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Coronary Artery Disease: HELP
Articles from Karolinska Institutions
Based on 177 articles published since 2008
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These are the 177 published articles about Coronary Artery Disease that originated from Karolinska Institutions during 2008-2019.
 
+ Citations + Abstracts
Pages: 1 · 2 · 3 · 4 · 5 · 6 · 7 · 8
1 Editorial Lung Function and Coronary Artery Disease Risk. 2018

Nowak, Christoph. ·Division of Family Medicine and Primary Care, Department of Neurobiology, Care Sciences and Society (NVS), Karolinska Institutet, Huddinge, Sweden. christoph.nowak@ki.se. ·Circ Genom Precis Med · Pubmed #29650768.

ABSTRACT: -- No abstract --

2 Editorial Serum S100A12: A Risk Marker or Risk Factor of Vascular Calcification in Chronic Kidney Disease. 2015

Lindholm, Bengt. ·Renal Medicine and Baxter Novum, Department of Clinical Science, Intervention and Technology, Karolinska Institutet, Stockholm, Sweden. ·Am J Nephrol · Pubmed #26278719.

ABSTRACT: -- No abstract --

3 Editorial Obstructive sleep apnoea and cardiovascular calcification. 2015

Bäck, Magnus / Stanke-Labesque, Françoise. ·Translational Cardiology, Karolinska Institutet, Stockholm, Sweden Department of Cardiology, Karolinska University Hospital, Stockholm, Sweden. · Université Grenoble Alpes, Grenoble, France INSERM U1042, HP2,Grenoble, France Department of Pharmacology, CHU, Grenoble, France. ·Thorax · Pubmed #26272928.

ABSTRACT: -- No abstract --

4 Editorial Women with nonobstructive coronary artery disease are not necessarily healthy. 2015

Schenck-Gustafsson, Karin / Johnston, Nina. ·1 Department of Cardiology Centre for Gender Medicine, Karolinska University Hospital , Stockholm, Sweden . ·J Womens Health (Larchmt) · Pubmed #25973797.

ABSTRACT: -- No abstract --

5 Editorial Recognition of resting heart calcification as a means to an end: an eye-opener in the application of dobutamine stress echocardiography in subjects with chest pain. 2015

Saha, Samir K / Govind, Satish C. ·Karolinska Institutet, Sundsvall, Sweden. · Narayana Institute of Cardiac Sciences, Bangalore, India. ·Echocardiography · Pubmed #25728209.

ABSTRACT: -- No abstract --

6 Review Bilateral Versus Single Internal Thoracic Artery Grafts. 2018

Persson, Michael / Sartipy, Ulrik. ·Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden. · Section of Cardiothoracic Surgery, Heart and Vascular Theme, Karolinska University Hospital, SE-171 76, Stockholm, Sweden. · Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden. Ulrik.Sartipy@karolinska.se. · Section of Cardiothoracic Surgery, Heart and Vascular Theme, Karolinska University Hospital, SE-171 76, Stockholm, Sweden. Ulrik.Sartipy@karolinska.se. ·Curr Cardiol Rep · Pubmed #29362968.

ABSTRACT: PURPOSE OF REVIEW: Several advances have been made in recent years to improve outcome for patients with coronary artery disease. One of the most debated topics regarding surgical treatment with coronary artery bypass grafting (CABG) is graft selection. This review aims to present the current status and scientific evidence for bilateral internal thoracic artery (BITA) grafting. RECENT FINDINGS: Observational studies and pooled analyses suggest that BITA grafting is associated with improved survival. Early results from a large randomized controlled trial report safety and efficacy of the method. The improved survival might be amplified in select groups, but with an increase in sternal wound-related complications. The benefit of BITA grafts seems to remain to an approximate age of 69 years at surgery. CABG with BITA grafts is likely associated with improved long-term survival at a cost of an increase in sternal wound infections. Ten-year results from the Arterial Revascularization Trial are expected in 2018, providing the best evidence regarding the method yet. Early results show it is a safe method in most patient categories considerable for CABG.

7 Review Association between preoperative depression and long-term survival following coronary artery bypass surgery - A systematic review and meta-analysis. 2016

Stenman, Malin / Holzmann, Martin J / Sartipy, Ulrik. ·Department of Cardiothoracic Surgery and Anesthesiology, Karolinska University Hospital, Stockholm, Sweden; Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden. Electronic address: Malin.Stenman@ki.se. · Department of Emergency Medicine, Karolinska University Hospital, Stockholm, Sweden; Department of Internal Medicine, Karolinska Institutet, Stockholm, Sweden. · Department of Cardiothoracic Surgery and Anesthesiology, Karolinska University Hospital, Stockholm, Sweden; Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden. ·Int J Cardiol · Pubmed #27505334.

ABSTRACT: BACKGROUND: Depression is common in patients with cardiovascular disease. The importance of preoperative depression for long-term survival following coronary artery bypass grafting (CABG) is not well known. The aim was to provide a summary estimate of the association between preoperative depression and long-term survival in adults who underwent CABG. METHODS: We did a systematic search of MEDLINE, EMBASE, Cochrane Library, PsycINFO, Web of Science, and PubMed from inception to November, 2015, including cohort studies with at least one month of follow-up that reported hazard ratios (HR) and 95% confidence intervals (CI) for long-term all-cause mortality following CABG in patients with preoperative depression compared to non-depressed patients. Two reviewers independently extracted data on populations, exposure, outcome, risk of bias, and quality of evidence. We calculated HR and 95% CIs for all-cause mortality using random-effects meta-analyses and performed subgroup and sensitivity analyses. RESULTS: Seven studies were included with a combined study population of 89,490 patients (4002 depressed/85,488 non-depressed). All studies observed a positive association between preoperative depression and all-cause mortality, and in 4 studies the association was statistically significant. Patients with depression had a pooled hazard ratio of 1.46 (95% CI: 1.23-1.73, p<0.0001) for all-cause mortality with moderate heterogeneity (I(2)=50.1%, p=0.061). CONCLUSIONS: This systematic review and meta-analysis indicates that patients with preoperative depression are at increased risk for long-term, all-cause mortality following CABG compared with those without depression. Systematic screening for depression prior to cardiac surgery could identify those at higher risk.

