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Ulrik Ø Andersen Department of Clinical Biochemistry, Rigshospitalet, Copenhagen, Denmark
Institute of Biomedical Sciences, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark

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Dijana Terzic Department of Clinical Biochemistry, Rigshospitalet, Copenhagen, Denmark
Institute of Biomedical Sciences, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark

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Nicolai Jacob Wewer Albrechtsen Department of Clinical Biochemistry, Rigshospitalet, Copenhagen, Denmark
Institute of Biomedical Sciences, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark
Novo Nordisk Foundation Centre for Protein Research, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark

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Peter Dall Mark Department of Clinical Biochemistry, Rigshospitalet, Copenhagen, Denmark
Institute of Biomedical Sciences, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark

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Peter Plomgaard Department of Clinical Biochemistry, Rigshospitalet, Copenhagen, Denmark
Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark

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Jens F Rehfeld Department of Clinical Biochemistry, Rigshospitalet, Copenhagen, Denmark

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Finn Gustafsson Department of Cardiology, Rigshospitalet, Copenhagen, Denmark

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Jens P Goetze Department of Clinical Biochemistry, Rigshospitalet, Copenhagen, Denmark
Institute of Biomedical Sciences, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark

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Aims

Neprilysin degrades natriuretic peptides in circulation and is also suggested to degrade the gut hormones gastrin and cholecystokinin. Neprilysin inhibition has become a therapeutic strategy and thus a regimen in need of further testing in terms of other hormonal axes besides natriuretic peptides. The aim of this study was to examine whether acute inhibition of neprilysin affects meal-induced responses in gastrin and cholecystokinin concentrations in healthy individuals.

Methods and results

Nine healthy young men were included in an open-labelled, randomized cross-over clinical trial. The participants received a standardized meal (25 g fat, 26 g protein, 42 g carbohydrate) on two separate days with or without a one-time dosage of sacubitril ((194 mg)/valsartan (206 mg)). Blood pressure, heart rate and blood samples were measured and collected during the experiment. Statistical differences between groups were assessed using area under the curve together with an ANOVA with a Bonferroni post hoc test. Sacubitril/valsartan increased the postprandial plasma concentrations of both gastrin and cholecystokinin (80% (AUC0-270 min, P = 0.004) and 60% (AUC0-270 min, P = 0.003), respectively) compared with the control meal. No significant hemodynamic effects were noted (blood pressure, AUC0-270 min, P = 0.86, heart rate, AUC0-270 min, P = 0.96).

Conclusion

Our study demonstrates that sacubitril/valsartan increases the postprandial plasma concentrations of gastrin and cholecystokinin in healthy individuals. The results thus suggest that neprilysin-mediated degradation of gastrin and cholecystokinin is physiologically relevant and may have a role in heart failure patients treated with sacubitril/valsartan.

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Myrtille Fouché Department of Anaesthesiology and Critical Care Medicine, Edouard Herriot Hospital, Hospices Civils de Lyon, Lyon, France

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Yves Bouffard Department of Anaesthesiology and Critical Care Medicine, Edouard Herriot Hospital, Hospices Civils de Lyon, Lyon, France

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Mary-Charlotte Le Goff Department of Anaesthesiology and Critical Care Medicine, Edouard Herriot Hospital, Hospices Civils de Lyon, Lyon, France

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Johanne Prothet Department of Anaesthesiology and Critical Care Medicine, Edouard Herriot Hospital, Hospices Civils de Lyon, Lyon, France

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François Malavieille Department of Anaesthesiology and Critical Care Medicine, Edouard Herriot Hospital, Hospices Civils de Lyon, Lyon, France

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Pierre Sagnard Department of Anaesthesiology and Critical Care Medicine, Edouard Herriot Hospital, Hospices Civils de Lyon, Lyon, France

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Françoise Christin Department of Anaesthesiology and Critical Care Medicine, Edouard Herriot Hospital, Hospices Civils de Lyon, Lyon, France

