Author: "Marketa Sjögren" / Topic: business.industry - Searchworks@Jio Institute Digital Library Search Results

47 results on '"Marketa Sjögren"'

1. The Gly82Ser polymorphism in the receptor for advanced glycation end products is associated with increased risk for coronary events in the general population

Author: Gunnar Engström, Jan-Åke Nilsson, Marketa Sjögren, Peter M. Nilsson, H. Grauen Larsen, Olle Melander, Alexandru Schiopu, and Marju Orho-Melander
Subjects: medicine.medical_specialty, education.field_of_study, business.industry, Population, Endocrinology, Increased risk, Glycation, Internal medicine, medicine, cardiovascular diseases, Cardiology and Cardiovascular Medicine, Receptor, business, education
Abstract: Background/Introduction Activation of the receptor for advanced glycation end products (RAGE) by AGEs and various immune mediators has pro-inflammatory and pro-atherogenic effects. RAGE also exists in a soluble form, sRAGE, that acts as a decoy receptor for RAGE ligands. Low plasma sRAGE has previously been found to be associated with a higher risk for major adverse coronary events (MACE) in the population. Purpose The purpose of our study was to examine the causality of the association, by exploring whether genetic variants that influence sRAGE are associated with atherosclerosis progression and incident MACE and mortality in the population. Methods We performed a genome-wide association study (GWAS) in 4192 individuals from a randomly selected subgroup of a population-based cohort. Subsequently, we explored the associations between the identified single nucleotide polymorphims (SNPs) associated with plasma sRAGE levels, baseline intima media thickness (IMT) and IMT progression in the common carotid artery during a median follow-up of 16.5 years. Further, we analyzed the prospective relationships between the sRAGE-associated SNPs, incident MACE and mortality in the entire population-based cohort of 29245 individuals. The median follow-up time from baseline was 21.2 years for MACE and 21.6 years for total mortality (time to event or end of follow-up). Results We found the minor alleles of two single nucleotide polymorphisms (SNPs), rs2070600 and rs204993, to be independently associated with lower plasma sRAGE. While rs204993 is a silent intronic mutation, rs2070600 is known to cause a Gly82Ser polymorphism in the ligand binding domain, enhancing RAGE propensity for activation. In Cox regression analyses, we found an association between the minor T (vs. C) allele of rs2070600 and increased risk for first-time MACE [HR 1.12 (1.02–1.23); P=0.023]. The association was independent of traditional cardiovascular risk factors, blood pressure-lowering medication and lipid-lowering medication at baseline. rs204993 was not associated with MACE. Neither SNP was associated with carotid IMT at baseline or with IMT progression. We did not identify any relationships with total mortality. Conclusions We demonstrate for the first time an independent link between a genetic RAGE determinant and the risk for MACE in the population. Despite both identified SNPs being associated with lower sRAGE levels, only the functional rs2070600 mutation was associated with MACE, suggesting that the link is probably due to the enhancement of RAGE function rather than to the sRAGE lowering effect. Funding Acknowledgement Type of funding source: Public Institution(s). Main funding source(s): This study was supported by grants from the Swedish Research Council and the Swedish Heart and Lung foundation.
Published: 2020
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2. Genetic inactivation of ANGPTL4 improves glucose homeostasis and is associated with reduced risk of diabetes

Author: Teresa Tusié-Luna, Svati H. Shah, Wen-Jane Lee, Amit Khera, Gonçalo R. Abecasis, Olle Melander, Alan R. Shuldiner, Connor A. Emdin, Kari Stefansson, Jesper Gromada, Andrew P. Morris, Lee-Ming Chuang, Omri Gottesman, Lars G. Fritsche, Pradeep Natarajan, Marju Orho-Melander, Daniel F. Gudbjartsson, Anubha Mahajan, Marylyn D. Ritchie, William E. Kraus, Tooraj Mirshahi, Colm O'Dushlaine, Jason Flannick, Nicholas J. Wareham, Anne Tybjærg-Hansen, Anders Berg Wulff, Rashmi B. Prasad, Aris Baras, Jonas B. Nielsen, Valgerdur Steinthorsdottir, Yii-Der Ida Chen, Jerome I. Rotter, Lukas Habegger, Samantha N. Fetterolf, David Altshuler, Om Prakash Dwivedi, Tanya M. Teslovich, Cristen J. Willer, Luca A. Lotta, Andrew J. Murphy, Joseph B. Leader, Cristopher V. Van Hout, Christopher D. Still, Ola Hansson, David Birtwell, Alexander Lopez, Daniel J. Rader, John D. Overton, Anthony Marcketta, Patrick Sulem, Peter N. Benotti, Jose C. Florez, Lydia Coulter Kwee, David J. Carey, Oddgeir L. Holmen, Kristian Hveem, Leif Groop, Sekar Kathiresan, Viktoria Gusarova, Unnur Thorsteinsdottir, Cassandra M. Hartle, Uyenlinh L. Mirshahi, H. Lester Kirchner, Shannon Bruse, Robert A. Scott, Michael F. Murray, Marketa Sjögren, Jeffrey G. Reid, Aeron Small, Børge G. Nordestgaard, Amr H. Wardeh, Chad M. Brummett, Mark I. McCarthy, Frederick E. Dewey, David H. Ledbetter, John Penn, Ingrid B. Borecki, Scott M. Damrauer, Hilma Holm, Michael Boehnke, George D. Yancopoulos, Institute for Molecular Medicine Finland, University of Helsinki, Centre of Excellence in Complex Disease Genetics, and HUS Abdominal Center
Subjects: Blood Glucose, Male, 0301 basic medicine, Insulin Resistance/genetics, General Physics and Astronomy, Type 2 diabetes, 030204 cardiovascular system & hematology, Inbred C57BL, Cardiovascular, HAN CHINESE, Whole Exome Sequencing, Mice, 0302 clinical medicine, Risk Factors, ANGPTL4, Homeostasis, Glucose homeostasis, lcsh:Science, Mice, Knockout, Lipoprotein lipase, Multidisciplinary, Diabetes, Lipoprotein Lipase/metabolism, REMNANT CHOLESTEROL, ADIPOSE-TISSUE, Female, Type 2, Heterozygote, medicine.medical_specialty, Knockout, Science, LIPOPROTEIN-LIPASE, HEART-DISEASE, Diabetes Mellitus, Type 2/etiology, Article, General Biochemistry, Genetics and Molecular Biology, Angiopoietin-like 4 Protein/deficiency, 03 medical and health sciences, Internal medicine, Diabetes mellitus, Exome Sequencing, Diabetes Mellitus, Genetics, medicine, Angiopoietin-Like Protein 4, Animals, Humans, Gene Silencing, GENOME-WIDE ASSOCIATION, Metabolic and endocrine, Genetic Association Studies, CHINESE POPULATION, Blood Glucose/metabolism, PLASMA-LIPIDS, business.industry, Case-control study, Genetic Variation, General Chemistry, Odds ratio, Atherosclerosis, medicine.disease, Mice, Inbred C57BL, Lipoprotein Lipase, 030104 developmental biology, Endocrinology, Diabetes Mellitus, Type 2, Amino Acid Substitution, Case-Control Studies, lcsh:Q, 3111 Biomedicine, ANGIOPOIETIN-LIKE PROTEIN-4, Insulin Resistance, business
Abstract: Angiopoietin-like 4 (ANGPTL4) is an endogenous inhibitor of lipoprotein lipase that modulates lipid levels, coronary atherosclerosis risk, and nutrient partitioning. We hypothesize that loss of ANGPTL4 function might improve glucose homeostasis and decrease risk of type 2 diabetes (T2D). We investigate protein-altering variants in ANGPTL4 among 58,124 participants in the DiscovEHR human genetics study, with follow-up studies in 82,766 T2D cases and 498,761 controls. Carriers of p.E40K, a variant that abolishes ANGPTL4 ability to inhibit lipoprotein lipase, have lower odds of T2D (odds ratio 0.89, 95% confidence interval 0.85–0.92, p = 6.3 × 10−10), lower fasting glucose, and greater insulin sensitivity. Predicted loss-of-function variants are associated with lower odds of T2D among 32,015 cases and 84,006 controls (odds ratio 0.71, 95% confidence interval 0.49–0.99, p = 0.041). Functional studies in Angptl4-deficient mice confirm improved insulin sensitivity and glucose homeostasis. In conclusion, genetic inactivation of ANGPTL4 is associated with improved glucose homeostasis and reduced risk of T2D., Genetic variation in ANGPTL4 is associated with lipid traits. Here, the authors find that predicted loss-of-function variants in ANGPTL4 are associated with glucose homeostasis and reduced risk of type 2 diabetes and that Angptl4−/− mice on a high-fat diet show improved insulin sensitivity.
Published: 2018
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3. A NEW GENETIC RISK SCORE FOR BLOOD PRESSURE STRONGLY ASSOCIATES WITH THE INCIDENCE OF HYPERTENSION AND CARDIOVASCULAR ENDPOINTS IN TWO SWEDISH COHORTS

Author: Alice Giontella, Marketa Sjögren, Luca Lotta, John Overton, Aris Baras, Regeneron Genetics Center, Fava Cristiano, and Olle Melander
Subjects: medicine.medical_specialty, Blood pressure, Physiology, business.industry, Incidence (epidemiology), Internal medicine, Internal Medicine, Medicine, Genetic risk, Cardiology and Cardiovascular Medicine, business
Published: 2021
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4. Orthostatic Hypotension and Novel Blood Pressure Associated Gene Variants in Older Adults: Data From the TILDA Study