8 Review Human Validation of Genes Associated With a Murine Atherosclerotic Phenotype. 2016

Pasterkamp, Gerard / van der Laan, Sander W / Haitjema, Saskia / Foroughi Asl, Hassan / Siemelink, Marten A / Bezemer, Tim / van Setten, Jessica / Dichgans, Martin / Malik, Rainer / Worrall, Bradford B / Schunkert, Heribert / Samani, Nilesh J / de Kleijn, Dominique P V / Markus, Hugh S / Hoefer, Imo E / Michoel, Tom / de Jager, Saskia C A / Björkegren, Johan L M / den Ruijter, Hester M / Asselbergs, Folkert W. ·From the Laboratory of Experimental Cardiology, Division Heart and Lungs (G.P., S.W.v.d.L., S.H., M.A.S., T.B., J.v.S., I.E.H., S.C.A.d.J., H.M.d.R.), Laboratory of Clinical Chemistry and Hematology, Division Laboratories and Pharmacy (G.P.), and Division Heart and Lungs, Department of Cardiology (F.W.A.), University Medical Center Utrecht, Utrecht, The Netherlands · Vascular Biology Unit, Department of Medical Biochemistry and Biophysics, Karolinska Institutet, Stockholm, Sweden (H.F.A., J.L.M.B.) · Institut für Schlaganfall- und Demenzforschung (ISD) Klinikum der Universität München, Munich, Germany (M.D., R.M.) · Munich Cluster for Systems Neurology (SyNergy), Munich, Germany (M.D.) · Department of Neurology, University of Virginia, Charlottesville (B.B.W.) · Klinik für Herz- und Kreislauferkrankungen, Deutsches Herzzentrum München, Technische Universität München, Munich, Germany (H.S.) · Deutsches Zentrum für Herz-Kreislauf-Forschung (DZHK) e.V., Partner Site Munich Heart Alliance, Munich, Germany (H.S.) · Department of Cardiovascular Sciences, University of Leicester, Leicester, United Kingdom (N.J.S.) · Leicester National Institute of Health Research Biomedical Research Unit in Cardiovascular Disease, Leicester, United Kingdom (N.J.S.) · Department of Surgery, National University of Singapore, Singapore (D.P.V.d.K.) · Cardiovascular Research Institute (CVRI), National University Health System, Singapore, Singapore (D.P.V.d.K.) · Interuniversity Cardiology Institute of the Netherlands, Utrecht, The Netherlands (D.P.V.d.K.) · Department of Neurosciences, University of Cambridge, Cambridge, United Kingdom (H.S.M.) · The Roslin Institute, University of Edinburgh, Edinburgh, United Kingdom (T.M.) · Department of Genetics and Genomic Sciences, Icahn Institute for Genomics and Multiscale Biology, Icahn School of Medicine at Mount Sinai, New York, NY (J.L.M.B.) · Department of Physiology, Institute of Biomedicine and Translational Medicine, University of Tartu, Tartu, Estoni ·Arterioscler Thromb Vasc Biol · Pubmed #27079880.

ABSTRACT: OBJECTIVE: The genetically modified mouse is the most commonly used animal model for studying the pathogenesis of atherosclerotic disease. We aimed to assess if mice atherosclerosis-related genes could be validated in human disease through examination of results from genome-wide association studies. APPROACH AND RESULTS: We performed a systematic review to identify atherosclerosis-causing genes in mice and carried out gene-based association tests of their human orthologs for an association with human coronary artery disease and human large artery ischemic stroke. Moreover, we investigated the association of these genes with human atherosclerotic plaque characteristics. In addition, we assessed the presence of tissue-specific cis-acting expression quantitative trait loci for these genes in humans. Finally, using pathway analyses we show that the putative atherosclerosis-causing genes revealed few associations with human coronary artery disease, large artery ischemic stroke, or atherosclerotic plaque characteristics, despite the fact that the majority of these genes have cis-acting expression quantitative trait loci. CONCLUSIONS: A role for genes that has been observed in mice for atherosclerotic lesion development could scarcely be confirmed by studying associations of disease development with common human genetic variants. The value of murine atherosclerotic models for selection of therapeutic targets in human disease remains unclear.

9 Review Animal models of diabetic macrovascular complications: key players in the development of new therapeutic approaches. 2015

Heinonen, Suvi E / Genové, Guillem / Bengtsson, Eva / Hübschle, Thomas / Åkesson, Lina / Hiss, Katrin / Benardeau, Agnes / Ylä-Herttuala, Seppo / Jönsson-Rylander, Ann-Cathrine / Gomez, Maria F. ·Bioscience, Cardiovascular and Metabolic Diseases, Innovative Medicines and Early Development, AstraZeneca R&D, 43183 Mölndal, Sweden. · Division of Vascular Biology, Department of Medical Biochemistry and Biophysics, Karolinska Institutet, 17177 Stockholm, Sweden. · Department of Clinical Sciences, Lund University Diabetes Centre (LUDC), Lund University, 20502 Malmö, Sweden. · R&D Diabetes Division, Translational Medicine, Sanofi-Aventis, 65926 Frankfurt am Main, Germany. · Department of Biotechnology and Molecular Medicine, A.I. Virtanen Institute for Molecular Sciences, University of Eastern Finland, 70210 Kuopio, Finland. · Pharmaceutical Division, pRED, CV and Metabolic Disease, Hoffmann-La Roche, 4070 Basel, Switzerland. ·J Diabetes Res · Pubmed #25785279.

ABSTRACT: Diabetes mellitus is a lifelong, incapacitating metabolic disease associated with chronic macrovascular complications (coronary heart disease, stroke, and peripheral vascular disease) and microvascular disorders leading to damage of the kidneys (nephropathy) and eyes (retinopathy). Based on the current trends, the rising prevalence of diabetes worldwide will lead to increased cardiovascular morbidity and mortality. Therefore, novel means to prevent and treat these complications are needed. Under the auspices of the IMI (Innovative Medicines Initiative), the SUMMIT (SUrrogate markers for Micro- and Macrovascular hard end points for Innovative diabetes Tools) consortium is working on the development of novel animal models that better replicate vascular complications of diabetes and on the characterization of the available models. In the past years, with the high level of genomic information available and more advanced molecular tools, a very large number of models has been created. Selecting the right model for a specific study is not a trivial task and will have an impact on the study results and their interpretation. This review gathers information on the available experimental animal models of diabetic macrovascular complications and evaluates their pros and cons for research purposes as well as for drug development.

