Karolinska Institutet, Karolinska University Hospital Solna, 171 76, Stockholm, Sweden. Lars.Ryden@ki.se. · European Society of Cardiology, Les Templiers, 2035 route des Colles, CS 80179 BIOT, 06903, Sophia Antipolis Cedex, France. Lars.Ryden@ki.se. · Institut Pasteur de Lille, Inserm U744, Université Lille Nord de France, 1 rue du Professeur Calmette B.P. 245, 59019, Lille, France. Philippe.amouyel@pasteur-lille.Fr. · European Society of Cardiology, Les Templiers, 2035 route des Colles, CS 80179 BIOT, 06903, Sophia Antipolis Cedex, France. jan.bruthans@seznam.cz. · Center for Cardiovascular Prevention, 1st School of Medicine, Charles University and Thomayer Hospital, Vídeňská 800, 140 59, Prague, Czech Republic. jan.bruthans@seznam.cz. · Cardiac Rehabilitation Unit, Cardiology Department, Hospital Universitario La Paz, Madrid, Spain. almudenacastroconde@yahoo.es. · European Society of Cardiology, Les Templiers, 2035 route des Colles, CS 80179 BIOT, 06903, Sophia Antipolis Cedex, France. renata.cifkova@ftn.cz. · Center for Cardiovascular Prevention, 1st School of Medicine, Charles University and Thomayer Hospital, Vídeňská 800, 140 59, Prague, Czech Republic. renata.cifkova@ftn.cz. · European Society of Cardiology, Les Templiers, 2035 route des Colles, CS 80179 BIOT, 06903, Sophia Antipolis Cedex, France. j.deckers@erasmusmc.nl. · Thoraxcenter's Department of Cardiology, Dr Molewaterplein 50, 3000 DR, Rotterdam, The Netherlands. j.deckers@erasmusmc.nl. · European Society of Cardiology, Les Templiers, 2035 route des Colles, CS 80179 BIOT, 06903, Sophia Antipolis Cedex, France. johan.desutter@ugent.be. · Department of Internal Medicine, University of Ghent, De Pintelaan 185, 9000, Ghent, Belgium. johan.desutter@ugent.be. · European Society of Cardiology, Les Templiers, 2035 route des Colles, CS 80179 BIOT, 06903, Sophia Antipolis Cedex, France. mdilic@bih.net.ba. · Clinical Center University of Sarajevo, Bolnička 25, 71000, Sarajevo, Bosnia and Herzegovina. mdilic@bih.net.ba. · Department of Cardiology of Shupyk's Medical Academy of Postgraduate Education, 9 Dorohozhyts'ka str, Kiev, 04112, Ukraine. marinadolzhenko@mail.ru. · European Society of Cardiology, Les Templiers, 2035 route des Colles, CS 80179 BIOT, 06903, Sophia Antipolis Cedex, France. a.a.erglis@stradini.lv. · University of Latvia, Pauls Stradins Clinical University Hospital, Pilsonu Street 13, Riga, 1002, Latvia. a.a.erglis@stradini.lv. · European Society of Cardiology, Les Templiers, 2035 route des Colles, CS 80179 BIOT, 06903, Sophia Antipolis Cedex, France. zlatko.fras@telemach.net. · Preventive Cardiology Unit, Division of Internal Medicine, University Medical Centre Ljubljana, Zaloška 7, 1525, Ljubljana, Slovenia. zlatko.fras@telemach.net. · Medical Faculty, University of Ljubljana, Vrazov trg 2, 1000, Ljubljana, Slovenia. zlatko.fras@telemach.net. · European Society of Cardiology, Les Templiers, 2035 route des Colles, CS 80179 BIOT, 06903, Sophia Antipolis Cedex, France. dgaita@cardiologie.ro. · Institutul de Boli Cardiovasculare, Universitatea de Medicina si Farmacie "Victor Babes", Timisoara, Romania. dgaita@cardiologie.ro. · Department of Cardiology, National Heart Hospital, 65, Konyovitsa, 1309, Sofia, Bulgaria. ngotcheva@abv.bg. · European Society of Cardiology, Les Templiers, 2035 route des Colles, CS 80179 BIOT, 06903, Sophia Antipolis Cedex, France. igoudev@cc.uoi.gr. · Cardiology Department of Medical School, University of Ioannina, Ioannina, Greece. igoudev@cc.uoi.gr. · Institute of Clinical Epidemiology and Biometry, University of Würzburg, Würzburg, Germany. E_Heuschma_P@klinik.uni-wuerzburg.de. · Comprehensive Heart Failure Center, University of Würzburg, Würzburg, Germany. E_Heuschma_P@klinik.uni-wuerzburg.de. · Clinical Trial Center Würzburg, University Hospital Würzburg, Josef-Schneider-Str. 2, 97080, Würzburg, Germany. E_Heuschma_P@klinik.uni-wuerzburg.de. · European Society of Cardiology, Les Templiers, 2035 route des Colles, CS 80179 BIOT, 06903, Sophia Antipolis Cedex, France. alius@cardio.it. · Clinic of Cardiovascular Diseases of Vilnius University, Santariskiu 2, 08661, Vilnius, Lithuania. alius@cardio.it. · Heart and Vascular Medicine of Vilnius University Hospital Santariskiu Clinics, Santariskiu 2, 08661, Vilnius, Lithuania. alius@cardio.it. · Kuopio University Hospital, Rakennus 5/6. Kerros, Puijonlaaksontie 2, 70210, Kuopio, Finland. seppo.lehto@varkaus.fi. · European Society of Cardiology, Les Templiers, 2035 route des Colles, CS 80179 BIOT, 06903, Sophia Antipolis Cedex, France. draganl1@sbb.rs. · Clinic for Internal Medicine Intermedica, Jovana Ristica 20/2, 18000, Nis, Serbia. draganl1@sbb.rs. · European Society of Cardiology, Les Templiers, 2035 route des Colles, CS 80179 BIOT, 06903, Sophia Antipolis Cedex, France. d.milicic@mail.inet.hr. · University of Zagreb School of Medicine and University Hospital Centre Zagreb, Kispaticeva 12, HR-10000, Zagreb, Croatia. d.milicic@mail.inet.hr. · The Adelaide and Meath Hospital, Tallaght, Dublin 24, Ireland. David.Moore@amnch.ie. · European Society of Cardiology, Les Templiers, 2035 route des Colles, CS 80179 BIOT, 06903, Sophia Antipolis Cedex, France. evnicor@cytanet.com.cy. · University of Nicosia Medical School, Nicosia General Hospital, 2029 Strovolos, Nicosia, Cyprus. evnicor@cytanet.com.cy. · National Research Center for Preventive Medicine of the Ministry of Healthcare of the Russian Federation, 10 Petroverigsky per, 101990, Moscow, Russia. oganov@gnicpm.ru. · Department of Epidemiology and Population Studies, Faculty of Health Sciences, Jafiellonian University Medical College, Grzegórzecka 20, 31-531, Cracow, Poland. andrzej.pajak@uj.edu.pl. · European Society of Cardiology, Les Templiers, 2035 route des Colles, CS 80179 BIOT, 06903, Sophia Antipolis Cedex, France. NPogosova@gnicpm.ru. · Federal Health Centre and Department of Chronic Noncommunicable Diseases Prevention, National Research Centre for Preventive Medicine, 10 Petroverigsky per, 101953, Moscow, Russia. NPogosova@gnicpm.ru. · European Society of Cardiology, Les Templiers, 2035 route des Colles, CS 80179 BIOT, 06903, Sophia Antipolis Cedex, France. zreiner@kbc-zagreb.hr. · University Hospital Centre Zagreb, School of Medicine, University of Zagreb, Kišpatićeva 12, 10000, Zagreb, Croatia. zreiner@kbc-zagreb.hr. · Department of Heart failure and Valve Disease, Skåne University Hospital, Lund, Sweden. Martin.Stagmo@skane.se. · Comprehensive Heart Failure Centre and Department of Medicine I, University of Würzburg, Straubmühlweg 2a, 97078, Würzburg, Germany. Stoerk_S@medizin.uni-wuerzburg.de. · European Society of Cardiology, Les Templiers, 2035 route des Colles, CS 80179 BIOT, 06903, Sophia Antipolis Cedex, France. lalet@hacettepe.edu.tr. · Hacettepe University, 06690, Ankara, Turkey. lalet@hacettepe.edu.tr. · Centre for Medical Research, School of Medicine, University of Banja Luka, Vuka Karadzica 6, 78000, Banja Luka, Republic of Srpska, Bosnia and Herzegovina. dule@blic.net. ·Cardiovasc Diabetol · Pubmed #26427624.