Author: Olle Melander, Marketa Sjögren, Aisling M O'Halloran, Daniel Carey, Eamon Laird, Artur Fedorowski, Ann Hever, and Rose Anne Kenny
Subjects: Male, Aging, Candidate gene, medicine.medical_specialty, Genotype, Population, Single-nucleotide polymorphism, Polymorphism, Single Nucleotide, Orthostatic vital signs, Hypotension, Orthostatic, Risk Factors, Internal medicine, Surveys and Questionnaires, Medicine, SNP, Humans, Longitudinal Studies, Allele, education, Alleles, Aged, education.field_of_study, business.industry, Genetic Variation, Blood Pressure Determination, Middle Aged, Minor allele frequency, Endocrinology, Blood pressure, Female, Geriatrics and Gerontology, business, Ireland
Abstract: Orthostatic hypotension (OH) is associated with increased risk of trauma and cardiovascular events. Recent studies have identified new genetic variants that influence orthostatic blood pressure (BP). The aim of this study was to investigate the associations of candidate gene loci with orthostatic BP responses in older adults. A total of 3,430 participants aged ≥50 years from The Irish Longitudinal Study on Ageing (TILDA) with BP measures and genetic data from 12 single-nucleotide polymorphism (SNP) linked to BP responses were analyzed. Orthostatic BP responses were recorded at each 10 s interval and were defined as OH (SBP drop ≥20 mmHg or DBP drop ≥10 mmHg) at the time-points 40, 90, and 110 s. We defined sustained OH (SOH) as a drop that exceeded consensus BP thresholds for OH at 40, 90, and 110 s after standing. Logistic regression analyses modeled associations between the candidate SNP alleles and OH. We report no significant associations between OH and measured SNPs after correction for multiple comparisons apart from the SNP rs5068 where proportion of the minor allele was significantly different between cases and controls for SOH 40 (p = .002). After adjustment for covariates in a logistic regression, those with the minor G allele (compared to the A allele) had a decreased incidence rate ratio (IRR) for SOH 40 (IRR 0.45, p = .001, 95% CI 0.29–0.72). Only one SNP linked with increased natriuretic peptide concentrations was associated with OH. These results suggest that genetic variants may have a weak impact on OH but needs verification in other population studies.
Published: 2019

5. Twelve–Single Nucleotide Polymorphism Genetic Risk Score Identifies Individuals at Increased Risk for Future Atrial Fibrillation and Stroke

Author: James J. Devlin, Patrick T. Ellinor, Gunnar Engström, Olle Melander, Judy Z. Louie, Dov Shiffman, J. Gustav Smith, Marketa Sjögren, Joseph J. Catanese, Hayato Tada, Sekar Kathiresan, and Steven A. Lubitz
Subjects: Advanced and Specialized Nursing, Fibrillation, medicine.medical_specialty, Neurology, business.industry, Proportional hazards model, Atrial fibrillation, Single-nucleotide polymorphism, medicine.disease, Diet and cancer, Internal medicine, Cohort, medicine, Physical therapy, Neurology (clinical), medicine.symptom, Cardiology and Cardiovascular Medicine, business, Stroke
Abstract: Background and Purpose— Atrial fibrillation (AF) is prevalent and there is a clinical need for biomarkers to identify individuals at higher risk for AF. Fixed throughout a life course and assayable early in life, genetic biomarkers may meet this need. Here, we investigate whether multiple single nucleotide polymorphisms together as an AF genetic risk score (AF-GRS) can improve prediction of one’s risk for AF. Methods— In 27 471 participants of the Malmö Diet and Cancer Study, a prospective, community-based cohort, we used Cox models that adjusted for established AF risk factors to assess the association of AF-GRS with incident AF and ischemic stroke. Median follow-up was 14.4 years for incident AF and 14.5 years for ischemic stroke. The AF-GRS comprised 12 single nucleotide polymorphisms that had been previously shown to be associated with AF at genome-wide significance. Results— During follow-up, 2160 participants experienced a first AF event and 1495 had a first ischemic stroke event. Participants in the top AF-GRS quintile were at increased risk for incident AF (hazard ratio, 2.00; 95% confidence interval, 1.73–2.31; P =2.7×10 –21 ) and ischemic stroke (hazard ratio, 1.23; 95% confidence interval, 1.04–1.46; P =0.02) when compared with the bottom quintile. Addition of the AF-GRS to established AF risk factors modestly improved both discrimination and reclassification ( P Conclusions— An AF-GRS can identify 20% of individuals who are at ≈2-fold increased risk for incident AF and at 23% increased risk for ischemic stroke. Targeting diagnostic or therapeutic interventions to this subset may prove clinically useful.
Published: 2014
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6. Genetic variation in NEDD4L, an epithelial sodium channel regulator, is associated with cardiovascular disease and cardiovascular death

Author: Jonas Dahlberg, Olle Melander, Bo Hedblad, Gunnar Engström, and Marketa Sjögren
Subjects: Male, Epithelial sodium channel, medicine.medical_specialty, Genotype, Physiology, Nedd4 Ubiquitin Protein Ligases, Ubiquitin-Protein Ligases, Population, Regulator, Blood Pressure, Disease, Polymorphism, Single Nucleotide, Cohort Studies, Internal medicine, Genetic variation, Internal Medicine, medicine, Humans, Prospective Studies, Sodium Chloride, Dietary, education, Aged, Sweden, NEDD4L, education.field_of_study, Endosomal Sorting Complexes Required for Transport, business.industry, Sodium channel, Middle Aged, 3. Good health, Cross-Sectional Studies, Blood pressure, Endocrinology, Cardiovascular Diseases, Female, Cardiology and Cardiovascular Medicine, business
Abstract: We have previously shown that genetic variance in NEDD4L, a regulating protein of a sodium channel in the distal nephron, has been associated with marginally higher blood pressure and enhanced salt sensitivity. Here, we tested if the genetic NEDD4L variation previously associated with salt sensitivity is related to population blood pressure, incidence of cardiovascular disease (CVD) and mortality.We genotyped the rs4149601 A→G and rs2288774 T→C NEDD4L variants in 27,564 participants of the Malmö Diet and Cancer Study. The genotype combination previously shown to be associated with salt sensitivity (rs4149601 GG+rs2288774 CC), which was present in 9.6% of participants, was related to cross sectional blood pressure as well as to CVD incidence and mortality during a median follow-up time of 14 years using Cox regression models.Carriers of the NEDD4L salt sensitivity-associated genotype had (mean ± SEM) higher systolic (142 ± 0.4 vs. 141 ± 0.1 mmHg, P = 0.002) and diastolic (86.0 ± 0.5 vs. 85.6 ± 0.2 mmHg, P = 0.025) blood pressure and multivariate adjusted hazards ratio (95% confidence interval) of CVD 1.13 (1.02-1.25, P = 0.018), coronary events 1.20 (1.06-1.37; P = 0.005) and cardiovascular mortality 1.17 (0.99-1.37; P = 0.055) than noncarriers but there was no significant difference in the incidence of stroke and total mortality.The NEDD4L salt sensitivity-associated genotype was associated with higher blood pressure, which may translate into increased risk for CVD morbidity and mortality. Interestingly, there was no association with stroke suggesting that the association is partially blood pressure independent.
Published: 2014
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7. Polygenetic risk for coronary artery disease increases hospitalization burden and mortality

Author: Peter Almgren, Olle Melander, and Marketa Sjögren
Subjects: lcsh:Diseases of the circulatory (Cardiovascular) system, medicine.medical_specialty, Genome-wide association study, 030204 cardiovascular system & hematology, Coronary artery disease, 03 medical and health sciences, 0302 clinical medicine, Diet and cancer, Internal medicine, Genetic predisposition, Risk of mortality, Medicine, 030212 general & internal medicine, Mortality, Prospective cohort study, Cause of death, Original Paper, Genetic risk score (GRS), business.industry, fungi, medicine.disease, 3. Good health, Coronary artery disease (CAD), Hospitalization, lcsh:RC666-701, Population study, Cardiology and Cardiovascular Medicine, business
Abstract: Background: Coronary artery disease (CAD) is a leading cause of death worldwide and increasing cost for society. Genome wide association studies (GWAS) have identified common variants associated with CAD. Combining single nucleotide polymorphisms (SNPs) into a genetic risk score (GRS) can estimate an individual's genetic burden. Objectives: To investigate whether GRS for CAD can predict hospitalization and mortality. Methods: 23,594 individuals without CAD at baseline and with full data for all covariates from the population based prospective study Malmö diet and cancer study were investigated. The association between hospitalizations was calculated by negative binomial regression and risk of mortality was calculated by Cox proportional hazards regression. The GRS was constructed from 50 SNPs. Results: The study population was divided into quintiles according to the value of GRS. During the mean follow-up time of 17.8 years, 17,254 individuals were hospitalized at least once. Individuals in the highest quintile of GRS were hospitalized 10% more often than individuals in the lowest quintile (IRR: 1.10 [95% CI 1.04–1.16], p = 0.001), mainly for cardiovascular reasons (IRR: 1.31 [95% CI 1.20–1.43], p = 5.17 × 10−10). These individuals had highly increased risk of CVD mortality (HR: 1.44 [1.25–1.66], p = 6.56 × 10−7) but not the risk of mortality due to other causes. Conclusion: Our results suggest that genetic predisposition for CAD can predict hospitalization burden and mortality, especially due to cardiovascular causes, independently of traditional risk factors. As the risk conferred by the GRS is partially modifiable, our results may help to reduce societal costs, individual suffering and prolong life. Keywords: Genetic risk score (GRS), Coronary artery disease (CAD), Hospitalization, Mortality
Published: 2019
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8. Are 25 SNPs from the CARDIoGRAM study associated with ischaemic stroke?

