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  • 1.
    Fortin, Elena
    et al.
    Karolinska Inst, Dept Med K2, Div Cardiol, Norrbacka S1 02, S-17176 Stockholm, Sweden..
    Ferrannini, Giulia
    Karolinska Inst, Dept Med K2, Div Cardiol, Norrbacka S1 02, S-17176 Stockholm, Sweden..
    Campi, Beatrice
    CNR, Inst Clin Physiol, Pisa, Italy..
    Mellbin, Linda
    Karolinska Inst, Dept Med K2, Div Cardiol, Norrbacka S1 02, S-17176 Stockholm, Sweden.;Karolinska Univ Hosp, Heart Vasc & Neuro Theme, Stockholm, Sweden..
    Norhammar, Anna
    Karolinska Inst, Dept Med K2, Div Cardiol, Norrbacka S1 02, S-17176 Stockholm, Sweden.;Capio St Gorans Hosp, Stockholm, Sweden..
    Näsman, Per
    KTH, School of Architecture and the Built Environment (ABE), Real Estate and Construction Management, Real Estate Economics and Finance.
    Saba, Alessandro
    Univ Pisa, Dept Pathol, Mass Spectrometry Lab, Pisa, Italy.;Santa Chiara Univ Hosp, Clin Pathol Lab, Pisa, Italy..
    Ferrannini, Ele
    CNR, Inst Clin Physiol, Pisa, Italy..
    Ryden, Lars
    Karolinska Inst, Dept Med K2, Div Cardiol, Norrbacka S1 02, S-17176 Stockholm, Sweden..
    Plasma mannose as a novel marker of myocardial infarction across different glycaemic states: A case control study2022In: Cardiovascular Diabetology, E-ISSN 1475-2840, Vol. 21, no 1, article id 195Article in journal (Refereed)
    Abstract [en]

    Background Plasma mannose, an emerging novel biomarker of insulin resistance, is associated with both diabetes mellitus and coronary atherosclerosis, but the relationship between mannose concentrations and myocardial infarction (MI) across different glycaemic states remains to be elucidated. The aim of this study was to investigate the independent association between mannose and a first MI in a group of subjects characterized according to their glycaemic state. Methods Fasting plasma mannose concentrations were analysed in 777 patients 6-10 weeks after a first myocardial infarction and in 770 matched controls by means of high-performance liquid chromatography coupled to tandem mass spectrometry. Participants without known diabetes mellitus were categorized by an oral glucose tolerance test (OGTT) as having normal glucose tolerance (NGT, n = 1045), impaired glucose tolerance (IGT, n = 246) or newly detected type 2 diabetes (T2DM, n = 112). The association between mannose and MI was investigated across these glycaemic states by logistic regression. Results Mannose levels increased across the glycaemic states (p < 0.0001) and were significantly associated with a first MI in the whole study population (odds ratio, OR: 2.2; 95% CI 1.4 to - 3.5). Considering the different subgroups separately, the association persisted only in subjects with NGT (adjusted OR: 2.0; 95% CI 1.2-3.6), but not in subgroups with glucose perturbations (adjusted OR: 1.8, 95% CI 0.8-3.7). Conclusions Mannose concentrations increased across worsening levels of glucose perturbations but were independently associated with a first MI only in NGT individuals. Thus, mannose might be a novel, independent risk marker for MI, possibly targeted for the early management of previously unidentified patients at high cardiovascular risk.