ABSTRACT: BACKGROUND: In order to influence every day clinical practice professional organisations issue management guidelines. Cross-sectional surveys are used to evaluate the implementation of such guidelines. The present survey investigated screening for glucose perturbations in people with coronary artery disease and compared patients with known and newly detected type 2 diabetes with those without diabetes in terms of their life-style and pharmacological risk factor management in relation to contemporary European guidelines. METHODS: A total of 6187 patients (18-80 years) with coronary artery disease and known glycaemic status based on a self reported history of diabetes (previously known diabetes) or the results of an oral glucose tolerance test and HbA1c (no diabetes or newly diagnosed diabetes) were investigated in EUROASPIRE IV including patients in 24 European countries 2012-2013. The patients were interviewed and investigated in order to enable a comparison between their actual risk factor control with that recommended in current European management guidelines and the outcome in previously conducted surveys. RESULTS: A total of 2846 (46%) patients had no diabetes, 1158 (19%) newly diagnosed diabetes and 2183 (35%) previously known diabetes. The combined use of all four cardioprotective drugs in these groups was 53, 55 and 60%, respectively. A blood pressure target of <140/90 mmHg was achieved in 68, 61, 54% and a LDL-cholesterol target of <1.8 mmol/L in 16, 18 and 28%. Patients with newly diagnosed and previously known diabetes reached an HbA1c <7.0% (53 mmol/mol) in 95 and 53% and 11% of those with previously known diabetes had an HbA1c >9.0% (>75 mmol/mol). Of the patients with diabetes 69% reported on low physical activity. The proportion of patients participating in cardiac rehabilitation programmes was low (≈40 %) and only 27% of those with diabetes had attended diabetes schools. Compared with data from previous surveys the use of cardioprotective drugs had increased and more patients were achieving the risk factor treatment targets. CONCLUSIONS: Despite advances in patient management there is further potential to improve both the detection and management of patients with diabetes and coronary artery disease.