Author: Ulf Kristoffersson, Katarina Jood, Bo Hedblad, Staffan Olsson, Hossein Delavaran, Olle Melander, Arne Lindgren, Peter Höglund, Christina Jern, Håkan Lövkvist, Gunnar Andsberg, Marketa Sjögren, Bo Norrving, Gunnar Engström, and J. G. Smith
Subjects: Adult, Male, Candidate gene, Pathology, medicine.medical_specialty, Adolescent, Genotype, Multifunction cardiogram, Single-nucleotide polymorphism, Genome-wide association study, Coronary Artery Disease, Polymorphism, Single Nucleotide, Coronary artery disease, Young Adult, Internal medicine, Humans, Medicine, SNP, Genetic Predisposition to Disease, Aged, Genetic association, Aged, 80 and over, business.industry, Odds ratio, Middle Aged, medicine.disease, Stroke, Phenotype, Neurology, Female, Neurology (clinical), business, Genome-Wide Association Study
Abstract: BACKGROUND AND PURPOSE: The Coronary Artery Disease Genome-Wide Replication and Meta-Analysis Study (CARDIoGRAM) reported 25 single-nucleotide polymorphisms (SNPs) on 15 chromosomes to be associated with coronary artery disease (CAD) risk. Because common vascular risk factors are shared between CAD and ischaemic stroke (IS), these SNPs may also be related to IS overall or one or more of its pathogenetic subtypes. METHODS: We performed a candidate gene study comprising 3986 patients with IS and 2459 control subjects. The 25 CAD-associated SNPs reported by CARDIoGRAM were examined by allelic association analysis including logistic regression. Weighted and unweighted genetic risk scores (GRSs) were also compiled and likewise analysed against IS. We furthermore considered the IS main subtypes large-vessel disease (LVD), small-vessel disease and cardioembolic stroke [according to Trial of Org 10172 in Acute Stroke Treatment (TOAST)] separately. RESULTS: SNP rs4977574 on chromosome 9p21.3 was associated with overall IS [odds ratio (OR) = 1.12; 95% confidence interval (CI): 1.04-1.20; P = 0.002] as well as LVD (OR = 1.36; 95% CI: 1.13-1.64; P = 0.001). No other SNP was significantly associated with IS or any of its main subtypes. Analogously, the GRSs did not show any noticeable effect. CONCLUSIONS: Besides the previously reported association with SNPs on chromosome 9p21, this study did not detect any significant association between IS and CAD-susceptible genetic variants. Also, GRSs compiled from these variants did not predict IS or any pathogenetic IS subtype, despite a total sample size of 6445 participants.
Published: 2013
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9. Genetic polymorphisms confer risk of atrial fibrillation in patients with heart failure: a population‐based study

Author: Pyotr G. Platonov, J. Gustav Smith, Olle Melander, Bo Hedblad, Christopher Newton-Cheh, Marketa Sjögren, and Gunnar Engström
Subjects: Male, medicine.medical_specialty, Pathology, Population, Genome-wide association study, Polymorphism, Single Nucleotide, Cohort Studies, Risk Factors, Internal medicine, Atrial Fibrillation, medicine, Humans, Genetic Predisposition to Disease, Prospective Studies, Prospective cohort study, education, Aged, Proportional Hazards Models, Aged, 80 and over, Heart Failure, Homeodomain Proteins, Sweden, education.field_of_study, Proportional hazards model, business.industry, Hazard ratio, Atrial fibrillation, Middle Aged, medicine.disease, Cohort, Cardiology, Female, Chromosomes, Human, Pair 4, Cardiology and Cardiovascular Medicine, business, Chromosomes, Human, Pair 16, Genome-Wide Association Study, Cohort study
Abstract: AIMS: Atrial fibrillation (AF) is a frequent co-morbidity in heart failure (HF) associated with increased mortality, but little is known about the mechanisms underlying AF onset in HF patients. We evaluated the association of cardiovascular and genetic risk factors with AF in HF patients. METHODS AND RESULTS: Individuals hospitalized for HF (n = 1040; 500 with AF) were identified from a large, population-based cohort study (n = 30 447; 2339 with AF). Genetic polymorphisms in the chromosomal regions 4q25 (rs2200733) and 16q22 (rs2106261) associated with AF in genome-wide association studies were genotyped. Association of cardiovascular risk factors and polymorphisms with AF was tested in HF patients and the entire cohort using both prospective and non-time-dependent models. Cardiovascular risk factors-hypertension, body mass index, sex, smoking, diabetes, and myocardial infarction-were associated with AF in the entire cohort but not in HF patients. In contrast, polymorphisms on chromosomes 16q22 and 4q25 were associated with AF both in the entire cohort and in HF patients, conferring 75% [95% confidence interval (CI) 35-126, P = 2 × 10(-5)] and 57% (95% CI 18-109, P = 0.002) increased risk of AF per copy in HF patients, respectively. In the entire cohort, AF risk in the presence of HF was multiplicatively magnified by genotype for 16q22 (P for interaction = 7 × 10(-4)) but not 4q25 (P = 0.83). In prospective analyses excluding patients with AF diagnosis prior to or simultaneously with HF diagnosis, 16q22 but not 4q25 remained robustly associated with AF (hazard ratio 1.96, 95% CI 1.40-2.73, P = 8 × 10(-5)). The proportion of AF diagnoses in HF patients attributable to polymorphisms was 19% and 12%, respectively. CONCLUSIONS: A polymorphism in the ZFHX3 gene, encoding a cardiac transcription factor, was associated with increased AF risk in HF patients, and the genetic association with AF was more pronounced in HF patients than in the general population.
Published: 2013
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10. Prediction of Blood Pressure Changes Over Time and Incidence of Hypertension by a Genetic Risk Score in Swedes

Author: Olle Melander, Martina Montagnana, Peter Almgren, Gian Cesare Guidi, Elisa Danese, Cristiano Fava, Pietro Minuz, Marketa Sjögren, Bo Hedblad, Gunnar Engström, and Peter M. Nilsson
Subjects: Adult, Male, medicine.medical_specialty, Genotype, Blood Pressure, Genome-wide association study, Single-nucleotide polymorphism, 030204 cardiovascular system & hematology, Polymorphism, Single Nucleotide, Prehypertension, Cohort Studies, 03 medical and health sciences, 0302 clinical medicine, Internal medicine, Diabetes mellitus, Prevalence, Internal Medicine, medicine, Humans, Cardiac and Cardiovascular Systems, Genetic Predisposition to Disease, genetic risk score, Prospective Studies, 030212 general & internal medicine, Prospective cohort study, Sweden, hypertension, incidence, prediction, business.industry, Incidence, Incidence (epidemiology), Middle Aged, medicine.disease, Obesity, Surgery, Blood pressure, Hypertension, Cardiology, Female, business
Abstract: Recent Genome-Wide Association Studies (GWAS) have pinpointed different single nucleotide polymorphisms consistently associated with blood pressure (BP) and hypertension prevalence. However, little data exist regarding single nucleotide polymorphisms predicting BP variation over time and hypertension incidence. The aim of this study was to confirm the association of a genetic risk score (GRS), based on 29 independent single nucleotide polymorphisms, with cross-sectional BP and hypertension prevalence and to challenge its prediction of BP change over time and hypertension incidence in >17 000 middle-aged Swedes participating in a prospective study, the Malmö Preventive Project, investigated at baseline and over a 23-year average period of follow-up. The GRS was associated with higher systolic and diastolic BP values both at baseline (β±SEM, 0.968±0.102 mm Hg and 0.585±0.064 mm Hg; P P P P P =6.7 E-07), independently from traditional risk factors. The relative weight of the GRS was lower in magnitude than obesity or prehypertension, but comparable with diabetes mellitus or a positive family history of hypertension. A C-statistics analysis does not show any improvement in the prediction of incident hypertension on top of traditional risk factors. Our data from a large cohort study show that a GRS is independently associated with BP increase and incidence of hypertension.
Published: 2013
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11. Genetic Variation Within the Interleukin-1 Gene Cluster and Ischemic Stroke

Author: Marketa Sjögren, Håkan Lövkvist, Gunnar Engström, Lukas Holmegaard, Bo Norrving, Christina Jern, Katarina Jood, Christian Blomstrand, Olle Melander, Sandra Olsson, and Arne Lindgren
Subjects: Male, medicine.medical_specialty, Pathology, Neurology, Genotype, Interleukin-1beta, Single-nucleotide polymorphism, Polymorphism, Single Nucleotide, Brain Ischemia, Diet and cancer, Polymorphism (computer science), Interleukin-1alpha, Internal medicine, Genetic variation, medicine, Humans, Stroke, Aged, Aged, 80 and over, Sweden, Advanced and Specialized Nursing, business.industry, Genetic Variation, Receptors, Interleukin-1, Recovery of Function, Middle Aged, medicine.disease, Pathophysiology, Interleukin 1 Receptor Antagonist Protein, Treatment Outcome, IL1A, Multigene Family, Female, Neurology (clinical), Cardiology and Cardiovascular Medicine, business, Interleukin-1
Abstract: Background and Purpose— Evidence is emerging that inflammation plays a key role in the pathophysiology of ischemic stroke (IS). The aim of this study was to investigate whether genetic variation in the interleukin-1α, interleukin-1β, and interleukin-1 receptor antagonist genes ( IL1A, IL1B , and IL1RN ) is associated with IS and/or any etiologic subtype of IS. Methods— Twelve tagSNPs were analyzed in the Sahlgrenska Academy Study on Ischemic Stroke (SAHLSIS), which comprises 844 patients with IS and 668 control subjects. IS subtypes were defined according to the Trial of Org 10172 in Acute Stroke Treatment criteria in SAHLSIS. The Lund Stroke Register and the Malmö Diet and Cancer study were used as a replication sample for overall IS (in total 3145 patients and 1793 control subjects). Results— The single nucleotide polymorphism rs380092 in IL1RN showed an association with overall IS in SAHLSIS (OR, 1.21; 95% CI, 1.02–1.43; P =0.03), which was replicated in the Lund Stroke Register and the Malmö Diet and Cancer study sample. An association was also detected in all samples combined (OR, 1.12; 95% CI, 1.04–1.21; P =0.03). Three single nucleotide polymorphisms in IL1RN (including rs380092) were nominally associated with the subtype of cryptogenic stroke in SAHLSIS, but the statistical significance did not remain after correction for multiple testing. Furthermore, increased plasma levels of interleukin-1 receptor antagonist were observed in the subtype of cryptogenic stroke compared with controls. Conclusion— This comprehensive study, based on a tagSNP approach and replication, presents support for the role of IL1RN in overall IS.
Published: 2012
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12. Pharmacogenetic implications for eight common blood pressure-associated single-nucleotide polymorphisms