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Davy Hayi-Slayman Department of Anaesthesiology and Critical Care Medicine, Edouard Herriot Hospital, Hospices Civils de Lyon, Lyon, France

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Arnaud Pasquer Department of Visceral Surgery, Edouard Herriot Hospital, Hospices Civils de Lyon, Lyon, France

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Gilles Poncet Department of Visceral Surgery, Edouard Herriot Hospital, Hospices Civils de Lyon, Lyon, France

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Thomas Walter Department of Hepatogastroenterology and Oncology, Edouard Herriot Hospital, Hospices Civils de Lyon, Lyon, France

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Thomas Rimmelé Department of Anaesthesiology and Critical Care Medicine, Edouard Herriot Hospital, Hospices Civils de Lyon, Lyon, France
EA 7426 Hospices Civils de Lyon-University Claude Bernard Lyon 1-Biomérieux ‘Pathophysiology of Injury-Induced Immunosuppression’ Pi3, Lyon, France

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Only few descriptions of intraoperative carcinoid syndrome (ioCS) have been reported. The primary objective of this study was to describe ioCS. A second aim was to identify risk factors of ioCS. We retrospectively analysed patients operated for small-bowel neuroendocrine tumour in our institution between 2007 and 2015, and receiving our preventive local regimen of octreotide continuous administration. ioCS was defined as highly probable in case of rapid (<5 min) arterial blood pressure changes ≥40%, not explained by surgical/anaesthetic management and regressive ≥20% after octreotide bolus injection. Probable cases were ioCS which did not meet all criteria of highly-probable ioCS. Suspected ioCS were detected on the anaesthesia record by an injection of octreotide due to a manifestation which did not meet the criteria for highly-probable or probable ioCS. A total of 81 patients (liver metastases: 59, prior carcinoid syndrome: 49, carcinoid heart disease: 7) were included; 139 ioCS occurred in 45 patients: 45 highly probable, 67 probable and 27 suspected. ioCs was hypertensive (91%) and/or hypotensive (29%). There was no factor, including the use of vasopressors, significantly associated with the occurrence of an ioCS. All surgeries were completed and one patient died from cardiac failure 4 days after surgery. After preoperative octreotide continuous infusion, ioCS were mainly hypertensive. No ioCS risk factors, including vasopressor use, were identified. No intraoperative carcinoid crisis occurred, suggesting the clinical relevance of a standardized octreotide prophylaxis protocol.

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Frans H H Leenen Brain and Heart Research Group, University of Ottawa Heart Institute, Ottawa, Ontario, Canada

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Mordecai P Blaustein Department of Physiology, University of Maryland School of Medicine, Baltimore, Maryland, USA
Department of Medicine, University of Maryland School of Medicine, Baltimore, Maryland, USA

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John M Hamlyn Department of Physiology, University of Maryland School of Medicine, Baltimore, Maryland, USA

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In the brain, angiotensinergic pathways play a major role in chronic regulation of cardiovascular and electrolyte homeostasis. Increases in plasma angiotensin II (Ang II), aldosterone, [Na+] and cytokines can directly activate these pathways. Chronically, these stimuli also activate a slow neuromodulatory pathway involving local aldosterone, mineralocorticoid receptors (MRs), epithelial sodium channels and endogenous ouabain (EO). This pathway increases AT1R and NADPH oxidase subunits and maintains/further increases the activity of angiotensinergic pathways. These brain pathways not only increase the setpoint of sympathetic activity per se, but also enhance its effectiveness by increasing plasma EO and EO-dependent reprogramming of arterial and cardiac function. Blockade of any step in this slow pathway or of AT1R prevents Ang II-, aldosterone- or salt and renal injury-induced forms of hypertension. MR/AT1R activation in the CNS also contributes to the activation of sympathetic activity, the circulatory and cardiac RAAS and increase in circulating cytokines in HF post MI. Chronic central infusion of an aldosterone synthase inhibitor, MR blocker or AT1R blocker prevents a major part of the structural remodeling of the heart and the decrease in LV function post MI, indicating that MR activation in the CNS post MI depends on aldosterone, locally produced in the CNS. Thus, Ang II, aldosterone and EO are not simply circulating hormones that act on the CNS but rather they are also paracrine neurohormones, locally produced in the CNS, that exert powerful effects in key CNS pathways involved in the long-term control of sympathetic and neuro-endocrine function and cardiovascular homeostasis.