19 Article Improved glycemic control due to sitagliptin is not related to cortisol or the surrogate marker IGFBP-1 for hepatic insulin sensitivity. 2015

Arnetz, Lisa / Hage, Camilla / Ekberg, Neda Rajamand / Alvarsson, Michael / Brismar, Kerstin / Norhammar, Anna / Mellbin, Linda. ·Department of Molecular Medicine and Surgery, Karolinska Institutet, Karolinska University Hospital Solna, 17176 Stockholm, Sweden; Dept. of Endocrinology, Metabolism and Diabetes, Karolinska University Hospital Solna, 17176 Stockholm, Sweden. Electronic address: Lisa.Arnetz@karolinska.se. · Cardiology Unit, Department of Medicine, Karolinska Institutet, 17176 Stockholm, Sweden. Electronic address: camilla.hage@karolinska.se. · Department of Molecular Medicine and Surgery, Karolinska Institutet, Karolinska University Hospital Solna, 17176 Stockholm, Sweden; Dept. of Endocrinology, Metabolism and Diabetes, Karolinska University Hospital Solna, 17176 Stockholm, Sweden. Electronic address: neda.ekberg@ki.se. · Department of Molecular Medicine and Surgery, Karolinska Institutet, Karolinska University Hospital Solna, 17176 Stockholm, Sweden; Dept. of Endocrinology, Metabolism and Diabetes, Karolinska University Hospital Solna, 17176 Stockholm, Sweden. Electronic address: michael.alvarsson@karolinska.se. · Department of Molecular Medicine and Surgery, Karolinska Institutet, Karolinska University Hospital Solna, 17176 Stockholm, Sweden; Dept. of Endocrinology, Metabolism and Diabetes, Karolinska University Hospital Solna, 17176 Stockholm, Sweden. Electronic address: kerstin.brismar@ki.se. · Cardiology Unit, Department of Medicine, Karolinska Institutet, 17176 Stockholm, Sweden. Electronic address: anna.norhammar@karolinska.se. · Cardiology Unit, Department of Medicine, Karolinska Institutet, 17176 Stockholm, Sweden. Electronic address: linda.mellbin@karolinska.se. ·Growth Horm IGF Res · Pubmed #26283275.