Author: Olle Melander, Thomas Hedner, Sverre E. Kjeldsen, Björn Wahlstrand, Marketa Sjögren, Viktor Hamrefors, and Peter Almgren
Subjects: Male, medicine.medical_specialty, Physiology, Population, Blood Pressure, Single-nucleotide polymorphism, 030204 cardiovascular system & hematology, Pharmacology, Essential hypertension, Polymorphism, Single Nucleotide, Gastroenterology, 03 medical and health sciences, 0302 clinical medicine, Internal medicine, Internal Medicine, medicine, Humans, Clinical significance, Diltiazem, Allele, education, Antihypertensive Agents, Aged, 030304 developmental biology, Sweden, 0303 health sciences, education.field_of_study, business.industry, Middle Aged, medicine.disease, 3. Good health, Blood pressure, Pharmacogenetics, Hypertension, Female, Cardiology and Cardiovascular Medicine, business, medicine.drug
Abstract: OBJECTIVE:: We aimed to test whether eight common recently identified single-nucleotide polymorphisms (SNPs), strongly associated with blood pressure (BP) in the population, also have impact on the degree of BP reduction by antihypertensive agents with different mechanisms. METHODS:: In 3863 Swedish hypertensive patients, we related number of unfavorable alleles of each SNP (i.e. alleles associated with higher baseline BP) to the magnitude of BP reduction during 6 months of monotherapy with either a beta-blocker, a thiazide diuretic or diltiazem. RESULTS:: For six SNPs (rs16998073, rs1378942, rs3184504, rs1530440, rs16948048, rs17367504) no pharmacogenetic interactions were suggested, whereas two SNPs showed nominal evidence of association with treatment response: PLCD3-rs12946454 associated with more SBP (beta = 1.53 mmHg per unfavorable allele; P = 0.010) and DBP (beta = 0.73 mmHg per unfavorable allele; P = 0.014) reduction in patients treated with diltiazem, in contrast to those treated with beta-blockers or diuretics wherein no treatment response association was found. CYP17A1-rs11191548 associated with less DBP reduction (beta = -1.26 mmHg per unfavorable allele; P = 0.018) in patients treated with beta-blockers or diuretics, whereas there was no treatment response association in diltiazem-treated patients. However, if accounting for multiple testing, the significant associations for rs12946454 and rs11191548 were attenuated. CONCLUSION:: For a majority of these, eight recently identified BP-associated SNPs, there are probably no important pharmacogenetic interactions for BP reduction with use of beta-blockers, diuretics or diltiazem. Whether the nominally significant associations for rs12946454 and rs11191548 are true signals and could be of possible clinical relevance for deciding treatment of polygenic essential hypertension should be further tested. (Less)
Published: 2012
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13. Orthostatic hypotension and novel blood pressure-associated gene variants: Genetics of Postural Hemodynamics (GPH) Consortium

Author: Peter Almgren, Olle Melander, Eric Boerwinkle, Francesco U.S. Mattace-Raso, Kathryn Rose, Kenneth Rice, Artur Fedorowski, Thomas J. Wang, Marketa Sjögren, Jacqueline C.M. Witteman, Martin G. Larson, Jerome I. Rotter, André G. Uitterlinden, Chunyu Liu, Albert Hofman, Germaine C. Verwoert, Bo Hedblad, Christopher Newton-Cheh, David Couper, Daniel Levy, Jennifer Karen Brody, Bruce M. Psaty, Nora Franceschini, Epidemiology, and Internal Medicine
Subjects: Male, Heterozygote, medicine.medical_specialty, Population, Blood Pressure, Single-nucleotide polymorphism, Genome-wide association study, 030204 cardiovascular system & hematology, Polymorphism, Single Nucleotide, Hypotension, Orthostatic, Adrenomedullin, 03 medical and health sciences, Orthostatic vital signs, Steroid 17-alpha-hydroxylase, 0302 clinical medicine, Gene Frequency, Clinical Research, Internal medicine, Genetic model, Genetics, Humans, Medicine, Natriuretic peptides, Allele, education, Antihypertensive Agents, Aged, education.field_of_study, Orthostatic hypotension, business.industry, Homozygote, Odds ratio, Middle Aged, Atherosclerosis, Genetic and protein markers of CVD, Single nucleotide polymorphism, 3. Good health, Blood pressure, Endocrinology, Female, Epidemiologic Methods, Cardiology and Cardiovascular Medicine, business, 030217 neurology & neurosurgery
Abstract: Aims Orthostatic hypotension (OH), an independent predictor of mortality and cardiovascular events, strongly correlates with hypertension. Recent genome-wide studies have identified new loci influencing blood pressure (BP) in populations, but their impact on OH remains unknown. Methods and results A total of 38 970 men and women of European ancestry from five population-based cohorts were included, of whom 2656 (6.8%) met the diagnostic criteria for OH (systolic/diastolic BP drop ≥20/10 mmHg within 3 min of standing). Thirty-one recently discovered BP-associated single nucleotide polymorphisms (SNPs) were examined using an additive genetic model and the major allele as referent. Relations between OH, orthostatic systolic BP response, and genetic variants were assessed by inverse variance-weighted meta-analysis. We found Bonferroni adjusted ( P < 0.0016) significant evidence for association between OH and the EBF1 locus (rs11953630, per-minor-allele odds ratio, 95% confidence interval: 0.90, 0.85–0.96; P = 0.001), and nominal evidence ( P < 0.05) for CYP17A1 (rs11191548: 0.85, 0.75–0.95; P = 0.005), and NPR3- C5orf23 (rs1173771: 0.92, 0.87–0.98; P = 0.009) loci. Among subjects not taking BP-lowering drugs, three SNPs within the NPPA/NPPB locus were nominally associated with increased risk of OH (rs17367504: 1.13, 1.02–1.24; P = 0.02, rs198358: 1.10, 1.01–1.20; P = 0.04, and rs5068: 1.22, 1.04–1.43; P = 0.01). Moreover, an ADM variant was nominally associated with continuous orthostatic systolic BP response in the adjusted model ( P = 0.04). Conclusion The overall association between common gene variants in BP loci and OH was generally weak and the direction of effect inconsistent with resting BP findings. These results suggest that OH and resting BP share few genetic components.
Published: 2012
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14. A large-sample assessment of possible association between ischaemic stroke and rs12188950 in the PDE4D gene

Author: Christina Jern, Ulf Kristoffersson, Arne Lindgren, Holger Luthman, Katarina Jood, Bo Hedblad, Gunnar Andsberg, Peter Höglund, Marketa Sjögren, Bo Norrving, Gunnar Engström, J. Gustav Smith, Sandra Olsson, Olle Melander, Håkan Lövkvist, and Hossein Delavaran
Subjects: Adult, Male, medicine.medical_specialty, Adolescent, Genotyping Techniques, Single-nucleotide polymorphism, Context (language use), Coronary Artery Disease, Polymorphism, Single Nucleotide, Article, Young Adult, Ischemia, Risk Factors, Internal medicine, Diabetes Mellitus, Odds Ratio, Genetics, medicine, Humans, Genetic Predisposition to Disease, Genetic Testing, Prospective Studies, Young adult, Prospective cohort study, Stroke, Alleles, Genetics (clinical), Aged, Aged, 80 and over, Sweden, business.industry, Smoking, Case-control study, Odds ratio, Middle Aged, medicine.disease, Cyclic Nucleotide Phosphodiesterases, Type 3, Confidence interval, Cyclic Nucleotide Phosphodiesterases, Type 4, Phenotype, Case-Control Studies, Hypertension, Female, business
Abstract: Previous reports have shown ambiguous findings regarding the possible associations between ischaemic stroke (IS) and single nucleotide polymorphisms (SNPs) in the phosphodiesterase 4D (PDE4D) gene region. The SNP rs12188950 (or SNP45) has often been studied in this context. We performed a multi-centre study involving a large sample of 2599 IS patients and 2093 control subjects from the south and west regions of Sweden to replicate previous studies regarding IS risk and rs12188950. Subjects from Lund Stroke Register (LSR), Malmö Diet and Cancer Study (MDC) and Sahlgrenska Academy Study on Ischemic Stroke (SAHLSIS) were enroled. Subgroups of participants with hypertension and participants
Published: 2012
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15. A myocardial infarction genetic risk score is associated with markers of carotid atherosclerosis

Author: Viktor Hamrefors, Peter Almgren, Bo Hedblad, Gunnar Engström, Marketa Sjögren, and Olle Melander
Subjects: 0303 health sciences, medicine.medical_specialty, Framingham Risk Score, business.industry, Single-nucleotide polymorphism, Odds ratio, 030204 cardiovascular system & hematology, medicine.disease, Coronary artery disease, 03 medical and health sciences, 0302 clinical medicine, Blood pressure, medicine.artery, Internal medicine, cardiovascular system, Internal Medicine, medicine, Cardiology, Population study, cardiovascular diseases, Common carotid artery, Myocardial infarction, business, 030304 developmental biology
Abstract: Objective: To assess whether a genetic risk score that was previously shown to be associated with myocardial infarction and coronary artery disease is also associated with markers of carotid atherosclerosis. Design: A total of 4022 middle-aged subjects from the general Swedish population were genotyped and individually assigned a genetic risk score based on 13 single-nucleotide polymorphisms (SNPs), previously associated with myocardial infarction and coronary artery disease. The genetic score (Score-MI) was then related to carotid bulb intima-media thickness (IMT), common carotid artery IMT and to the occurrence of carotid plaques in the study population. Results: Score-MI was associated with IMT of the bulb (P
Published: 2011
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16. Serine/threonine kinase 39 is a candidate gene for primary hypertension especially in women: results from two cohort studies in Swedes