  • 2.
    Fortin, Elena
    et al.
    Karolinska Inst, Dept Med Solna, Stockholm, Sweden.
    Lundin, Magnus
    Karolinska Inst, Dept Clin Physiol, Stockholm, Sweden.
    Mellbin, Linda
    Karolinska Inst, Dept Med Solna, Stockholm, Sweden; Karolinska Univ Hosp, Cardiol Unit, Stockholm, Sweden.
    Norhammar, Anna
    Karolinska Inst, Dept Med Solna, Stockholm, Sweden; Capio St Gorans Hosp, Stockholm, Sweden.
    Näsman, Per
    KTH, School of Architecture and the Built Environment (ABE), Real Estate and Construction Management, Real Estate Economics and Finance.
    Smetana, Stina
    Karolinska Univ Hosp, Cardiol Unit, Stockholm, Sweden.
    Sörensson, Peder
    Karolinska Inst, Dept Med Solna, Stockholm, Sweden; Karolinska Inst, Dept Clin Physiol, Stockholm, Sweden.
    Ferrannini, Ele
    CNR, Dept Clin Physiol, Pisa, Italy.
    Rydén, Lars
    Karolinska Inst, Dept Med Solna, Stockholm, Sweden.
    Ferrannini, Giulia
    Karolinska Inst, Dept Med Solna, Stockholm, Sweden; Södertälje Hosp, Internal Med Unit, Södertälje, Stockholm, Sweden.
    Empagliflozin improves insulin sensitivity in patients with recent acute coronary syndrome and newly detected dysglycaemia: Experiences from the randomized, controlled SOCOGAMI trial2023In: Cardiovascular Diabetology, E-ISSN 1475-2840, Vol. 22, no 1, p. 208-Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Empagliflozin reduces the risk of cardiovascular disease (CVD) in patients with type 2 diabetes (T2DM) and high cardiovascular risk via mechanisms which have not been fully explained. The mechanisms of such benefit have not been fully understood, and whether empagliflozin can be safely administered as first-line treatment in patients with CVD at the initial stages of glycaemic perturbations remains to be established. We investigated the effects of empagliflozin on insulin resistance, insulin sensitivity and β-cell function indexes in patients with a recent acute coronary event and newly detected dysglycaemia, i.e., impaired glucose tolerance (IGT) or T2DM. METHODS: Forty-two patients (mean age 67.5 years, 19% females) with a recent myocardial infarction (n = 36) or unstable angina (n = 6) and newly detected dysglycaemia were randomized to either empagliflozin 25 mg daily (n = 20) or placebo (n = 22). Patients were investigated with stress-perfusion cardiac magnetic resonance imaging before randomization, 7 months after the start of study drug and 3 months following its cessation. Indexes of insulin resistance, sensitivity and β-cell function were calculated based on glucose and insulin values from 2-hour oral glucose tolerance tests (OGTT) and fasting C-peptide. The differences in glucose, insulin, C-peptide, mannose levels and indexes between the two groups were computed by repeated measures ANOVA including an interaction term between the treatment allocation and the time of visit. RESULTS: After 7 months, empagliflozin significantly decreased glucose and insulin values during the OGTT, whereas C-peptide, mannose and HbA1c did not differ. Empagliflozin significantly improved insulin sensitivity indexes but did not impact insulin resistance and β-cell function. After cessation of the drug, all indexes returned to initial levels. Insulin sensitivity indexes were inversely correlated with left ventricular mass at baseline. CONCLUSIONS: Empagliflozin improved insulin sensitivity indexes in patients with a recent coronary event and drug naïve dysglycaemia. These findings support the safe use of empagliflozin as first-line glucose-lowering treatment in patients at very high cardiovascular risk with newly diagnosed dysglycaemia. TRIAL REGISTRATION NUMBER: EudraCT number 2015-004571-73.