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Susanna Cirera
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Sophia G Moesgaard Department of Veterinary Clinical and Animal Sciences, Novo Nordisk A/S, Department of Clinical Biochemistry, Department of Cardiothoracic and Vascular Surgery, Department of Clinical Biochemistry, Department of Veterinary Disease Biology, Department of Clinical Chemistry, Faculty of Health and Medical Sciences, University of Copenhagen, Frederiksberg C, Denmark

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Nora E Zois Department of Veterinary Clinical and Animal Sciences, Novo Nordisk A/S, Department of Clinical Biochemistry, Department of Cardiothoracic and Vascular Surgery, Department of Clinical Biochemistry, Department of Veterinary Disease Biology, Department of Clinical Chemistry, Faculty of Health and Medical Sciences, University of Copenhagen, Frederiksberg C, Denmark

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Nathja Ravn Department of Veterinary Clinical and Animal Sciences, Novo Nordisk A/S, Department of Clinical Biochemistry, Department of Cardiothoracic and Vascular Surgery, Department of Clinical Biochemistry, Department of Veterinary Disease Biology, Department of Clinical Chemistry, Faculty of Health and Medical Sciences, University of Copenhagen, Frederiksberg C, Denmark

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Jens P Goetze Department of Veterinary Clinical and Animal Sciences, Novo Nordisk A/S, Department of Clinical Biochemistry, Department of Cardiothoracic and Vascular Surgery, Department of Clinical Biochemistry, Department of Veterinary Disease Biology, Department of Clinical Chemistry, Faculty of Health and Medical Sciences, University of Copenhagen, Frederiksberg C, Denmark
Department of Veterinary Clinical and Animal Sciences, Novo Nordisk A/S, Department of Clinical Biochemistry, Department of Cardiothoracic and Vascular Surgery, Department of Clinical Biochemistry, Department of Veterinary Disease Biology, Department of Clinical Chemistry, Faculty of Health and Medical Sciences, University of Copenhagen, Frederiksberg C, Denmark

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Signe E Cremer Department of Veterinary Clinical and Animal Sciences, Novo Nordisk A/S, Department of Clinical Biochemistry, Department of Cardiothoracic and Vascular Surgery, Department of Clinical Biochemistry, Department of Veterinary Disease Biology, Department of Clinical Chemistry, Faculty of Health and Medical Sciences, University of Copenhagen, Frederiksberg C, Denmark

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Tom Teerlink Department of Veterinary Clinical and Animal Sciences, Novo Nordisk A/S, Department of Clinical Biochemistry, Department of Cardiothoracic and Vascular Surgery, Department of Clinical Biochemistry, Department of Veterinary Disease Biology, Department of Clinical Chemistry, Faculty of Health and Medical Sciences, University of Copenhagen, Frederiksberg C, Denmark

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Páll S Leifsson Department of Veterinary Clinical and Animal Sciences, Novo Nordisk A/S, Department of Clinical Biochemistry, Department of Cardiothoracic and Vascular Surgery, Department of Clinical Biochemistry, Department of Veterinary Disease Biology, Department of Clinical Chemistry, Faculty of Health and Medical Sciences, University of Copenhagen, Frederiksberg C, Denmark

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Jesper L Honge Department of Veterinary Clinical and Animal Sciences, Novo Nordisk A/S, Department of Clinical Biochemistry, Department of Cardiothoracic and Vascular Surgery, Department of Clinical Biochemistry, Department of Veterinary Disease Biology, Department of Clinical Chemistry, Faculty of Health and Medical Sciences, University of Copenhagen, Frederiksberg C, Denmark