Author: Bo Hedblad, Gunnar Engström, Elisa Danese, Marketa Sjögren, Cristiano Fava, Olle Melander, Martina Montagnana, Peter Almgren, Pietro Minuz, Gian C Guidi, and Peter Nilsson
Subjects: Male, medicine.medical_specialty, Candidate gene, hypertension, Genotype, Physiology, Single-nucleotide polymorphism, Protein Serine-Threonine Kinases, Polymorphism, Single Nucleotide, Gastroenterology, Cohort Studies, Ste20-related proline-alanine-rich kinase, Polymorphism (computer science), Internal medicine, Internal Medicine, medicine, Humans, genetics, Aged, Sweden, Sex Characteristics, business.industry, Incidence (epidemiology), Estrogen Replacement Therapy, blood pressure, Odds ratio, Middle Aged, Endocrinology, Blood pressure, serine/threonine kinase 39, Cohort, Female, Menopause, Cardiology and Cardiovascular Medicine, business, Genome-Wide Association Study, Cohort study
Abstract: BACKGROUND: As recently pinpointed by a genome-wide association study the serine/threonine kinase 39 (STK39) is a candidate gene for hypertension. This kinase is strongly implicated in sodium reabsorption by the kidney through its modulating effect on furosemide-sensitive and thiazide-sensitive channels. The aim of our study was to test the effects of the STK39 rs35929607A>G polymorphism on blood pressure (BP) levels and the prevalence and incidence of hypertension in middle-aged Swedes participating in two urban-based surveys in Malmo (Sweden). METHODS: The rs35929607A>G polymorphism was genotyped in 5634 participants included in the cardiovascular cohort of the 'Malmo Diet and Cancer-cardiovascular arm' (MDC-CVA) study and successively in 17 894 participants of the 'Malmo Preventive Project' (MPP) both at baseline and at reinvestigation after a mean of 23 years. The effect of the same single nucleotide polymorphism on salt sensitivity was tested in 39 participants of the Salt Reduction to Avoid Hypertension study. RESULTS: Both before and after adjustment for covariates, the functional rs35929607A>G polymorphism was associated with higher SBP and DBP values in the MDC-CVA, but not in the MPP. In both surveys, the polymorphism was associated with hypertension prevalence; after adjustment using the autosomal-dominant model, the odds ratio for hypertension ranged between 1.077 (MPP at baseline) and 1.151 (MDC-CVA) with P-value less than 0.05. After stratification for sex, the results remained statistically significant in women, but not in men. Carriers of the G-allele displayed an increase in salt sensitivity. CONCLUSION: Our results from two large cohort studies support previous evidence about the association of the STK39 rs35929607A>G variant with hypertension, especially in women. If further confirmed in successive studies, owing to its pivotal role in sodium reabsorption at the renal tubule level, STK39 might prove to be a suitable target for antihypertensive therapy. The greater effect of the STK39 rs35929607A>G polymorphism in women with respect to men deserves further investigation. (Less)
Published: 2011
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17. A17553 High BMI increases hospitalization burden and mortality

Author: Peter Almgren, Olle Melander, and Marketa Sjögren
Subjects: medicine.medical_specialty, Physiology, business.industry, Emergency medicine, Internal Medicine, Medicine, Cardiology and Cardiovascular Medicine, business
Published: 2018
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18. Genetic prediction of the metabolic syndrome

Author: Valeriya Lyssenko, B Isomaa, Marju Orho-Melander, Tiinamaija Tuomi, Peter Almgren, Marketa Sjögren, Dragi Anevski, Marja-Riitta Taskinen, Leif Groop, and Publica
Subjects: Peroxisome proliferator-activated receptor gamma, medicine.medical_specialty, Adiponectin, business.industry, Endocrinology, Diabetes and Metabolism, nutritional and metabolic diseases, General Medicine, Type 2 diabetes, medicine.disease, Endocrinology, Diabetes mellitus, Internal medicine, Internal Medicine, Medicine, SNP, PPARGC1A, Metabolic syndrome, business, Prospective cohort study
Abstract: Background: The metabolic syndrome (MetS) is a constellation of factors associated with increased risk of cardiovascular disease (CVD) and type 2 diabetes (T2D). It has been difficult to identify an underlying unifying pathogenic mechanism for the different components. As the syndrome shows high heritability one way to search for such common mechanisms could to be to try to identify genetic variants contributing to MetS. Methods: In total 1937 of 2293 non-diabetic individuals participating in the Botnia prospective study were free of MetS at baseline (M/F: 873/1064; age 44 ± 14 years; BMI 25 ± 4 kg/m2; 25% had IFG or IGT or both). Variants in the peroxisome proliferator-activated receptor gamma (PPARG P12A), 1-, 2- and 3-adrenergic receptor (ADRB1 G389R; ADRB2 Q27E; ADRB3 W64R), adiponectin (APM1 SNP -11,377 C > G, 276 G > T, I2019D), and PPARG co-activator-1 alpha (PPARGC1A G482S) genes were studied for their ability to predict MetS defined using the NCEP ATPIII criteria. We also repeated the analyses using the WHO and IDF criteria for defining MetS. Results: During a median 6-year follow-up, 267 (13.8%) persons developed MetS. The PPARG (PP) (HR 1.49 [1.10-3.01], P = 0.011) and the ADRB1 G389R (GG/GR) (1.43 [1.14-1.80], P = 0.0022) predicted future MetS. ADRB1 G389R and ADRB3 W64R variants showed an interaction effect, implying that the MetS risk was further increased if an individual carried both GG/GR and RR/WR genotypes (2.02 [1.34-3.05], P < 0.001). Among the individual MetS components, the PP (PPARG) and GG/GR (ADRB1) genotypes were associated with increase in triglycerides (coefficient 0.016 and 0.0162, P < 0.05; respectively). In addition, the GG/GR genotypes (coefficient 0.013, P = 0.036) were also associated with increase in fasting glucose concentrations over time. Variants in the ADRB2, APM1 and PPARGC1A genes did not influence risk of future MetS. Conclusion: We demonstrate in a prospective study that variants in the PPARG and ADRB1 gene.
Published: 2008
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19. Genetic vasopressin 1b receptor variance in overweight and diabetes mellitus

Author: Peter M. Nilsson, Bo Hedblad, Sofia Enhörning, Olle Melander, Joachim Struck, and Marketa Sjögren
Subjects: Male, medicine.medical_specialty, Receptors, Vasopressin, endocrine system, Genotype, Endocrinology, Diabetes and Metabolism, Population, 030209 endocrinology & metabolism, Single-nucleotide polymorphism, 030204 cardiovascular system & hematology, Overweight, Endocrinology and Diabetes, Polymorphism, Single Nucleotide, Body Mass Index, Cohort Studies, 03 medical and health sciences, 0302 clinical medicine, Endocrinology, Copeptin, Internal medicine, medicine, Diabetes Mellitus, Humans, Obesity, Prospective Studies, Prospective cohort study, education, Abdominal obesity, Aged, Sweden, education.field_of_study, business.industry, urogenital system, Glycopeptides, Genetic Variation, General Medicine, Middle Aged, 3. Good health, nervous system, Obesity, Abdominal, Cohort, Clinical Study, Female, medicine.symptom, business, hormones, hormone substitutes, and hormone antagonists, Cohort study
Abstract: ObjectiveRecently, imbalance in the vasopressin (AVP) system, measured as elevated levels of copeptin (the C-terminal part of the AVP pro-hormone) in plasma, was linked to the development of abdominal obesity and diabetes mellitus (DM). Here, we aim to investigate if the genetic variation of the human AVP receptor 1b gene (AVPR1B) is associated with measures of obesity and DM.DesignMalmö Diet and Cancer study (MDC) is a population-based prospective cohort examined 1991–1996.MethodsFour tag single nucleotide polymorphisms (SNPs: rs35810727, rs28373064, rs35439639, rs35608965) of AVPR1B were genotyped in the cardiovascular cohort (n=6103) of MDC (MDC-CC) and associated with measures of obesity and DM. Significant SNPs were replicated in another 24 344 MDC individuals (MDC replication cohort).ResultsIn MDC-CC, the major allele of rs35810727 was associated with elevated BMI (β-coefficient±s.e.m.; 0.30±0.14, P=0.03) and waist (0.78±0.36, P=0.03) after age and gender adjustment. The association with BMI was replicated in the MDC replication cohort (0.21±0.07, P=0.003), whereas that with waist was not significant. In MDC-CC there was no association between the major allele of rs35810727 and DM, but in the complete MDC cohort (n=30 447) the major allele of rs35810727 was associated with DM (OR (95% CI); 1.10 (1.00–1.20), P=0.04).ConclusionsGenetic variance of AVPR1B contributes to overweight. Furthermore, our data indicate a link between AVPR1B variance and DM development. Our data point at a relationship between the disturbance of the pharmacologically modifiable AVP system and the body weight regulation.
Published: 2016

20. [PP.07.09] GENETIC RISK SCORE AND CARDIOVASCULAR COMPLICATIONS IN PATIENTS WITH HYPERTENSION

Author: Michal Hoffmann, Marketa Sjögren, Wojciech Sobiczewski, Marcin Wirtwein, Marcin Gruchała, Olle Melander, and K. Narkiewicz
Subjects: medicine.medical_specialty, Physiology, business.industry, Internal medicine, Internal Medicine, Medicine, In patient, Genetic risk, Cardiology and Cardiovascular Medicine, business
Published: 2016
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21. [OP.2A.08] RELATIONSHIP BETWEEN SELECTED DNA POLYMORPHISMS AND CORONARY ARTERY DISEASE COMPLICATIONS

Author: Marcin Wirtwein, Wojciech Sobiczewski, Olle Melander, Marcin Gruchała, Marketa Sjögren, and K. Narkiewicz
Subjects: medicine.medical_specialty, Physiology, business.industry, Dna polymorphism, 030204 cardiovascular system & hematology, medicine.disease, Coronary artery disease, 03 medical and health sciences, 0302 clinical medicine, Internal medicine, Internal Medicine, Cardiology, medicine, 030212 general & internal medicine, Cardiology and Cardiovascular Medicine, business
Published: 2017
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22. Cardiovascular consequences of a polygenetic component of blood pressure in an urban-based longitudinal study: the Malmö diet and cancer