10 Review Genome-wide significant loci: how important are they? Systems genetics to understand heritability of coronary artery disease and other common complex disorders. 2015

Björkegren, Johan L M / Kovacic, Jason C / Dudley, Joel T / Schadt, Eric E. ·Department of Genetics and Genomic Sciences, Icahn Institute for Genomics and Multiscale Biology, Icahn School of Medicine at Mount Sinai, New York, New York; Cardiovascular Institute, Icahn School of Medicine at Mount Sinai, New York, New York; Division of Vascular Biology, Department of Medical Biochemistry and Biophysics, Karolinska Institutet, Stockholm, Sweden; Department of Pathological Anatomy and Forensic Medicine, University of Tartu, Tartu, Estonia. Electronic address: johan.bjorkegren@mssm.edu. · Cardiovascular Institute, Icahn School of Medicine at Mount Sinai, New York, New York. · Department of Genetics and Genomic Sciences, Icahn Institute for Genomics and Multiscale Biology, Icahn School of Medicine at Mount Sinai, New York, New York. ·J Am Coll Cardiol · Pubmed #25720628.

ABSTRACT: Genome-wide association studies (GWAS) have been extensively used to study common complex diseases such as coronary artery disease (CAD), revealing 153 suggestive CAD loci, of which at least 46 have been validated as having genome-wide significance. However, these loci collectively explain <10% of the genetic variance in CAD. Thus, we must address the key question of what factors constitute the remaining 90% of CAD heritability. We review possible limitations of GWAS, and contextually consider some candidate CAD loci identified by this method. Looking ahead, we propose systems genetics as a complementary approach to unlocking the CAD heritability and etiology. Systems genetics builds network models of relevant molecular processes by combining genetic and genomic datasets to ultimately identify key "drivers" of disease. By leveraging systems-based genetic approaches, we can help reveal the full genetic basis of common complex disorders, enabling novel diagnostic and therapeutic opportunities.

11 Review The role of matrix metalloproteinases in atherothrombosis. 2011

Ketelhuth, Daniel F J / Bäck, Magnus. ·Department of Medicine, Karolinska Institutet, Stockholm, Sweden. Daniel.Ketelhuth@ki.se ·Curr Atheroscler Rep · Pubmed #21271310.

ABSTRACT: The matrix metalloproteinase (MMP) family of enzymes is involved in arterial wall extracellular matrix degradation and remodeling. The latter activities have been implicated in a number of normal and pathologic processes, such as atherosclerotic lesion formation and progression, plaque destabilization and rupture, but also in plaque stabilization and healing. As a result, the MMPs have been explored as both therapeutic targets and diagnostic tools for the treatment and diagnosis of atherosclerotic cardiovascular diseases. In this review, we summarize experimental findings, genetic associations, and the biomarker potential of MMPs in atherothrombosis. In addition, the regulation and expression of MMPs in atherosclerotic plaques is discussed, with an emphasis on the role of lipid-derived inflammatory mediators as modulators of MMP activity.

12 Review FDG-PET imaging of atherosclerosis: Do we know what we see? 2010

Sheikine, Yuri / Akram, Kamran. ·Noninvasive Cardiovascular Imaging Program, Department of Radiology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA. yuri.sheikine@ki.se ·Atherosclerosis · Pubmed #20202637.

ABSTRACT: Imaging atherosclerosis may help to identify subjects harboring rupture-prone atherosclerotic plaques who may benefit from preventive interventions. Potential of plaques to rupture depends on their structural changes and metabolic activation, which are difficult to assess using anatomic imaging modalities. Recent studies suggested that functional imaging with positron emission tomography (PET) utilizing fluorine-18-labeled 2-deoxy-d-glucose (FDG) has the potential to assess plaque metabolism and add to prediction of vascular risk. Aortic, iliac, and carotid plaques can be detected with FDG-PET, even though not all plaques exhibit high FDG uptake. Detection of coronary artery plaques is more cumbersome due to technical limitations of PET and fast movement of these vessels during cardiac and respiratory cycles. Studies on substrate accumulating FDG in plaques are contradictory and mostly do not extend beyond correlation analyses. Vascular FDG uptake has an excellent short-term stability, but larger fluctuations of uptake long-term, which may complicate interpretation of such changes in therapeutic trials. FDG uptake in major arteries correlates with some cardiovascular risk factors and atherosclerosis markers, but clinical utility of such correlations is unclear. What is more important is that recently reported studies in cancer patients showed correlation between higher baseline FDG uptake and subsequent cardiovascular mortality. Anti-atherogenic therapy and therapeutic lifestyle changes seem to decrease vascular FDG uptake but it is not clear whether the latter predicts subsequent lower morbidity and mortality. These initial findings suggest that vascular FDG-PET may in the future find some utility in management of patients with atherosclerosis, but a number of important issues need to be addressed first. We need to: (1) determine optimal standard ways of performing imaging and quantifying vascular FDG uptake; (2) understand molecular mechanisms governing FDG accumulation in plaques; (3) perform studies prospectively linking vascular FDG uptake to cardiovascular events in non-cancer patients. As of today, vascular FDG-PET is not ready for its prime time in clinical practice.

13 Review Implications of abnormal glucose metabolism in patients with coronary artery disease. 2008

Anselmino, Matteo / Wallander, Märit / Norhammar, Anna / Mellbin, Linda / Rydén, Lars. ·Department of Medicine, Karolinska Institute, Stockholm, Sweden. ·Diab Vasc Dis Res · Pubmed #18958838.

ABSTRACT: Abnormal glucose metabolism and type 2 diabetes mellitus (T2DM) are becoming increasingly common. It has been recently confirmed that the period of time prior to the development of diabetes, when patients have impaired glucose tolerance, may also predispose them to increased cardiovascular risk. Therefore prevention and management of T2DM and its antecedents must have high priority when allocating healthcare resources. The present review summarises some information on detection, management and treatment of abnormal glucose metabolism in patients with established coronary artery disease, highlighting the importance of early detection of abnormal glucose metabolism in order to prevent the progression of prediabetes to T2DM and to delay the occurrence of those macrovascular and microvascular complications that impair quality of life and diminish survival.

14 Review Identifying the susceptibility genes for coronary artery disease: from hyperbole through doubt to cautious optimism. 2008

Hamsten, A / Eriksson, P. ·Atherosclerosis Research Unit, Department of Medicine, Center for Molecular Medicine, Karolinska University Hospital, Karolinska Institutet, Stockholm, Sweden. anders.hamsten@ki.se ·J Intern Med · Pubmed #18410597.