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J Michael Hasenkam Department of Veterinary Clinical and Animal Sciences, Novo Nordisk A/S, Department of Clinical Biochemistry, Department of Cardiothoracic and Vascular Surgery, Department of Clinical Biochemistry, Department of Veterinary Disease Biology, Department of Clinical Chemistry, Faculty of Health and Medical Sciences, University of Copenhagen, Frederiksberg C, Denmark

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Lisbeth H Olsen Department of Veterinary Clinical and Animal Sciences, Novo Nordisk A/S, Department of Clinical Biochemistry, Department of Cardiothoracic and Vascular Surgery, Department of Clinical Biochemistry, Department of Veterinary Disease Biology, Department of Clinical Chemistry, Faculty of Health and Medical Sciences, University of Copenhagen, Frederiksberg C, Denmark

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Objective

Non-ischemic mitral regurgitation (MR) is primarily caused by myxomatous mitral valve (MV) disease leading to adaptive remodeling, enlargement, and dysfunction of the left ventricle. The aim of this study was to examine the regulation of plasma markers and several cardiac key genes in a novel porcine model of non-ischemic MR.

Methods and results

Twenty-eight production pigs (Sus scrofa) were randomized to experimental MR or sham surgery controls. MR was induced by external suture(s) through the posterior MV leaflet and quantified using echocardiography. The experimental group was subdivided into mild MR (mMR, MR=20–50%, n=10) and moderate/severe MR (sMR, MR >50%, n=6) and compared with controls (CON, MR ≤10%, n=12). Eight weeks postoperatively, follow-up examinations were performed followed by killing. Circulating concentrations of pro-atrial natriuretic peptide (proANP), l-arginine, asymmetric dimethylarginine, and symmetric dimethylarginine (SDMA) were measured. MV, anterior papillary muscle, and left ventricular free wall tissues were collected to quantify mRNA expression of eNOS (NOS3), iNOS (NOS2), MMP9, MMP14, ANP (NPPA), BNP (NPPB), and TGFB1, 2, and 3 and five microRNAs by quantitative real-time PCR. Pigs with sMR displayed markedly increased plasma proANP and SDMA concentrations compared with both controls and mMR (P<0.05). The expression of all genes examined differed significantly between the three localizations in the heart. miR-21 and miR-133a were differently expressed among the experimental groups (P<0.05).

Conclusions

Plasma proANP and SDMA levels and tissue expression of miR-21 and miR-133a are associated with severity of chronic MR in an experimental porcine model.

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Jing Hong Department of Endocrinology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China

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Wen-Yue Liu Department of Endocrinology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China

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Xiang Hu Department of Endocrinology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China

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Fei-Fei Jiang Department of Endocrinology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China

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Ze-Ru Xu Department of Endocrinology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China

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Fang Li Department of Endocrinology, Ruian Traditional Chinese Medicine Hospital, Wenzhou, China

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Fei-Xia Shen Department of Endocrinology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China

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Hong Zhu Department of Endocrinology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China

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Background

A prolonged heart rate-corrected QT interval (QTc) has been associated with peripheral artery disease (PAD) in the general population. However, no study to date has identified a link between prolonged QTc and the severity of PAD in patients with diabetes mellitus and foot ulcers (DFUs). This study aimed to investigate this relationship.

Methods

This multicenter study enrolled 281 patients with DFUs. The severity of PAD was classified into no severe PAD group (without stenosis or occlusion) and severe PAD group (with stenosis or occlusion) based on duplex ultrasonography. The association of prolonged QTc with severe PAD was evaluated in a multivariable mixed-effect logistic regression model, with the hospital as a random effect. Directed acyclic graphs were used to drive the selection of variables to fit the regression model.