Author: Bo Hedblad, Peter Almgren, Peter M. Nilsson, Pietro Minuz, Angela Tagetti, Therese Ohlsson, Cristiano Fava, Olle Melander, Gunnar Engström, and Marketa Sjögren
Subjects: Adult, Male, Longitudinal study, medicine.medical_specialty, Urban Population, Physiology, Population, Single-nucleotide polymorphism, Genome-wide association study, Blood Pressure, Disease, Kaplan-Meier Estimate, 030204 cardiovascular system & hematology, Polymorphism, Single Nucleotide, Cohort Studies, 03 medical and health sciences, 0302 clinical medicine, Diet and cancer, Genetic, cardiovascular mortality, Risk Factors, Internal medicine, Neoplasms, Internal Medicine, medicine, Humans, Genetic Predisposition to Disease, Longitudinal Studies, Genetic risk, Polymorphism, education, 030304 developmental biology, Aged, Genetics, Sweden, 0303 health sciences, education.field_of_study, business.industry, Incidence, Middle Aged, Cardiovascular disease, 3. Good health, Diet, Blood pressure, Cardiovascular Diseases, Genetic, Polymorphism, blood pressure, Female, Cardiology and Cardiovascular Medicine, business
Abstract: A recently published genome wide association study identified 29 single nucleotide polymorphisms (SNPs) influencing blood pressure (BP). Case-control studies suggest that a genetic risk score (GRS) based on these 29 SNPs affect the risk of cardiovascular disease (CVD), but its role for CVD at population level is unknown. Here, we prospectively evaluate the impact of this polygenetic BP component on CVD morbidity and mortality in a large urban-based middle-aged population.The 29 previously BP associated SNPs were genotyped in the Swedish Malmö Diet and Cancer Study; (n = 27,003 with at least 24 valid SNPs). The number of BP elevating alleles of each SNPs, weighted by their effect size in the discovery studies, was summed into a BP-GRS.Using regression models, we found significant associations of the BP-GRS, cross-sectionally, with BP and hypertension prevalence, prospectively, with incident cardiovascular morbidity and mortality during 14.2 ± 3.2 years of follow-up. After adjustment for traditional cardiovascular risk factors (TRF), including hypertension, the BP-GRS remained significantly associated only with CVDs [in terms of strokes and coronary artery disease; hazard ratio 1.15; 95% confidence interval (CI) 1.06-1.24 comparing the third vs. first tertile; P = 0.003]. Calibration, discrimination and reclassification analyses did not show a meaningful increment in prediction using the BP-GRS in addition to the model encompassing only the TRF.The polygenetic component of BP influences risk of cardiovascular morbidity and mortality. However, the effect size is small and unlikely to be useful for prediction at the population level.
Published: 2014

23. A MULTI-LOCUS GENETIC RISK SCORE IS ASSOCIATED WITH INCIDENT ATRIAL FIBRILLATION AND ISCHEMIC STROKE AMONG 27,471 PARTICIPANTS FROM A PROSPECTIVE COHORT STUDY

Author: Sekar Kathiresan, J. Gustav Smith, Marketa Sjögren, Joseph J. Catanese, Gunnar Engström, James J. Devlin, Dov Shiffman, Judy Z. Louie, and Olle Melander
Subjects: medicine.medical_specialty, business.industry, Atrial fibrillation, Retrospective cohort study, Locus (genetics), medicine.disease, Internal medicine, Ischemic stroke, Cardiology, Medicine, Genetic risk, business, Prospective cohort study, Cardiology and Cardiovascular Medicine
Published: 2014
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24. Smoking modifies the associated increased risk of future cardiovascular disease by genetic variation on chromosome 9p21

Author: George Hindy, Viktor Hamrefors, Peter Almgren, Marju Orho-Melander, Marketa Sjögren, Olle Melander, Gunnar Engström, J. Gustav Smith, Bo Hedblad, and Klas Gränsbo
Subjects: Male, Epidemiology, Myocardial Infarction, Disease, Coronary Artery Disease, 030204 cardiovascular system & hematology, Cardiovascular, 0302 clinical medicine, Gene Frequency, Risk Factors, Surveys and Questionnaires, Genotype, Medicine, Cardiac and Cardiovascular Systems, Prospective Studies, Registries, Genetics, 0303 health sciences, Multidisciplinary, Incidence, Smoking, Middle Aged, 3. Good health, Survival Rate, Stroke, Cardiovascular Diseases, Genetic Epidemiology, Educational Status, Female, Public Health, Chromosomes, Human, Pair 9, Environmental Health, Research Article, Tobacco Control, Science, Single-nucleotide polymorphism, Endocrinology and Diabetes, Polymorphism, Single Nucleotide, Environmental Epidemiology, 03 medical and health sciences, Chromosome (genetic algorithm), Genetic variation, Genetic predisposition, Humans, Genetic Predisposition to Disease, cardiovascular diseases, Allele frequency, Biology, Cardiovascular Disease Epidemiology, 030304 developmental biology, Aged, Proportional Hazards Models, Lifecourse Epidemiology, Sweden, business.industry, Proportional hazards model, Acute Cardiovascular Problems, Genetics of Disease, Genetic Polymorphism, business, Population Genetics
Abstract: AimsGenetic predisposition for cardiovascular disease (CVD) is likely to be modified by environmental exposures. We tested if the associated risk of CVD and CVD-mortality by the single nucleotide polymorphism rs4977574 on chromosome 9p21 is modified by life-style factors.Methods and resultsA total of 24,944 middle-aged subjects (62% females) from the population-based Malmö-Diet-and-Cancer-Cohort were genotyped. Smoking, education and physical activity-levels were recorded. Subjects were followed for 15 years for incidence of coronary artery disease (CAD; N = 2309), ischemic stroke (N = 1253) and CVD-mortality (N = 1156). Multiplicative interactions between rs4977574 and life-style factors on endpoints were tested in Cox-regression-models. We observed an interaction between rs4977574 and smoking on incident CAD (P = 0.035) and CVD-mortality (P = 0.012). The hazard ratios (HR) per risk allele of rs4977574 were highest in never smokers (N = 9642) for CAD (HR = 1.26; 95% CI 1.13-1.40; PConclusionSmoking may modify the associated risk of CAD and CVD-mortality conferred by genetic variation on chromosome 9p21. Whether the observed attenuation of the genetic risk reflects a pathophysiological mechanism or is a result of smoking being such a strong risk-factor that it may eliminate the associated genetic effect, requires further investigation.
Published: 2014

25. A genetic risk score for hypertension associates with the risk of ischemic stroke in a Swedish case-control study

Author: Arne Lindgren, Cristiano Fava, Katarina Jood, Bo Hedblad, Christina Jern, Håkan Lövkvist, Sandra Olsson, Gunnar Engström, Olle Melander, Bo Norrving, and Marketa Sjögren
Subjects: Male, medicine.medical_specialty, Genetic risk score, stroke, hypertension, Genotype, Genome-wide association study, Bioinformatics, Polymorphism, Single Nucleotide, Article, Brain Ischemia, Diet and cancer, Gene Frequency, Risk Factors, Diabetes mellitus, Internal medicine, Genetics, medicine, Humans, Genetic Predisposition to Disease, Prospective Studies, Registries, Prospective cohort study, Stroke, Genetics (clinical), Aged, Proportional Hazards Models, Aged, 80 and over, Sweden, business.industry, Proportional hazards model, Case-control study, Middle Aged, medicine.disease, Blood pressure, Case-Control Studies, Hypertension, Female, business, Genome-Wide Association Study
Abstract: Genetic risk scores (GRS), summing up the total effect of several single-nucleotide polymorphisms (SNPs) in genes associated with either coronary risk or cardiovascular risk factors, have been tested for association with ischemic stroke with conflicting results. Recently an association was found between a GRS based on 29 SNPs discovered by genome-wide association studies and hypertension. The aim of our study was to investigate the possible association of the same GRS with ischemic stroke on top of other 'traditional risk factors', also testing its potential improvement in indices of discrimination and reclassification, in a Swedish case-control study. Twenty-nine SNPs were genotyped in 3677 stroke cases and 2415 controls included in the Lund Stroke Register (LSR), the Malmo Diet and Cancer (MDC) study and the Sahlgrenska Academy Study on Ischemic Stroke (SAHLSIS). The analysis was conducted in the combined sample, and separately for the three studies. After adjustment for hypertension, diabetes mellitus and smoking habits, the GRS was associated with ischemic stroke in the combined sample (OR (95% CI) 1.086 (1.029-1.147) per SD increase in the GRS P=0.003) with similar trends in all three samples: LSR (1.050 (0.967-1.140); P=0.25), MDC (1.168 (1.060-1.288); P=0.002) and SAHLSIS (1.124 (0.997-1.267); P=0.055). Measures of risk discrimination and reclassification improved marginally using the GRS. A blood pressure GRS is independently associated with ischemic stroke risk in three Swedish case-control studies, however, the effect size is low and adds marginally to prediction of stroke on top of traditional risk factors including hypertension.
Published: 2014

26. Ceruloplasmin and atrial fibrillation: evidence of causality from a population-based Mendelian randomization study

Author: Peter M. Nilsson, Bo Hedblad, S. Adamsson Eryd, Gunnar Engström, Olle Melander, Marketa Sjögren, and J. G. Smith
Subjects: Adult, Male, medicine.medical_specialty, Bioinformatics, Polymorphism, Single Nucleotide, Cohort Studies, Gene Frequency, Internal medicine, Mendelian randomization, Epidemiology, Atrial Fibrillation, Internal Medicine, medicine, Odds Ratio, Humans, Promoter Regions, Genetic, Sweden, biology, business.industry, Incidence (epidemiology), Incidence, Ceruloplasmin, Atrial fibrillation, Mendelian Randomization Analysis, Middle Aged, medicine.disease, Endocrinology, biology.protein, Biomarker (medicine), Gene polymorphism, business, Biomarkers, Cohort study, Follow-Up Studies
Abstract: Inflammatory diseases and inflammatory markers secreted by the liver, including C-reactive protein (CRP) and ceruloplasmin, have been associated with incident atrial fibrillation (AF). Genetic studies have not supported a causal relationship between CRP and AF, but the relationship between ceruloplasmin and AF has not been studied. The purpose of this Mendelian randomization study was to explore whether genetic polymorphisms in the gene encoding ceruloplasmin are associated with elevated ceruloplasmin levels, and whether such genetic polymorphisms are also associated with the incidence of AF.Genetic polymorphisms in the ceruloplasmin gene (CP) were genotyped in a population-based cohort study of men from southern Sweden (Malmö Preventive Project; n = 3900). Genetic polymorphisms associated with plasma ceruloplasmin concentration were also investigated for association with incident AF (n = 520) during a mean follow-up of 29 years in the same cohort. Findings were replicated in an independent case-control sample (The Malmö AF cohort; n = 2247 cases, 2208 controls).A single nucleotide polymorphism (rs11708215, minor allele frequency 0.12) located in the CP gene promoter was strongly associated with increased levels of plasma ceruloplasmin (P = 9 × 10(-10) ) and with AF in both the discovery cohort [hazard ratio 1.24 per risk allele, 95% confidence interval (CI) 1.06-1.44, P = 0.006] and the replication cohort (odds ratio 1.13, 95% CI 1.02-1.26, P = 0.02).Our findings indicate a causal role of ceruloplasmin in AF pathophysiology and suggest that ceruloplasmin might be a mediator in a specific inflammatory pathway that causally links inflammatory diseases and incidence of AF.
Published: 2013