ABSTRACT: The genetic basis of coronary artery disease (CAD) is complex, and the fact that an alarmingly high proportion of reported associations between genetic variants and CAD are not replicated has generated uncertainty as to whether molecular genetics is ever going to deliver on the promises delivered in the late 1990s. However, during 2007, the first generation of large-scale genome-wide association studies using high-density, single nucleotide polymorphism genotyping arrays have revealed genetic variants that are robustly associated with CAD and CAD-related traits such as type 2 diabetes and obesity. In particular, a robust susceptibility locus for CAD has been identified on chromosome 9p21. Also, evidence has been obtained that multiple rare alleles with fairly strong phenotypic effects may contribute to the genetic heritability of CAD, in addition to common variants with a modest impact on risk. Furthermore, new mechanistic connections have been discovered between different common complex diseases including CAD. This review focuses on the challenges and recent advances of molecular genetics in dissecting the molecular pathophysiology of atherothrombosis and defining novel targets for treatment.

15 Clinical Trial The Accuracy of Point-of-Care Equipment for Glucose Measurement in Screening for Dysglycemia in Patients with Coronary Artery Disease. 2018

Shahim, Bahira / Kjellström, Barbro / Gyberg, Viveca / Jennings, Catriona / Smetana, Stina / Rydén, Lars. ·1 Cardiology Unit, Department of Medicine, Karolinska Institutet , Stockholm, Sweden . · 2 Department of Neurobiology, Care Sciences and Society, Centre for Family Medicine, Karolinska Institutet , Huddinge, Sweden . · 3 Faculty of Medicine, NHLI Imperial College London , Hammersmith Campus, London, United Kingdom . ·Diabetes Technol Ther · Pubmed #30074818.

ABSTRACT: BACKGROUND: Point-of-care equipment for measuring glucose saves time and costs for both patients and professionals and minimizes preanalytic errors when screening for or managing dysglycemia, that is, impaired glucose tolerance and type 2 diabetes. The accuracy of such devices has, however, been questioned compared with analyses at an accredited hospital laboratory. OBJECTIVE: To investigate the agreement between glucose measurements made by the point-of-care HemoCue MATERIAL: Patients with established coronary artery disease (CAD) recruited in Sweden and the United Kingdom within the auspices of the European Action on Secondary and primary Prevention by Intervention to Reduce Events (EUROASPIRE) V survey (n = 87; 18-80 years) with or without previously known dysglycemia were investigated. Plasma glucose values collected in the fasting state (n = 85) and 60 (n = 57) and 120 (n = 72) min after a glucose load were analyzed both using HemoCue monitors and local hospital laboratories. The two measurement techniques were compared using a bias plot according to Bland-Altman, the surveillance error grid, and Spearman correlation test. RESULTS: The bias plot method showed small differences between the HemoCue and local hospital laboratory methods, the HemoCue and central hospital laboratory, and the local hospital laboratories and the central hospital laboratory. In the surveillance error grid, 98.6% of the values were in the deep green zone, indicating no risk and the remaining values (1.4%) were within the light green zone, indicating "slight lower risk." CONCLUSION: The HemoCue point-of-care system is accurate for dysglycemia screening in patients with CAD.

16 Clinical Trial Ticagrelor pharmacokinetics and pharmacodynamics in patients with NSTEMI after a 180-mg loading dose. 2017

Holm, Manne / Tornvall, Per / Westerberg, Julia / Rihan Hye, Shaym / van der Linden, Jan. ·a Department of Cardiothoracic Surgery and Anesthesiology , Karolinska University Hospital, Stockholm, Sweden. · b Department of Molecular Medicine and Surgery , Karolinska Institutet, Stockholm, Sweden. · c Department of Science and Education, Södersjukhuset (Stockholm South General Hospital) , Karolinska Institutet , Stockholm , Sweden. ·Platelets · Pubmed #28150519.

ABSTRACT: The pharmacokinetics after a 180-mg loading dose (LD) of ticagrelor has not been thoroughly investigated in NSTEMI patients. We aimed to compare the ticagrelor uptake and on-treatment platelet reactivity between non-ST-segment elevation myocardial infarction (NSTEMI) patients and a control group of patients with stable coronary artery disease (SCAD) undergoing elective percutaneous coronary intervention. We performed an observational, prospective, single-center study including 40 NSTEMI patients and 20 SCAD controls. Key exclusion criteria included ongoing opioid treatment. Both groups received a 180-mg ticagrelor LD, and blood samples were taken pre-dose and 1, 2, 3, 4, 5, and 6 hours post-LD. Plasma concentrations of ticagrelor and its active metabolite AR-C124910XX were determined by validated methods. Platelet aggregation was tested using ADP-induced multiple electrode aggregometry. The primary endpoint was the time to maximal ticagrelor concentration (T

17 Clinical Trial Effect of arginase inhibition on ischemia-reperfusion injury in patients with coronary artery disease with and without diabetes mellitus. 2014

Kövamees, Oskar / Shemyakin, Alexey / Pernow, John. ·Department of Medicine, Karolinska Institutet, Stockholm, Sweden. ·PLoS One · Pubmed #25072937.

ABSTRACT: BACKGROUND: Arginase competes with nitric oxide synthase for their common substrate L-arginine. Up-regulation of arginase in coronary artery disease (CAD) and diabetes mellitus may reduce nitric oxide bioavailability contributing to endothelial dysfunction and ischemia-reperfusion injury. Arginase inhibition reduces infarct size in animal models. Therefore the aim of the current study was to investigate if arginase inhibition protects from endothelial dysfunction induced by ischemia-reperfusion in patients with CAD with or without type 2 diabetes ( CLINICAL TRIAL REGISTRATION NUMBER: NCT02009527). METHODS: Male patients with CAD (n = 12) or CAD + type 2 diabetes (n = 12), were included in this cross-over study with blinded evaluation. Endothelium-dependent vasodilatation was assessed by flow-mediated dilatation (FMD) of the radial artery before and after 20 min ischemia-reperfusion during intra-arterial infusion of the arginase inhibitor (Nω-hydroxy-nor-L-arginine, 0.1 mg/min) or saline. RESULTS: The forearm ischemia-reperfusion was well tolerated. Endothelium-independent vasodilatation was assessed by sublingual nitroglycerin. Ischemia-reperfusion decreased FMD in patients with CAD from 12.7±5.2% to 7.9±4.0% during saline administration (P<0.05). Nω-hydroxy-nor-L-arginine administration prevented the decrease in FMD in the CAD group (10.3±4.3% at baseline vs. 11.5±3.6% at reperfusion). Ischemia-reperfusion did not significantly reduce FMD in patients with CAD + type 2 diabetes. However, FMD at reperfusion was higher following nor-NOHA than following saline administration in both groups (P<0.01). Endothelium-independent vasodilatation did not differ between the occasions. CONCLUSIONS: Inhibition of arginase protects against endothelial dysfunction caused by ischemia-reperfusion in patients with CAD. Arginase inhibition may thereby be a promising therapeutic strategy in the treatment of ischemia-reperfusion injury.