Results

Patients with severe PAD had longer QTc than those without. Based on the multivariable mixed-effect logistic regression model, a prolonged QTc was positively associated with severe PAD (odds ratio (OR) = 2.61; 95% CI: 1.07–6.35) and severe DFUs (Wagner grade score ≥ 3) (OR = 2.87; 95% CI: 1.42–5.81).

Conclusions

A prolonged QTc was associated with severe PAD in patients with DFUs. Further research is required to ascertain whether the association is causal.

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Signe Frøssing Department of Internal Medicine, Center of Endocrinology and Metabolism, Herlev Gentofte Hospital, Copenhagen, Denmark
Faculty of Health and Medical Sciences, Copenhagen University, Copenhagen, Denmark

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Malin Nylander Faculty of Health and Medical Sciences, Copenhagen University, Copenhagen, Denmark
Department of Obstetrics & Gynecology, Herlev Gentofte Hospital, Copenhagen, Denmark

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Caroline Kistorp Department of Internal Medicine, Center of Endocrinology and Metabolism, Herlev Gentofte Hospital, Copenhagen, Denmark
Faculty of Health and Medical Sciences, Copenhagen University, Copenhagen, Denmark

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Sven O Skouby Faculty of Health and Medical Sciences, Copenhagen University, Copenhagen, Denmark
Department of Obstetrics & Gynecology, Herlev Gentofte Hospital, Copenhagen, Denmark

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Jens Faber Department of Internal Medicine, Center of Endocrinology and Metabolism, Herlev Gentofte Hospital, Copenhagen, Denmark
Faculty of Health and Medical Sciences, Copenhagen University, Copenhagen, Denmark

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Context

Women with polycystic ovary syndrome (PCOS) have an increased risk of cardiovascular disease (CVD), and biomarkers can be used to detect early subclinical CVD. Midregional-pro-adrenomedullin (MR-proADM), midregional-pro-atrial natriuretic peptide (MR-proANP) and copeptin are all associated with CVD and part of the delicate system controlling fluid and hemodynamic homeostasis through vascular tonus and diuresis. The GLP-1 receptor agonist liraglutide, developed for treatment of type 2 diabetes (T2D), improves cardiovascular outcomes in patients with T2D including a decrease in particular MR-proANP.

Objective

To investigate if treatment with liraglutide in women with PCOS reduces levels of the cardiovascular biomarkers MR-proADM, MR-proANP and copeptin.

Methods

Seventy-two overweight women with PCOS were treated with 1.8 mg/day liraglutide or placebo for 26 weeks in a placebo-controlled RCT. Biomarkers, anthropometrics, insulin resistance, body composition (DXA) and visceral fat (MRI) were examined.

Results

Baseline median (IQR) levels were as follows: MR-proADM 0.52 (0.45–0.56) nmol/L, MR-proANP 44.8 (34.6–56.7) pmol/L and copeptin 4.95 (3.50–6.50) pmol/L. Mean percentage differences (95% CI) between liraglutide and placebo group after treatment were as follows: MR-proADM −6% (−11 to 2, P = 0.058), MR-proANP −25% (−37 to −11, P = 0.001) and copeptin +4% (−13 to 25, P = 0.64). Reduction in MR-proANP concentration correlated with both increased heart rate and diastolic blood pressure in the liraglutide group. Multiple regression analyses with adjustment for BMI, free testosterone, insulin resistance, visceral fat, heart rate and eGFR showed reductions in MR-proANP to be independently correlated with an increase in the heart rate.

Conclusion

In an RCT, liraglutide treatment in women with PCOS reduced levels of the cardiovascular risk biomarkers MR-proANP with 25% and MR-proADM with 6% (borderline significance) compared with placebo. The decrease in MR-proANP was independently associated with an increase in the heart rate.