27. Smoking and obesity associated BDNF gene variance predicts total and cardiovascular mortality in smokers

Author: Gunnar Engström, Marketa Sjögren, Sara Halldén, Björn Wahlstrand, Olle Melander, Michal Hoffmann, Krzysztof Narkiewicz, Thomas Hedner, and Bo Hedblad
Subjects: Male, Time Factors, medicine.medical_treatment, Smoking Prevention, 030204 cardiovascular system & hematology, Body Mass Index, 0302 clinical medicine, Diet and cancer, Gene Frequency, Risk Factors, Epidemiology, Odds Ratio, Cardiac and Cardiovascular Systems, Prospective Studies, Prospective cohort study, 2. Zero hunger, Incidence, Smoking, Age Factors, Middle Aged, 3. Good health, Phenotype, Cardiovascular Diseases, Female, Cardiology and Cardiovascular Medicine, medicine.medical_specialty, Polymorphism, Single Nucleotide, Risk Assessment, 03 medical and health sciences, Sex Factors, Internal medicine, medicine, Humans, Genetic Predisposition to Disease, Obesity, Psychiatry, Aged, Proportional Hazards Models, Sweden, Proportional hazards model, business.industry, Brain-Derived Neurotrophic Factor, Odds ratio, medicine.disease, Multivariate Analysis, Smoking cessation, Smoking Cessation, business, Body mass index, Risk Reduction Behavior, 030217 neurology & neurosurgery
Abstract: OBJECTIVE: The brain derived neurotrophic factor (BDNF) locus has been implicated in psychiatric and substance related disorders. Recent genome-wide association studies (GWAS) have shown strong associations between single nucleotide polymorphisms in BDNF, smoking behaviour and high body mass index (BMI). Our aim was to test whether genetic BDNF variation alters the risk of smoking related morbidity and mortality. DESIGN: Cox proportional hazards models were used to relate the BDNF rs4923461(A/G) polymorphisms to all-cause, cancer and cardiovascular mortality and cardiovascular disease (CVD) incidence adjusted for age, sex, BMI, and smoking quantity. SETTING: The Malmö Diet and Cancer Study (MDCS), a population based prospective cohort study (n=30 447). PATIENTS: We obtained complete data on 25 071 subjects, of whom 6507 were current smokers and 18 564 were non-smokers who underwent a baseline examination from 1991-1996. MAIN OUTCOME MEASURES: During a mean follow-up time of 12 years, 1049 deaths (346 cardiovascular deaths and 492 cancer deaths) and 802 incident CVD events occurred among current smokers. RESULTS: The major allele (A) of rs4923461 was significantly associated with ever having smoked (p=0.03) and high BMI (p=0.001). The A-allele was associated with risk of all-cause (HR=1.12, 95% CI 1.00 to 1.25; p
Published: 2013

28. Chromosome 9p21 genetic variation explains 13% of cardiovascular disease incidence but does not improve risk prediction

Author: Bo Hedblad, Olle Melander, Marketa Sjögren, Gunnar Engström, Klas Gränsbo, Peter Almgren, and J. G. Smith
Subjects: Male, Genotype, 030204 cardiovascular system & hematology, Logistic regression, Polymorphism, Single Nucleotide, Risk Assessment, 03 medical and health sciences, 0302 clinical medicine, Risk Factors, Genetic variation, Internal Medicine, Medicine, Humans, Prospective Studies, Alleles, 030304 developmental biology, Proportional Hazards Models, Genetics, 0303 health sciences, business.industry, Incidence (epidemiology), Incidence, Hazard ratio, Genetic Variation, Middle Aged, Confidence interval, 3. Good health, Logistic Models, Quartile, Cardiovascular Diseases, Attributable risk, Population study, Female, business, Chromosomes, Human, Pair 9, Demography
Abstract: OBJECTIVES: To evaluate the proportion of cardiovascular disease (CVD) incidence that is explained by genetic variation at chromosome 9p21 and to test whether such variation adds incremental information with regard to CVD prediction, beyond traditional risk factors. DESIGN, SETTING AND PARTICIPANTS: rs4977574 on chromosome 9p21 was genotyped in 24 777 subjects from the Malmo Diet and Cancer study who were free from CVD prior to the baseline examination. Association between genotype and incident CVD (n = 2668) during a median follow-up of 11.7 years was evaluated in multivariate Cox proportional hazard models. Analyses were performed in quartiles of baseline age, and linear trends in effect size across age groups were estimated in logistic regression models. RESULTS: In additive models, chromosome 9p21 significantly predicted CVD in the entire population (hazard ratio 1.17 per G allele, 95% confidence interval 1.11-1.23, P < 0.001). Effect estimates increased from the highest (Q4) to the lowest quartile (Q1) of baseline age, but this trend was not significant. The overall population attributable risk conferred by chromosome 9p21 in fully adjusted models was 13%, ranging from 17% in Q1 to 11% in Q4. Addition of chromosome 9p21 to traditional risk factors only marginally improved predictive accuracy. CONCLUSION: The high population attributable risk conferred by chromosome 9p21 suggests that future interventions interfering with downstream mechanisms of the genetic variation may affect CVD incidence over a broad range of ages. However, variation of chromosome 9p21 alone does not add clinically meaningful information in terms of CVD prediction beyond traditional risk factors at any age. (Less)
Published: 2013

29. Genetic associations with valvular calcification and aortic stenosis

Author: Marketa Sjögren, Albert V. Smith, Gina M. Peloso, David S. Owens, Sigurdur Sigurdsson, Kathleen F. Kerr, Vilmundur Gudnason, Markus M. Nöthen, Rajeev Malhotra, Hagen Kälsch, Sonali Pechlivanis, Raimund Erbel, Emanuele Di Angelantonio, Sekar Kathiresan, Quenna Wong, Jesper van der Pals, George Thanassoulis, J. Gustav Smith, Tamara B. Harris, Matthew A. Allison, Michael H. Criqui, Thor Aspelund, Christopher J. O'Donnell, John Danesh, Yongmei Liu, Susan R. Heckbert, Olle Melander, Shih-Jen Hwang, Matthew J. Budoff, L. Adrienne Cupples, Wendy S. Post, Anne Tybjærg-Hansen, Kevin D. O'Brien, Pia R. Kamstrup, Catherine Y. Campbell, Børge G. Nordestgaard, Thomas W. Mühleisen, Jerome I. Rotter, and Muriel J. Caslake
Subjects: Male, diagnostic imaging [Aortic Valve], genetics [Calcinosis], Heart Valve Diseases, Medizin, Genome-wide association study, 030204 cardiovascular system & hematology, ethnology [Heart Valve Diseases], ethnology [Aortic Valve Stenosis], genetics [Aortic Valve Stenosis], 0302 clinical medicine, Epidemiology, diagnostic imaging [Mitral Valve], 0303 health sciences, education.field_of_study, Calcinosis, General Medicine, Middle Aged, 3. Good health, Aortic Valve, cardiovascular system, Cardiology, Population study, Mitral Valve, Female, medicine.medical_specialty, Population, pathology [Mitral Valve], Polymorphism, Single Nucleotide, Article, 03 medical and health sciences, genetics [Lipoprotein(a)], Internal medicine, medicine, diagnostic imaging [Aortic Valve Stenosis], Humans, ddc:610, education, 030304 developmental biology, Aged, business.industry, Calcific aortic valve stenosis, pathology [Aortic Valve], Odds ratio, Aortic Valve Stenosis, Mendelian Randomization Analysis, diagnostic imaging [Heart Valve Diseases], medicine.disease, Stenosis, Linear Models, genetics [Heart Valve Diseases], business, Tomography, X-Ray Computed, Calcification, Genome-Wide Association Study, Lipoprotein(a)
Abstract: Limited information is available regarding genetic contributions to valvular calcification, which is an important precursor of clinical valve disease.We determined genomewide associations with the presence of aortic-valve calcification (among 6942 participants) and mitral annular calcification (among 3795 participants), as detected by computed tomographic (CT) scanning; the study population for this analysis included persons of white European ancestry from three cohorts participating in the Cohorts for Heart and Aging Research in Genomic Epidemiology consortium (discovery population). Findings were replicated in independent cohorts of persons with either CT-detected valvular calcification or clinical aortic stenosis.One SNP in the lipoprotein(a) (LPA) locus (rs10455872) reached genomewide significance for the presence of aortic-valve calcification (odds ratio per allele, 2.05; P=9.0×10(-10)), a finding that was replicated in additional white European, African-American, and Hispanic-American cohorts (P0.05 for all comparisons). Genetically determined Lp(a) levels, as predicted by LPA genotype, were also associated with aortic-valve calcification, supporting a causal role for Lp(a). In prospective analyses, LPA genotype was associated with incident aortic stenosis (hazard ratio per allele, 1.68; 95% confidence interval [CI], 1.32 to 2.15) and aortic-valve replacement (hazard ratio, 1.54; 95% CI, 1.05 to 2.27) in a large Swedish cohort; the association with incident aortic stenosis was also replicated in an independent Danish cohort. Two SNPs (rs17659543 and rs13415097) near the proinflammatory gene IL1F9 achieved genomewide significance for mitral annular calcification (P=1.5×10(-8) and P=1.8×10(-8), respectively), but the findings were not replicated consistently.Genetic variation in the LPA locus, mediated by Lp(a) levels, is associated with aortic-valve calcification across multiple ethnic groups and with incident clinical aortic stenosis. (Funded by the National Heart, Lung, and Blood Institute and others.).
Published: 2013
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30. ISH NIA PS 03-06 Genetic risk score determines cardiovascular complications in patients with stable coronary artery disease