18 Clinical Trial Feasibility of myocardial performance index for evaluation of left ventricular function during dobutamine stress echocardiography before and after coronary artery bypass grafting. 2014

Hashemi, Nashmil / Samad, Bassem A / Hedman, Anders / Brodin, Lars-Åke / Alam, Mahbubul. ·Department of Clinical Physiology, Karolinska University Hospital, Huddinge, Stockholm, Sweden. ·Echocardiography · Pubmed #24354348.

ABSTRACT: AIMS: Myocardial performance index (MPI) is a measure of combined systolic and diastolic myocardial function. In patients with coronary artery disease (CAD) an increase in MPI is consistent with myocardial dysfunction. The objectives of this study were to characterize the changes in MPI after coronary artery bypass graft (CABG) at rest and at peak dobutamine stress echocardiography (DSE). METHODS AND RESULTS: Thirty-six patients diagnosed with CAD and accepted for CABG were studied by standard echocardiography and DSE 1 month prior and 3 month after CABG. The MPI was calculated using pulsed-wave tissue Doppler imaging (PW-TDI) of the left ventricular (LV) wall-motion velocity. At baseline, ejection fraction (EF; 42.7 ± 8%) and wall-motion score index (WMSI; 1.1 ± 0.2) were impaired at rest as well as at peak DSE (EF; 49.2 ± 9 and WMSI 1.4 ± 0.2). MPI was prolonged both at rest (0.61 ± 0.13) and at peak DSE (0.78 ± 0.16). After CABG, EF and WMSI did not improve at rest (43.7 ± 8% and 1.1 ± 0.2, respectively). On the other hand, MPI improved substantially both at rest (0.45 ± 0.08; P < 0.001) and at peak DSE (0.56 ± 0.1; P < 0.001). At peak DSE an improvement of EF (54.2 ± 9; P < 0.05) and WMSI (1.1 ± 0.16; P < 0.001) was seen as well. CONCLUSION: Myocardial performance index shows significant improvement after CABG in patients with CAD both at rest and peak DSE and appears to be a sensitive measure of myocardial function.

19 Article Functional regulatory mechanism of smooth muscle cell-restricted LMOD1 coronary artery disease locus. 2018

Nanda, Vivek / Wang, Ting / Pjanic, Milos / Liu, Boxiang / Nguyen, Trieu / Matic, Ljubica Perisic / Hedin, Ulf / Koplev, Simon / Ma, Lijiang / Franzén, Oscar / Ruusalepp, Arno / Schadt, Eric E / Björkegren, Johan L M / Montgomery, Stephen B / Snyder, Michael P / Quertermous, Thomas / Leeper, Nicholas J / Miller, Clint L. ·Department of Surgery, Division of Vascular Surgery, Stanford University School of Medicine, Stanford, California, United States of America. · Stanford Cardiovascular Institute, Stanford University School of Medicine, Stanford, California, United States of America. · Department of Genetics, Stanford University School of Medicine, Stanford, California, United States of America. · Department of Medicine, Division of Cardiovascular Medicine, Stanford University School of Medicine, Stanford, California, United States of America. · Department of Biology, Stanford University School of Medicine, Stanford, California, United States of America. · Department of Pathology, Stanford University School of Medicine, Stanford, California, United States of America. · Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden. · Department of Genetics and Genomic Sciences, Icahn Institute for Genomics and Multiscale Biology, Icahn School of Medicine at Mount Sinai, New York, United States of America. · Clinical Gene Networks AB, Stockholm, Sweden. · Department of Cardiac Surgery, Tartu University Hospital, Tartu, Estonia. · Department of Medical Biochemistry and Biophysics, Vascular Biology Unit, Karolinska Institutet, Stockholm, Sweden. · Department of Physiology, Institute of Biomedicine and Translation Medicine, University of Tartu, Tartu, Estonia. · Center for Public Health Genomics, Department of Public Health Sciences, Department of Biochemistry and Molecular Genetics, and Department of Biomedical Engineering, University of Virginia, Charlottesville, Virginia, United States of America. ·PLoS Genet · Pubmed #30444878.

ABSTRACT: Recent genome-wide association studies (GWAS) have identified multiple new loci which appear to alter coronary artery disease (CAD) risk via arterial wall-specific mechanisms. One of the annotated genes encodes LMOD1 (Leiomodin 1), a member of the actin filament nucleator family that is highly enriched in smooth muscle-containing tissues such as the artery wall. However, it is still unknown whether LMOD1 is the causal gene at this locus and also how the associated variants alter LMOD1 expression/function and CAD risk. Using epigenomic profiling we recently identified a non-coding regulatory variant, rs34091558, which is in tight linkage disequilibrium (LD) with the lead CAD GWAS variant, rs2820315. Herein we demonstrate through expression quantitative trait loci (eQTL) and statistical fine-mapping in GTEx, STARNET, and human coronary artery smooth muscle cell (HCASMC) datasets, rs34091558 is the top regulatory variant for LMOD1 in vascular tissues. Position weight matrix (PWM) analyses identify the protective allele rs34091558-TA to form a conserved Forkhead box O3 (FOXO3) binding motif, which is disrupted by the risk allele rs34091558-A. FOXO3 chromatin immunoprecipitation and reporter assays show reduced FOXO3 binding and LMOD1 transcriptional activity by the risk allele, consistent with effects of FOXO3 downregulation on LMOD1. LMOD1 knockdown results in increased proliferation and migration and decreased cell contraction in HCASMC, and immunostaining in atherosclerotic lesions in the SMC lineage tracing reporter mouse support a key role for LMOD1 in maintaining the differentiated SMC phenotype. These results provide compelling functional evidence that genetic variation is associated with dysregulated LMOD1 expression/function in SMCs, together contributing to the heritable risk for CAD.