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Jan Calissendorff Department of Endocrinology, Metabolism and Diabetes, Karolinska University Hospital, Stockholm, Sweden
Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden

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Henrik Falhammar Department of Endocrinology, Metabolism and Diabetes, Karolinska University Hospital, Stockholm, Sweden
Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden

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Background

Graves’ disease is a common cause of hyperthyroidism. Three therapies have been used for decades: pharmacologic therapy, surgery and radioiodine. In case of adverse events, especially agranulocytosis or hepatotoxicity, pre-treatment with Lugol’s solution containing iodine/potassium iodide to induce euthyroidism before surgery could be advocated, but this has rarely been reported.

Methods

All patients hospitalised due to uncontrolled hyperthyroidism at the Karolinska University Hospital 2005–2015 and treated with Lugol’s solution were included. All electronic files were carefully reviewed manually, with focus on the cause of treatment and admission, demographic data, and effects of iodine on thyroid hormone levels and pulse frequency.

Results

Twenty-seven patients were included. Lugol’s solution had been chosen due to agranulocytosis in 9 (33%), hepatotoxicity in 2 (7%), other side effects in 11 (41%) and poor adherence to medication in 5 (19%). Levels of free T4, free T3 and heart rate decreased significantly after 5–9 days of iodine therapy (free T4 53–20 pmol/L, P = 0.0002; free T3 20–6.5 pmol/L, P = 0.04; heart rate 87–76 beats/min P = 0.0007), whereas TSH remained unchanged. Side effects were noted in 4 (15%) (rash n = 2, rash and vomiting n = 1, swelling of fingers n = 1). Thyroidectomy was performed in 26 patients (96%) and one was treated with radioiodine; all treatments were without serious complications.

Conclusion

Treatment of uncontrolled hyperthyroidism with Lugol’s solution before definitive treatment is safe and it decreases thyroid hormone levels and heart rate. Side effects were limited. Lugol’s solution could be recommended pre-operatively in Graves’ disease with failed medical treatment, especially if side effects to anti-thyroid drugs have occurred.

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Richard P Steeds Department of Cardiology, University Hospitals Birmingham (Queen Elizabeth), NHS Hospitals Foundation Trust, Birmingham, UK
Institute of Cardiovascular Sciences, University of Birmingham, Birmingham, UK

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Vandana Sagar Centre for Liver and Gastrointestinal Research, Institute of Immunology and Immunotherapy, University of Birmingham, Birmingham, UK

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Shishir Shetty Centre for Liver and Gastrointestinal Research, Institute of Immunology and Immunotherapy, University of Birmingham, Birmingham, UK

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Tessa Oelofse Departments of Anaesthesia and Intensive Care, University Hospitals Birmingham (Queen Elizabeth), NHS Hospitals Foundation Trust, Birmingham, UK

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Harjot Singh Departments of Anaesthesia and Intensive Care, University Hospitals Birmingham (Queen Elizabeth), NHS Hospitals Foundation Trust, Birmingham, UK

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Raheel Ahmad Department of Cardiology, University Hospitals Birmingham (Queen Elizabeth), NHS Hospitals Foundation Trust, Birmingham, UK

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Elizabeth Bradley Therapy Services (Dietetics), University Hospitals Birmingham (Queen Elizabeth), NHS Hospitals Foundation Trust, Birmingham, UK

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Rachel Moore Departments of Anaesthesia and Intensive Care, University Hospitals Birmingham (Queen Elizabeth), NHS Hospitals Foundation Trust, Birmingham, UK

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Suzanne Vickrage Birmingham Neuroendocrine Tumour Centre, University Hospitals Birmingham (Queen Elizabeth), NHS Hospitals Foundation Trust, Birmingham, UK

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Stacey Smith Birmingham Neuroendocrine Tumour Centre, University Hospitals Birmingham (Queen Elizabeth), NHS Hospitals Foundation Trust, Birmingham, UK

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Ivan Yim Department of Cardiothoracic Surgery, University Hospitals Birmingham (Queen Elizabeth), NHS Hospitals Foundation Trust, Birmingham, UK

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Yasir S Elhassan Centre for Endocrinology, Diabetes and Metabolism, Birmingham Health Partners, Birmingham, UK
Institute of Metabolism and Systems Research, University of Birmingham, Birmingham, UK