  • 3.
    Jin, Han
    et al.
    KTH, Centres, Science for Life Laboratory, SciLifeLab. KTH, School of Engineering Sciences in Chemistry, Biotechnology and Health (CBH), Protein Science, Systems Biology. Central Laboratory, Tianjin Medical University General Hospital, Tianjin, China; Department of Pathology, Cardiovascular Research Institute Maastricht (CARIM), Maastricht UMC+, Maastricht, the Netherlands.
    Zhang, Cheng
    KTH, Centres, Science for Life Laboratory, SciLifeLab. KTH, School of Engineering Sciences in Chemistry, Biotechnology and Health (CBH), Protein Science, Systems Biology.
    Nagenborg, Jan
    Department of Pathology, Cardiovascular Research Institute Maastricht (CARIM), Maastricht UMC+, Maastricht, the Netherlands.
    Juhasz, Peter
    PJConsulting, Natick, MA, USA.
    Ruder, Adele V.
    Department of Pathology, Cardiovascular Research Institute Maastricht (CARIM), Maastricht UMC+, Maastricht, the Netherlands.
    Sikkink, Cornelis J.J.M.
    Zuyderland Medical Centre, Sittard-Geleen, The Netherlands.
    Mees, Barend M.E.
    Department of Surgery, Maastricht UMC+, Maastricht, the Netherlands.
    Waring, Olivia
    Department of Pathology, Cardiovascular Research Institute Maastricht (CARIM), Maastricht UMC+, Maastricht, the Netherlands.
    Sluimer, Judith C.
    Department of Pathology, Cardiovascular Research Institute Maastricht (CARIM), Maastricht UMC+, Maastricht, the Netherlands; Centre for Cardiovascular Science, University of Edinburgh, Edinburgh, Scotland.
    Neumann, Dietbert
    Department of Pathology, Cardiovascular Research Institute Maastricht (CARIM), Maastricht UMC+, Maastricht, the Netherlands.
    Goossens, Pieter
    Department of Pathology, Cardiovascular Research Institute Maastricht (CARIM), Maastricht UMC+, Maastricht, the Netherlands.
    Donners, Marjo M.P.C.
    Department of Pathology, Cardiovascular Research Institute Maastricht (CARIM), Maastricht UMC+, Maastricht, the Netherlands.
    Mardinoglu, Adil
    KTH, Centres, Science for Life Laboratory, SciLifeLab. KTH, School of Engineering Sciences in Chemistry, Biotechnology and Health (CBH), Protein Science, Systems Biology. Science for Life Laboratory (SciLifeLab), KTH-Royal Institute of Technology, Solna, Sweden; Centre for Host-Microbiome Interactions, Faculty of Dentistry, Oral & Craniofacial Sciences, King’s College London, London, UK.
    Biessen, Erik A.L.
    Department of Pathology, Cardiovascular Research Institute Maastricht (CARIM), Maastricht UMC+, Maastricht, the Netherlands; Institute for Molecular Cardiovascular Research, RWTH Aachen University, Aachen, Germany.
    Genome-scale metabolic network of human carotid plaque reveals the pivotal role of glutamine/glutamate metabolism in macrophage modulating plaque inflammation and vulnerability2024In: Cardiovascular Diabetology, E-ISSN 1475-2840, Vol. 23, no 1, article id 240Article in journal (Refereed)
    Abstract [en]

    Background: Metabolism is increasingly recognized as a key regulator of the function and phenotype of the primary cellular constituents of the atherosclerotic vascular wall, including endothelial cells, smooth muscle cells, and inflammatory cells. However, a comprehensive analysis of metabolic changes associated with the transition of plaque from a stable to a hemorrhaged phenotype is lacking. Methods: In this study, we integrated two large mRNA expression and protein abundance datasets (BIKE, n = 126; MaasHPS, n = 43) from human atherosclerotic carotid artery plaque to reconstruct a genome-scale metabolic network (GEM). Next, the GEM findings were linked to metabolomics data from MaasHPS, providing a comprehensive overview of metabolic changes in human plaque. Results: Our study identified significant changes in lipid, cholesterol, and inositol metabolism, along with altered lysosomal lytic activity and increased inflammatory activity, in unstable plaques with intraplaque hemorrhage (IPH+) compared to non-hemorrhaged (IPH−) plaques. Moreover, topological analysis of this network model revealed that the conversion of glutamine to glutamate and their flux between the cytoplasm and mitochondria were notably compromised in hemorrhaged plaques, with a significant reduction in overall glutamate levels in IPH+ plaques. Additionally, reduced glutamate availability was associated with an increased presence of macrophages and a pro-inflammatory phenotype in IPH+ plaques, suggesting an inflammation-prone microenvironment. Conclusions: This study is the first to establish a robust and comprehensive GEM for atherosclerotic plaque, providing a valuable resource for understanding plaque metabolism. The utility of this GEM was illustrated by its ability to reliably predict dysregulation in the cholesterol hydroxylation, inositol metabolism, and the glutamine/glutamate pathway in rupture-prone hemorrhaged plaques, a finding that may pave the way to new diagnostic or therapeutic measures.