20 Article Variation in preoperative antithrombotic strategy, severe bleeding, and use of blood products in coronary artery bypass grafting: results from the multicentre E-CABG registry. 2018

Biancari, Fausto / Mariscalco, Giovanni / Gherli, Riccardo / Reichart, Daniel / Onorati, Francesco / Faggian, Giuseppe / Franzese, Ilaria / Santarpino, Giuseppe / Fischlein, Theodor / Rubino, Antonino S / Maselli, Daniele / Nardella, Saverio / Salsano, Antonio / Nicolini, Francesco / Zanobini, Marco / Saccocci, Matteo / Ruggieri, Vito G / Bounader, Karl / Perrotti, Andrea / Rosato, Stefano / D'Errigo, Paola / D'Andrea, Vito / De Feo, Marisa / Tauriainen, Tuomas / Gatti, Giuseppe / Dalén, Magnus. ·Heart Center, Turku University Hospital, University of Turku, Turku, Finland. · Department of Surgery, University of Turku, Hämeentie 11, PO Box, Turku, Finland. · Department of Surgery, Oulu University Hospital and University of Oulu, Kajaanintie 50, Oulu, Finland. · Department of Cardiovascular Sciences, Clinical Sciences Wing, University of Leicester, Glenfield, Hospital, Groby Road, Leicester, Leicestershire, UK. · Department of Cardiovascular Sciences, Cardiac Surgery Unit, S. Camillo, -Forlanini Hospital, Circonvallazione Gianicolense, 87, Rome, Italy. · Hamburg University Heart Center, Martinistraße 52, Hamburg, Germany. · Department of Cardiovascular Surgery, Division of Cardiovascular Surgery, Verona University Hospital, P. Le Stefani 1, Verona, Italy. · Department of Cardiovascular Surgery, Cardiovascular Center, Paracelsus Medical University, Nuremberg, Germany and Città di Lecce Hospital GVM Care&Research, Strada Provinciale per Arnesano km 4, Lecce LE, Italy. · Department of Cardiovascular Surgery, Centro Clinico-Diagnostico "G.B. Morgagni", Centro Cuore, Via della Resistenza, 31, Pedara CT, Italy. · Department of Cardiovascular Surgery, St. Anna Hospital, Catanzaro, Viale Papa Pio X, 111, Catanzaro, Italy. · Division of Cardiac Surgery, University of Genoa, Largo Rosanna Benzi, 10, Genova GE, Italy. · Division of Cardiac Surgery, University of Parma, Via Gramsci 14 - Parma, Italy. · Department of Cardiac Surgery, Centro Cardiologico - Fondazione Monzino IRCCS, University of Milan, Via Carlo Parea, 4, Milan MI, Italy. · Division of Cardiothoracic and Vascular Surgery, Robert Debré University Hospital, Rue du Général Koenig, Reims, France. · Division of Cardiothoracic and Vascular Surgery, Pontchaillou University Hospital, 2 Rue Henri le Guilloux, Rennes, France. · Department of Thoracic and Cardio-Vascular Surgery, University Hospital Jean Minjoz, 3 Boulevard Alexandre Fleming, Besançon, France. · National Center of Global Health, Istituto Superiore di Sanità, Via Giano della Bella 34, Rome RM, Italy. · Department of Cardiovascular Diseases, University of Campania "Luigi Vanvitelli", Piazza Luigi Miraglia, 2, Naples, Italy. · Division of Cardiac Surgery, Ospedali Riuniti, via Farneto 3, Trieste, Italy. · Department of Molecular Medicine and Surgery, Department of Cardiac Surgery, Karolinska Institutet, Karolinska University Hospital, Karolinska Universitetssjukhuset, Karolinska vägen, Solna, Sweden. ·Eur Heart J Qual Care Clin Outcomes · Pubmed #29939246.

ABSTRACT: Aims: No data exists on inter-institutional differences in terms of adherence to international guidelines regarding the discontinuation of antithrombotics and rates of severe bleeding in coronary artery bypass grafting (CABG). Methods and results: This is an analysis of 7118 patients from the prospective multicentre European CABG (E-CABG) registry who underwent isolated CABG in 15 European centres. Preoperative pause of P2Y12 receptor antagonists shorter than that suggested by the 2017 ESC guidelines (overall 11.6%) ranged from 0.7% to 24.8% between centres (adjusted P < 0.0001) and increased the rate of severe-massive bleeding [E-CABG bleeding grades 2-3, OR 1.66, 95% confidence interval (CI) 1.27-2.17; Universal Definition of Perioperative Bleeding (UDPB) bleeding grades 3-4, OR 1.50, 95% CI 1.16-1.93]. The incidence of resternotomy for bleeding (overall 2.6%) ranged from 0% to 6.9% (adjusted P < 0.0001), and surgical site bleeding (overall 59.6%) ranged from 0% to 84.6% (adjusted P = 0.003). The rate of the UDPB bleeding grades 3-4 (overall 8.4%) ranged from 3.7% to 22.3% (P < 0.0001), and of the E-CABG bleeding grades 2-3 (overall 6.5%) ranged from 0.4% to 16.4% between centres (P < 0.0001). Resternotomy for bleeding (adjusted OR 5.04, 95% CI 2.85-8.92), UDPB bleeding grades 3-4 (adjusted OR 6.61, 95% CI 4.42-9.88), and E-CABG bleeding grades 2-3 (adjusted OR 8.71, 95% CI 5.76-13.15) were associated with an increased risk of hospital/30-day mortality. Conclusions: Adherence to the current guidelines on the early discontinuation of P2Y12 receptor antagonists is of utmost importance to reduce excessive bleeding and early mortality after CABG. Inter-institutional variation should be considered for a correct interpretation of the results in multicentre studies evaluating perioperative bleeding and use of blood products.