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Hema Venkataraman Centre for Endocrinology, Diabetes and Metabolism, Birmingham Health Partners, Birmingham, UK

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John Ayuk Centre for Endocrinology, Diabetes and Metabolism, Birmingham Health Partners, Birmingham, UK

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Stephen Rooney Department of Cardiothoracic Surgery, University Hospitals Birmingham (Queen Elizabeth), NHS Hospitals Foundation Trust, Birmingham, UK

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Tahir Shah Birmingham Neuroendocrine Tumour Centre, University Hospitals Birmingham (Queen Elizabeth), NHS Hospitals Foundation Trust, Birmingham, UK
Department of Hepatology and Liver Transplantation, University Hospitals Birmingham (Queen Elizabeth), NHS Hospitals Foundation Trust, Birmingham, UK

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Carcinoid heart disease (CHD) is a consequence of valvular fibrosis triggered by vasoactive substances released from neuroendocrine tumours, classically in those with metastatic disease and resulting in tricuspid and pulmonary valve failure. CHD affects one in five patients who have carcinoid syndrome (CS). Valve leaflets become thickened, retracted and immobile, resulting most often in regurgitation that causes right ventricular dilatation and ultimately, right heart failure. The development of CHD heralds a significantly worse prognosis than those patients with CS who do not develop valvular disease. Diagnosis requires a low threshold of suspicion in all patients with CS, since symptoms occur late in the disease process and clinical signs are difficult to elicit. As a result, routine screening is recommended using the biomarker, N-terminal pro-natriuretic peptide, and regular echocardiography is then required for diagnosis and follow-up. There is no direct medical therapy for CHD, but the focus of non-surgical care is to control CS symptoms, reduce tumour load and decrease hormone levels. Valve surgery improves long-term outcome for those with severe disease compared to medical management, although peri-operative mortality remains at between 10 and 20% in experienced centres. Therefore, care needs to be multidisciplinary at all stages, with clear discussion with the patient and between teams to ensure optimum outcome for these often-complex patients.

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Alexander Tacey Institute for Health and Sport (IHES), Victoria University, Melbourne, Victoria, Australia
Department of Medicine-Western Health, Australian Institute for Musculoskeletal Science (AIMSS), Melbourne Medical School, The University of Melbourne, Melbourne, Victoria, Australia

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Lewan Parker Institute for Health and Sport (IHES), Victoria University, Melbourne, Victoria, Australia
Institute for Physical Activity and Nutrition, Deakin University, Geelong, Victoria, Australia

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Bu B Yeap Medical School, University of Western Australia, and Department of Endocrinology and Diabetes, Fiona Stanley Hospital, Perth, Western Australia, Australia

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John Joseph PathWest Laboratory Medicine, Sir Charles Gairdner Hospital, Perth, Western Australia, Australia

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Ee M Lim PathWest Laboratory Medicine, Sir Charles Gairdner Hospital, Perth, Western Australia, Australia

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Andrew Garnham Institute for Health and Sport (IHES), Victoria University, Melbourne, Victoria, Australia

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David L Hare University of Melbourne and the Department of Cardiology, Austin Health, Melbourne, Victoria, Australia

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Tara Brennan-Speranza Department of Physiology and Bosch Institute for Medical Research, University of Sydney, Sydney, New South Wales, Australia

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Itamar Levinger Institute for Health and Sport (IHES), Victoria University, Melbourne, Victoria, Australia
Department of Medicine-Western Health, Australian Institute for Musculoskeletal Science (AIMSS), Melbourne Medical School, The University of Melbourne, Melbourne, Victoria, Australia