  • 4.
    Meziani, Sara
    et al.
    Karolinska Inst, Dept Med Solna, Solnavagen 1, S-17176 Stockholm, Sweden..
    Ferrannini, Giulia
    Karolinska Inst, Dept Med Solna, Solnavagen 1, S-17176 Stockholm, Sweden..
    Bjerre, Mette
    Aarhus Univ, Dept Clin Med, Med Steno Aarhus Res Lab, Aarhus, Denmark..
    Hansen, Troels K.
    Aarhus Univ Hosp, Steno Diabet Ctr Aarhus, Aarhus, Denmark..
    Ritsinger, Viveca
    Karolinska Inst, Dept Med Solna, Solnavagen 1, S-17176 Stockholm, Sweden.;Reg Kronoberg, Dept Res & Dev, Växjö, Sweden..
    Norhammar, Anna
    Karolinska Inst, Dept Med Solna, Solnavagen 1, S-17176 Stockholm, Sweden.;Capio St Gorans Hosp, Stockholm, Sweden..
    Gyberg, Viveca
    Karolinska Inst, Dept Med Solna, Solnavagen 1, S-17176 Stockholm, Sweden..
    Näsman, Per
    KTH, School of Architecture and the Built Environment (ABE), Real Estate and Construction Management, Real Estate Economics and Finance.
    Ryden, Lars
    Karolinska Inst, Dept Med Solna, Solnavagen 1, S-17176 Stockholm, Sweden..
    Mellbin, Linda G.
    Karolinska Inst, Dept Med Solna, Solnavagen 1, S-17176 Stockholm, Sweden.;Karolinska Univ Hosp, Cardiol Unit, Stockholm, Sweden..
    Mannose-binding lectin does not explain the dismal prognosis after an acute coronary event in dysglycaemic patients: A report from the GAMI cohort2022In: Cardiovascular Diabetology, E-ISSN 1475-2840, Vol. 21, no 1, article id 129Article in journal (Refereed)
    Abstract [en]

    Background Mannose binding lectin (MBL) has been suggested to be associated with an impaired cardiovascular prognosis in dysglycaemic conditions, but results are still contrasting. Our aims are (i) to examine whether MBL levels differ between patients with an acute myocardial infarction (MI) and healthy controls and between subgroups with different glucose tolerance status, and (ii) to investigate the relation between MBL and future cardiovascular events. Methods MBL levels were assessed at discharge and after 3 months in 161 AMI patients without any previously known glucose perturbations and in 183 age- and gender-matched controls from the Glucose metabolism in patients with Acute Myocardial Infarction (GAMI) study. Participants were classified as having dysglycaemia, i.e. type 2 diabetes or impaired glucose tolerance, or not by an oral glucose tolerance test. The primary outcome was a composite of cardiovascular events comprising cardiovascular death, AMI, stroke or severe heart failure during 11 years of follow-up. Total and cardiovascular mortality served as secondary outcomes. Results At hospital discharge patients had higher MBL levels (median 1246 mu g/L) than three months later (median 575 mu g/L; p < 0.01), the latter did not significantly differ from those in the controls (801 mu g/L; p = 0.47). MBL levels were not affected by dysglycaemia either in patients or controls. Independent of glycaemic state, increasing MBL levels did not predict any of the studied outcomes in patients. In unadjusted analyses increasing MBL levels predicted cardiovascular events (hazard ratio HR: 1.67, 95% confidence interval CI 1.06-2.64) and total mortality (HR 1.53, 95% CI 1.12-2.10) in the control group. However, this did not remain in adjusted analyses. Conclusions Patients had higher MBL levels than controls during the hospital phase of AMI, supporting the assumption that elevated MBL reflects acute stress. MBL was not found to be independently associated with cardiovascular prognosis in patients with AMI regardless of glucose state.