21 Article Prognosis in relation to high-sensitivity cardiac troponin T levels in patients with myocardial infarction and non-obstructive coronary arteries. 2018

Hjort, Marcus / Lindahl, Bertil / Baron, Tomasz / Jernberg, Tomas / Tornvall, Per / Eggers, Kai M. ·Uppsala Clinical Research Center, Uppsala University, Uppsala, Sweden; Department of Medical Sciences, Uppsala University, Uppsala, Sweden. Electronic address: marcus.hjort@medsci.uu.se. · Uppsala Clinical Research Center, Uppsala University, Uppsala, Sweden; Department of Medical Sciences, Uppsala University, Uppsala, Sweden. · Department of Clinical Sciences, Danderyd Hospital, Karolinska Institutet, Stockholm, Sweden. · Department of Clinical Science and Education, Södersjukhuset, Karolinska Institutet, Stockholm, Sweden. · Department of Medical Sciences, Uppsala University, Uppsala, Sweden. ·Am Heart J · Pubmed #29898850.

ABSTRACT: BACKGROUND: Myocardial infarction (MI) with non-obstructive coronary arteries (MINOCA) is a recently recognized condition where biomarkers and prognosis are less well studied than in MI with obstructive coronary artery disease (MI-CAD). We therefore aimed to investigate the one-year prognostic value of high-sensitivity cardiac troponin T (hs-cTnT) levels in MINOCA in comparison to MI-CAD. METHODS: In this registry-based cohort study, we used data from patients with a discharge diagnosis of MI, admitted between 2009 and 2013 to Swedish hospitals using the hs-cTnT assay. Only patients without previously known coronary artery disease were considered. Patients with and without coronary stenosis >50% were regarded to have MI-CAD and MINOCA, respectively. Assessed outcomes included all-cause mortality, cardiovascular (CV) mortality and major CV events (MACE), defined as the composite of CV death or admissions for non-fatal MI, heart failure (HF) or ischemic stroke. RESULTS: The study cohort consisted of 1639 MINOCA and 17,304 MI-CAD patients. In adjusted analyses, hs-cTnT (ln) in MINOCA patients predicted all-cause mortality (HR 1.32 [95% CI 1.11-1.56]), CV mortality (HR 2.11 [95% CI 1.51-2.96]) and MACE (HR 1.44 [95% CI 1.20-1.72]). Hs-cTnT (ln) also predicted readmissions for HF (HR 1.51 [95% CI 1.51-2.96]) but not non-fatal MI or stroke. Interaction analyses suggested that hs-cTnT (ln) was at least as prognostic in patients with MINOCA compared to MI-CAD. CONCLUSIONS: Hs-cTnT levels in MINOCA patients are strong and independent predictors of adverse outcome. Consideration of hs-cTnT levels is important for risk assessment of MINOCA patients.

22 Article Serum magnesium levels and risk of coronary artery disease: Mendelian randomisation study. 2018

Larsson, Susanna C / Burgess, Stephen / Michaëlsson, Karl. ·Unit of Nutritional Epidemiology, Institute of Environmental Medicine, Karolinska Institutet, 171 77, Stockholm, Sweden. susanna.larsson@ki.se. · MRC Biostatistics Unit, University of Cambridge, Cambridge, UK. · Department of Public Health and Primary Care, University of Cambridge, Cambridge, UK. · Department of Surgical Sciences, Uppsala University, Uppsala, Sweden. ·BMC Med · Pubmed #29769070.

ABSTRACT: BACKGROUND: Observational studies have shown that serum magnesium levels are inversely associated with risk of cardiovascular disease, but whether this association is causal is unknown. We conducted a Mendelian randomisation study to investigate whether serum magnesium levels may be causally associated with coronary artery disease (CAD). METHODS: This Mendelian randomisation analysis is based on summary-level data from the CARDIoGRAMplusC4D consortium's 1000 Genomes-based genome-wide association meta-analysis of 48 studies with a total of 60,801 CAD cases and 123,504 non-cases. Six single-nucleotide polymorphisms associated with serum magnesium levels at genome-wide significance were used as instrumental variables. RESULTS: A genetic predisposition to higher serum magnesium levels was inversely associated with CAD. In conventional Mendelian randomisation analysis, the odds ratio of CAD was 0.88 (95% confidence interval [CI] 0.78 to 0.99; P = 0.03) per 0.1-mmol/L (about 1 standard deviation) increase in genetically predicted serum magnesium levels. Results were consistent in sensitivity analyses using the weighted median and heterogeneity-penalised model averaging methods, with odds ratios of 0.84 (95% CI 0.72 to 0.98; P = 0.03) and 0.83 (95% CI 0.71 to 0.96; P = 0.02), respectively. CONCLUSIONS: This study based on genetics provides evidence that serum magnesium levels are inversely associated with risk of CAD. Randomised controlled trials elucidating whether magnesium supplementation lowers the risk of CAD, preferably in a setting at higher risk of hypomagnesaemia, are warranted.

23 Article Stent thrombosis rates the first year and beyond with new- and old-generation drug-eluting stents compared to bare metal stents. 2018

Varenhorst, Christoph / Lindholm, Martin / Sarno, Giovanna / Olivecrona, Göran / Jensen, Ulf / Nilsson, Johan / Carlsson, Jörg / James, Stefan / Lagerqvist, Bo. ·Uppsala Clinical Research Center, Uppsala University, Uppsala, Sweden. christoph.varenhorst@medsci.uu.se. · Department of Medical Sciences, Cardiology, Uppsala University, Dag Hammarsköldsväg 14B, 75337, Uppsala, Sweden. christoph.varenhorst@medsci.uu.se. · Department of Internal Medicine, Cardiology, Västerås County Hospital, Västerås, Sweden. · Uppsala Clinical Research Center, Uppsala University, Uppsala, Sweden. · Department of Medical Sciences, Cardiology, Uppsala University, Dag Hammarsköldsväg 14B, 75337, Uppsala, Sweden. · Department of Cardiology, Lund University, Lund, Sweden. · Department of Clinical Science and Education, Södersjukhuset, Karolinska Institutet, Stockholm, Sweden. · Department of Cardiology, Heart Centre, Umeå University, Umeå, Sweden. · Faculty of Health and Life Sciences, Linnaeus University, Kalmar, Sweden. ·Clin Res Cardiol · Pubmed #29667015.