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The aim of this study was to investigate the effect of a single dose of prednisolone on (A) high-intensity interval cycling performance and (B) post-exercise metabolic, hormonal and haematological responses. Nine young men participated in this double-blind, randomised, cross-over study. The participants completed exercise sessions (4 × 4 min cycling bouts at 90–95% of peak heart rate), 12 h after ingesting prednisolone (20 mg) or placebo. Work load was adjusted to maintain the same relative heart rate between the sessions. Exercise performance was measured as total work performed. Blood samples were taken at rest, immediately post exercise and up to 3 h post exercise. Prednisolone ingestion decreased total work performed by 5% (P < 0.05). Baseline blood glucose was elevated following prednisolone compared to placebo (P < 0.001). Three hours post exercise, blood glucose in the prednisolone trial was reduced to a level equivalent to the baseline concentration in the placebo trial (P > 0.05). Prednisolone suppressed the increase in blood lactate immediately post exercise (P < 0.05). Total white blood cell count was elevated at all time-points with prednisolone (P < 0.01). Androgens and sex hormone-binding globulin were elevated immediately after exercise, irrespective of prednisolone or placebo. In contrast, prednisolone significantly reduced the ratio of testosterone/luteinizing hormone (P < 0.01). Acute prednisolone treatment impairs high-intensity interval cycling performance and alters metabolic and haematological parameters in healthy young men. Exercise may be an effective tool to minimise the effect of prednisolone on blood glucose levels.

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Akinori Sairaku Department of Cardiovascular Medicine, Hiroshima University Graduate School of Biomedical and Health Sciences, Hiroshima, Japan

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Yukiko Nakano Department of Cardiovascular Medicine, Hiroshima University Graduate School of Biomedical and Health Sciences, Hiroshima, Japan

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Yuko Uchimura Department of Cardiovascular Medicine, Hiroshima University Graduate School of Biomedical and Health Sciences, Hiroshima, Japan

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Takehito Tokuyama Department of Cardiovascular Medicine, Hiroshima University Graduate School of Biomedical and Health Sciences, Hiroshima, Japan

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Hiroshi Kawazoe Department of Cardiovascular Medicine, Hiroshima University Graduate School of Biomedical and Health Sciences, Hiroshima, Japan

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Yoshikazu Watanabe Department of Cardiovascular Medicine, Hiroshima University Graduate School of Biomedical and Health Sciences, Hiroshima, Japan

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Hiroya Matsumura Department of Cardiovascular Medicine, Hiroshima University Graduate School of Biomedical and Health Sciences, Hiroshima, Japan

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Yasuki Kihara Department of Cardiovascular Medicine, Hiroshima University Graduate School of Biomedical and Health Sciences, Hiroshima, Japan

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Background

The impact of subclinical hypothyroidism on the cardiovascular risk is still debated. We aimed to measure the relationship between subclinical hypothyroidism and the left atrial (LA) pressure.

Methods

The LA pressures and thyroid function were measured in consecutive patients undergoing atrial fibrillation (AF) ablation, who did not have any known heart failure, structural heart disease, or overt thyroid disease.

Results

Subclinical hypothyroidism (4.5≤ thyroid-stimulating hormone <19.9 mIU/L) was present in 61 (13.0%) of the 471 patients included. More subclinical hypothyroidism patients than euthyroid patients (55.7% vs 40.2%; P=0.04).’euthyroid patients had persistent or long-standing persistent AF (55.7% vs 40.2%; P = 0.04). The mean LA pressure (10.9 ± 4.7 vs 9.1 ± 4.3 mmHg; P = 0.002) and LA V-wave pressure (17.4 ± 6.5 vs 14.3 ± 5.9 mmHg; P < 0.001) were, respectively, higher in the patients with subclinical hypothyroidism than in the euthyroid patients. After an adjustment for potential confounders, the LA pressures remained significantly higher in the subclinical hypothyroidism patients. A multiple logistic regression model showed that subclinical hypothyroidism was independently associated with a mean LA pressure of >18 mmHg (odds ratio 3.94, 95% CI 1.28 11.2; P = 0.02).

Conclusions

Subclinical hypothyroidism may increase the LA pressure in AF patients.

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