  • 5.
    Riccio, Alessia
    et al.
    Cardiology Unit, Department of Medicine Solna, Karolinska Institute Stockholm, Stockholm, Sweden; Department of Clinical and Molecular Medicine, Sapienza University of Rome, Rome, Italy.
    Fortin, Elena
    Cardiology Unit, Department of Medicine Solna, Karolinska Institute Stockholm, Stockholm, Sweden.
    Mellbin, Linda
    Cardiology Unit, Department of Medicine Solna, Karolinska Institute Stockholm, Stockholm, Sweden; Heart, Vascular and Neuro Theme, Karolinska University Hospital, Stockholm, Sweden.
    Norhammar, Anna
    Cardiology Unit, Department of Medicine Solna, Karolinska Institute Stockholm, Stockholm, Sweden; Capio St Görans Hospital, Stockholm, Sweden.
    Näsman, Per
    KTH, School of Architecture and the Built Environment (ABE). Cardiology Unit, Department of Medicine Solna, Karolinska Institute Stockholm, Stockholm, Sweden.
    Rydén, Lars
    Cardiology Unit, Department of Medicine Solna, Karolinska Institute Stockholm, Stockholm, Sweden; Heart, Vascular and Neuro Theme, Karolinska University Hospital, Stockholm, Sweden.
    Sesti, Giorgio
    Department of Clinical and Molecular Medicine, Sapienza University of Rome, Rome, Italy.
    Ferrannini, Giulia
    Cardiology Unit, Department of Medicine Solna, Karolinska Institute Stockholm, Stockholm, Sweden; Internal Medicine Unit, Södertälje hospital, Södertälje, Sweden.
    Sex differences in the association between insulin resistance and non-fatal myocardial infarction across glycaemic states2024In: Cardiovascular Diabetology, E-ISSN 1475-2840, Vol. 23, no 1, article id 25Article in journal (Refereed)
    Abstract [en]

    Background: Females are generally less prone to cardiovascular (CV) events than males, but this protection is trumped by diabetes. The mechanism behind the increased relative risk in females with diabetes is not fully understood. Insulin resistance (IR) is suggested to be a more important contributor to CV morbidity in females than in males. We aim to investigate differences in the association between IR indexes (Homeostatic Model Assessment of IR - HOMA-IR, visceral adiposity index – VAI, and triglycerides/high-density lipoprotein-cholesterol - TG/HDL-C index), and a first non-fatal myocardial infarction (MI) across different glycaemic states. Methods: IR indexes were calculated in a population with (n = 696) and without (n = 707) a first non-fatal MI, free from known diabetes. MI cases were investigated at least six weeks after the event. All participants were categorized by an oral glucose tolerance test as having normal glucose tolerance, impaired fasting glucose, impaired glucose tolerance, or newly diagnosed diabetes. Comparison of proportion of glycaemic states by sex was tested by chi-square test. The associations between sex, a first non-fatal MI, IR indexes, and traditional CV risk factors were analysed by multivariate logistic regression models. Continuous variables were logarithmically transformed. Results: Of the total population 19% were females and 81% males, out of whom 47% and 50% had a first non-fatal MI, respectively. Compared with males, females were older, less often smokers, with lower body mass index and higher total cholesterol and high-density lipoprotein cholesterol levels. The proportion of glycaemic states did not differ between the sexes (p = 0.06). Females were less insulin resistant than males, especially among cases and with normal glucose tolerance. In logistic regression models adjusted for major CV risk factors including sex, the associations between VAI and TG/HDL-C index and a first non-fatal MI remained significant only in females (odds ratios and 95% confidence intervals: 1.7, 1.0-2.9, and 1.9, 1.1–3.4 respectively). Conclusions: These results support the assumption that IR indexes based on anthropometrics and lipid panel, i.e., VAI and TG/HDL-C, could be a better measure of IR and CV-predictor for non-fatal MI in females, even without glycaemic perturbations.

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