ABSTRACT: OBJECTIVES: Old-generation drug-eluting coronary stents (o-DES) have despite being safe and effective been associated with an increased propensity of late stent thrombosis (ST). We evaluated ST rates in o-DES, new-generation DES (n-DES) and bare metal stents (BMS) the first year (< 1 year) and beyond 1 year (> 1 year). METHODS: We evaluated all implantations with BMS, o-DES (Cordis Cypher, Boston Scientific Taxus Liberté and Medtronic Endeavor) and n-DES in the Swedish coronary angiography and angioplasty registry (SCAAR) between 1 January 2007 and 8 January 2014 (n = 207 291). All cases of ST (n = 2 268) until 31 December 2014 were analyzed. RESULTS: The overall risk of ST was lower in both n-DES and o-DES compared with BMS up to 1 year (n-DES versus BMS: adjusted risk ratio (RR) 0.48 (0.41-0.58) and o-DES versus BMS: 0.56 (0.46-0.67), both p < 0.001). From 1 year after stent implantation and onward, the risk for ST was higher in o-DES compared with BMS [adjusted RR, 1.82 (1.47-2.25], p < 0.001). N-DES were associated with similar low ST rates as BMS from 1 year and onward [adjusted RR 1.21 (0.94-1.56), p = 0.135]. CONCLUSION: New-generation DES were associated with lower ST rates in comparison to BMS during the first-year post-stenting. After 1 year, n-DES and BMS were associated with similar ST rates. TRIAL REGISTRATION: This study was a retrospective observational study and as such did not require clinical trial database registration.

24 Article Predictors of adverse outcome in patients with myocardial infarction with non-obstructive coronary artery (MINOCA) disease. 2018

Nordenskjöld, A M / Baron, T / Eggers, K M / Jernberg, T / Lindahl, B. ·Department of Cardiology, Faculty of Medicine and Health, Örebro University, Örebro, Sweden. Electronic address: anna.nordenskjold@regionorebrolan.se. · Department of Medical Sciences, Uppsala Clinical Research Center, Uppsala University, Uppsala, Sweden. · Department of Clinical Sciences, Cardiology, Danderyd Hospital, Karolinska Institute, Stockholm, Sweden. ·Int J Cardiol · Pubmed #29563017.

ABSTRACT: BACKGROUND: Myocardial infarction (MI) with non-obstructive coronary arteries (MINOCAs) is an increasingly recognized entity. No previous study has evaluated predictors for new major adverse cardiacvascular events (MACEs) and death in patients with MINOCA. METHODS: We conducted an observational study of MINOCA patients recorded between July 2003 and June 2013 and followed until December 2013 for outcome events. Out of 199,163 MI admissions, 9092 consecutive unique patients with MINOCA were identified. The mean age was 65.5 years and 62% were women. MACE was defined as all-cause mortality, rehospitalization for acute MI, ischemic stroke and heart failure. Hazard ratio and 95% confidence interval (HR; 95% CI) was calculated using Cox-regression. RESULTS: A total of 2147 patients (24%) experienced a new MACE and 1254 patients (14%) died during the mean follow-up of 4.5 years. Independent predictors for MACE after adjustment, were older age (1.05; 1.04-1.06), diabetes (1.44; 1.21-1.70), hypertension (1.25; 1.09-1.43), current smoking (1.38; 1.15-1.66), previous myocardial infarction (1.38; 1.04-2.82), previous stroke (1.69; 1.35-2.11), peripheral vascular disease (1.55; 1.97-2.23), chronic obstructive pulmonary disease (1.63; 1.32-2.00), reduced left ventricular ejection fraction (2.00; 1.54-2.60), lower level of total cholesterol (0.88; 0.83-0.94) and higher level of creatinine (1.01; 1.00-1.03). Independent predictors for all cause death were age, current smoking, diabetes, cancer, chronic obstructive pulmonary disease, previous stroke, reduced left ventricular fraction, lower level of total cholesterol and higher levels of creatinine and CRP. CONCLUSIONS: The clinical factors predicting new MACE and death of MINOCA patients seem to be strikingly similar to factors previously shown to predict new cardiovascular events in patients with MI and obstructive coronary artery disease.

25 Article Lack of genetic susceptibility in takotsubo cardiomyopathy: a case-control study. 2018

Mattsson, Emma / Saliba-Gustafsson, Peter / Ehrenborg, Ewa / Tornvall, Per. ·Department of Clinical Science and Education Södersjukhuset, Karolinska Institutet, Sjukhusbacken 10, 11883, Stockholm, Sweden. · Department of Medicine, Solna Center for Molecular Medicine (CMM), Karolinska University Hospital L8:03, Karolinska Institutet, Stockholm, Sweden. · Department of Clinical Science and Education Södersjukhuset, Karolinska Institutet, Sjukhusbacken 10, 11883, Stockholm, Sweden. Per.tornvall@ki.se. ·BMC Med Genet · Pubmed #29514624.

ABSTRACT: BACKGROUND: Takotsubo cardiomyopathy (TCM), also known as "broken heart syndrome", is a type of heart failure characterized by transient ventricular dysfunction in the absence of obstructive coronary lesions. Although associated with increased levels of catecholamines, pathophysiological mechanisms are unknown. Relapses and family heritability indicate a genetic predisposition. Several small studies have investigated associations between three different loci; the β1-adrenic receptor (ADRB1), G-protein-coupled receptor kinase 5 (GRK5), Bcl-associated athanogene 3 (BAG3) and TCM but no consensus has been reached. METHODS: Participants were recruited using the Swedish Coronary Angiography and Angioplasty Register (SCAAR). TCM patients without coronary artery disease (CAD)(n = 258) were identified and age- and sex-matched subjects with (n = 164) and without (n = 243) CAD were selected as controls. DNA was isolated from saliva and genotyped for candidate single nucleotide polymorphisms in the ADRB1, GRK5 and BAG3 genes. Allele frequencies and Odds Ratios (OR) with 95% Confidence Intervals (CI) for the investigated polymorphisms were compared, respectively calculated for TCM patients and controls. RESULTS: There were no differences in allele frequencies between TCM patients and controls. OR (CI) for TCM patients having at least one minor allele using controls as reference were 1.07 (0.75-1.55) for ADRB1, 0.45 (0.11-1.85) for GRK5 and 1.27 (0.74-2.19) for BAG3. CONCLUSION: By genotyping a large takotsubo cohort, we demonstrate a lack of association between candidate SNPs in the ADRB1, GRK5 and BAG3 genes, earlier suggested to contribute to TCM. Our result indicates a need to expand the search for new genetic candidates contributing to TCM.

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