ABSTRACT: IMPORTANCE: Elevated cortisol levels and dysregulated insulin-like growth factor binding protein-1 (IGFBP-1; a marker of hepatic insulin sensitivity) are both related to insulin resistance and glucose abnormalities. It is unknown whether improvement in these parameters is related to improved glucose metabolism during treatment with sitagliptin. OBJECTIVE: To determine whether improved insulin sensitivity and beta-cell function during treatment with sitagliptin is related to lower cortisol levels and/or improved regulation of IGFBP-1 in patients with recent acute coronary syndrome (ACS) and newly discovered glucose abnormalities. DESIGN: Samples were taken from The BEta-cell function in Glucose abnormalities and Acute Myocardial Infarction (BEGAMI) trial, a double-blinded, placebo-controlled randomized clinical trial on the efficacy and safety of sitagliptin for patients with ACS and newly discovered glucose abnormalities. SETTING: Cardiology departments (cardiac ICU and outpatient clinic) in two hospitals in Stockholm, Sweden. PARTICIPANTS: Subjects hospitalized (or recently hospitalized) for ACS, in whom an oral glucose tolerance test revealed previously unknown glucose abnormalities. INTERVENTIONS: Subjects were randomized to sitagliptin 100mg once daily (n=34) or placebo (n=37) for twelve weeks. Oral glucose tolerance test (OGTT) and randomization occurred after stabilization median 7 days after ACS. MAIN OUTCOMES AND MEASURES: Fasting serum cortisol and IGFBP-1 were analyzed before OGTT, around 8a.m., and after at 10a.m. The latter time point was chosen as the spread in cortisol levels around is small then, allowing improved chances to detect differences between groups. RESULTS: Glucose tolerance and insulin sensitivity improved in both groups, while HbA1c and indices of β-cell function improved only in the sitagliptin group as reported previously. Both groups displayed decreased cortisol levels around 10a.m. (from 338±21 to 278±14 nmol/L, p=0.038, in the sitagliptin group; from 343±17 to 302±15 nmol/L, p=0.017, in the placebo group), and improved correlation between fasting log-IGFBP-1 and insulin. CONCLUSIONS AND RELEVANCE: These findings suggest that a stress-related elevation in cortisol may have negative impact on glucose tolerance in patients with recent ACS. However, improved glycemic control with sitagliptin does not appear to be related to changes in cortisol levels or hepatic insulin sensitivity as assessed by IGFBP-1.

20 Article Detection of circulating hcmv-miR-UL112-3p in patients with glioblastoma, rheumatoid arthritis, diabetes mellitus and healthy controls. 2014

Mohammad, Abdul-Aleem / Rahbar, Afsar / Lui, Weng-Onn / Davoudi, Belghis / Catrina, Anca / Stragliotto, Giuseppe / Mellbin, Linda / Hamsten, Anders / Rydén, Lars / Yaiw, Koon-Chu / Söderberg-Nauclér, Cecilia. ·Experimental Cardiovascular Research Unit, Department of Medicine-Solna, Center for Molecular Medicine, Karolinska Institute, Stockholm, Sweden. · Department of Oncology-Pathology, Karolinksa Institutet, Cancer Center Karolinska, Karolinska University Hospital, Stockholm, Sweden. · Rheumatology Unit, Department of Medicine, Karolinska University Hospital, Karolinska Institutet, Stockholm, Sweden. · Cardiology Unit, Department of Medicine Solna, Karolinska Institute, Stockholm, Sweden. · Atherosclerosis Research Unit, Center for Molecular Medicine, Karolinska Institute, Stockholm, Sweden. ·PLoS One · Pubmed #25462570.

ABSTRACT: BACKGROUND: microRNAs (miRNA) are 18-22 nucleotides long non-coding RNAs that regulate gene expression at a post-transcriptional level. Human cytomegalovirus (HCMV) encodes at least 26 known mature miRNAs. hcmv-miR-UL112-3p (miR-UL112-3p) is the most well characterized HCMV miRNA, which is suggested to play role in establishment and maintenance of viral latency. Elevated miR-UL112-3p levels have been reported to be present in plasma of patients with hypertension. OBJECTIVES: In this study, we aimed to quantify miR-UL112-3p levels in the plasma/serum of patients with Diabetes Mellitus (DM; from the DIGAMI-2 cohort), Glioblastoma multiforme (GBM), Rheumatoid Arthritis (RA) and Healthy Controls (HC). STUDY DESIGN: Total RNA was isolated from plasma/serum samples of 87 patients and controls, a TaqMan miRNA assay was performed to detect miR-UL112-3p and the copy numbers were normalized to 10 ng of total RNA. HCMV IgG and IgM were analysed using ELISA. RESULTS: HCMV miR-UL112-3p was detected in 14/27 (52%) of DM, 5/20 (25%) of GBM, 1/20 (5%) of RA patients and in 2/20 (10%) of HC, respectively. Anti-HCMV IgG was detected in 85%, 65%, 75% of patients and 70% of HC, respectively. Anti-HCMV IgM was found only in one GBM patient of 87 examined patients and controls. CONCLUSIONS: A higher prevalence of miR-UL112-3p was detected in DM and GBM patients than in RA patients and HC. Elevated levels of miR-UL112-3p and higher prevalence of HCMV IgG were observed in DM patients. Whether the presence of circulating miR-UL112-3p denotes a biomarker of HCMV latency or active replication in patients warrants further investigation.