Author: Michal Hoffmann, Krzysztof Narkiewicz, Olle Melander, Marcin Wirtwein, Wojciech Sobiczewski, Marketa Sjögren, and Marcin Gruchała
Subjects: medicine.medical_specialty, Physiology, business.industry, medicine.disease, Coronary artery disease, Internal medicine, Internal Medicine, Cardiology, Medicine, In patient, Medical emergency, Genetic risk, Cardiology and Cardiovascular Medicine, business
Published: 2016
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31. [PP.07.02] AMBULATORY SYSTOLIC-DIASTOLIC PRESSURE REGRESSION INDEX IS GENETICALLY DETERMINED IN HYPERTENSIVE PATIENTS WITH CORONARY HEART DISEASE

Author: Marcin Gruchała, Marketa Sjögren, K. Narkiewicz, Olle Melander, Michal Hoffmann, and Marcin Wirtwein
Subjects: medicine.medical_specialty, Index (economics), Blood pressure, Physiology, business.industry, Internal medicine, Ambulatory, Internal Medicine, medicine, Cardiology, Cardiology and Cardiovascular Medicine, business, Coronary heart disease
Published: 2016
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32. [PS 03-25] ELEVATED AMBULATORY SYSTOLIC-DIASTOLIC PRESSURE REGRESSION INDEX IS GENETICALLY DETERMINED IN PATIENTS WITH CORONARY HEART DISEASE

Author: Michal Hoffmann, Marcin Wirtwein, Wojciech Sobiczewski, Krzysztof Narkiewicz, Marcin Gruchała, Olle Melander, and Marketa Sjögren
Subjects: medicine.medical_specialty, Index (economics), Physiology, business.industry, Coronary heart disease, Regression, Blood pressure, Internal medicine, Ambulatory, Internal Medicine, medicine, Cardiology, In patient, Cardiology and Cardiovascular Medicine, business
Published: 2016
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33. [PP.07.03] GENETIC RISK SCORE AND DIPPING PROFILE IN HYPERTENSIVE PATIENTS WITH CORONARY HEART DISEASE

Author: Olle Melander, Michal Hoffmann, Marcin Wirtwein, Wojciech Sobiczewski, K. Narkiewicz, Marcin Gruchała, and Marketa Sjögren
Subjects: medicine.medical_specialty, Framingham Risk Score, Physiology, business.industry, Internal medicine, Internal Medicine, medicine, Cardiology, Genetic risk, Cardiology and Cardiovascular Medicine, business, Coronary heart disease
Published: 2016
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34. OS 30-05 GENETIC RISK SCORE DETERMINES DIPPING PROFILE IN PATIENTS WITH CORONARY HEART DISEASE

Author: Marcin Gruchała, Marketa Sjögren, Michal Hoffmann, Olle Melander, Wojciech Sobiczewski, and Marcin Wirtwein
Subjects: medicine.medical_specialty, Framingham Risk Score, Physiology, business.industry, Internal medicine, Internal Medicine, Cardiology, Medicine, In patient, Genetic risk, Cardiology and Cardiovascular Medicine, business, Coronary heart disease
Published: 2016
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35. CHROMOSOME 9P21 CDKN2A/CDKN2B GENE VARIATION EXPLAINS 12&percnt; OF INCIDENT CARDIOVASCULAR EVENTS IN THE POPULATION BUT DOES NOT ADD INCREMENTAL VALUE ON RISK PREDICTION BEYOND TRADITIONAL RISK FACTORS- THE MALMö DIET AND CANCER STUDY

Author: Marketa Sjögren, Peter Almgren, Gunnar Engström, Olle Melander, Bo Hedblad, Gustav Smith, and Klas Gränsbo
Subjects: Genetics, Oncology, medicine.medical_specialty, education.field_of_study, business.industry, Population, Context (language use), Disease, Diet and cancer, CDKN2A, Internal medicine, CDKN2B, medicine, Dependant, Prospective cohort study, education, business, Cardiology and Cardiovascular Medicine
Abstract: Context: The clinical utility and age dependant effects of the strongest single cardiovascular disease (CVD) susceptibility gene variant identified thus far (on chromosome 9p21) has not yet been evaluated in any large homogeneous prospective cohort study. We tested in a large prospective cohort
Published: 2012
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36. A variant upstream of the CDH13 adiponectin receptor gene and metabolic syndrome in Swedes

Author: Peter Almgren, Bo Hedblad, Martina Montagnana, Cristiano Fava, Alessandro Lechi, Marketa Sjögren, Pietro Minuz, Olle Melander, Gunnar Engström, Gian Cesare Guidi, and Elisa Danese
Subjects: Male, medicine.medical_specialty, Genotype, Metabolic Syndrome, Disease, Polymorphism, Single Nucleotide, Pathogenesis, Cohort Studies, Diet and cancer, CDH13, Adiponectin Receptor Gene, Sex Factors, Polymorphism (computer science), Internal medicine, medicine, Humans, Obesity, Promoter Regions, Genetic, Triglycerides, Aged, Adiponectin receptor 1, Sweden, Adiponectin, business.industry, Cholesterol, HDL, Homozygote, Middle Aged, medicine.disease, Cadherins, Endocrinology, Cohort, Hypertension, Female, Metabolic syndrome, Menopause, Cardiology and Cardiovascular Medicine, business, Follow-Up Studies
Abstract: Metabolic syndrome (MetS) constitutes a worldwide epidemic burst accounting for billions of cardiovascular disease events and deaths. The genetic basis of MetS is largely unknown. The rs11646213 T → A polymorphism maps at 16q23.3 upstream of the CDH13 gene codifying for cadherin-13 (also known as T-cadherin or H-cadherin), which is considered a vascular adiponectin receptor. This and other single-nucleotide polymorphisms have been associated with hypertension and adiponectin level in separate studies. The aim of the present study was to evaluate the effect of the CDH13 rs11646213 T → A polymorphism on individual components of MetS and on MetS. The polymorphism was genotyped in the cardiovascular cohort of the Malmo Diet and Cancer Study (n = 4,942) and successively in the Malmo Preventive Project (n = 17,675) cohort at baseline and after an average of 23 years of follow-up (reinvestigation). Four different definitions of MetS were applied to these cohorts. In the cardiovascular arm, CDH13 rs11646213 AA homozygotic women showed a trend toward higher triglycerides and lower high-density lipoprotein cholesterol and presented a higher MetS score (composite sum of MetS phenotypes). MetS (Adult Treatment Panel III definition) was more prevalent in AA homozygotic women compared to T-carriers, a result confirmed in the Malmo Preventive Project cohort at baseline and at reinvestigation with an increased risk from 19% to 45% in AA homozygotic women. In conclusion, the CDH13 rs11646213 T > A polymorphism was consistently associated with MetS in Swedish women recruited in 2 large cohorts. In light of the role of cadherin-13 as a vascular receptor for adiponectin, our study supports the genetic basis for the role of adiponectin in MetS pathogenesis.
Published: 2011

37. Lack of association between genetic variations in the KALRN region and ischemic stroke

Author: Bo Norrving, Michael Nilsson, Christina Jern, Sandra Olsson, Marketa Sjögren, Arne Lindgren, Olle Melander, and Katarina Jood
Subjects: Oncology, Male, medicine.medical_specialty, Clinical Biochemistry, Single-nucleotide polymorphism, Protein Serine-Threonine Kinases, Bioinformatics, KALRN gene, Polymorphism, Single Nucleotide, Brain Ischemia, Risk Factors, Internal medicine, Genetic variation, medicine, Guanine Nucleotide Exchange Factors, Humans, Genetic Predisposition to Disease, Aged, Sweden, Cardioembolic stroke, business.industry, General Medicine, Stroke, Case-Control Studies, Ischemic stroke, Female, business
Abstract: Objectives: To investigate whether KALRN gene variation is associated with ischemic stroke (IS). Design and methods: Associations to overall IS and IS subtypes were investigated in SAHLSIS, which comprises 844 patients with IS and 668 controls. Results: Associations between KALRN SNPs and overall IS and cardioembolic stroke were detected. Associations for overall IS were investigated in two additional Swedish samples, but could not be replicated. Conclusion: KALRN gene variation is not associated with overall IS. (C) 2011 The Canadian Society of Clinical Chemists. Published by Elsevier Inc. All rights reserved.
Published: 2011

38. Genetic variant on chromosome 12p13 does not show association to ischemic stroke in 3 Swedish case-control studies

Author: Katarina Jood, Håkan Lövkvist, Marketa Sjögren, J. Gustav Smith, Bo Norrving, Arne Lindgren, Gunnar Engström, Sandra Olsson, Christina Jern, and Olle Melander
Subjects: Male, medicine.medical_specialty, Population, Single-nucleotide polymorphism, Polymorphism, Single Nucleotide, Brain Ischemia, Brain ischemia, Risk Factors, Internal medicine, medicine, Humans, education, Stroke, Aged, Advanced and Specialized Nursing, Aged, 80 and over, Sweden, education.field_of_study, Chromosomes, Human, Pair 12, Cerebral infarction, business.industry, Case-control study, Odds ratio, Middle Aged, medicine.disease, Surgery, Minor allele frequency, Case-Control Studies, Female, Neurology (clinical), Cardiology and Cardiovascular Medicine, business, Genome-Wide Association Study
Abstract: Background and Purpose— In a genome-wide association study and subsequent case-control studies, the single-nucleotide polymorphism rs12425791 on chromosome 12p13 was reported to be associated with ischemic stroke, but this could not be validated in a recent well-powered study. We therefore investigated whether an association between ischemic stroke and rs12425791 could be detected in 3 different case-control studies from the southwest of Sweden. Methods— We examined 3606 patients with ischemic stroke and 2528 controls from 3 independent case-controls studies. Results— No significant association between ischemic stroke and the single-nucleotide polymorphism rs12425791 was detected in any of the 3 case-control samples or in the samples combined. The odds ratio for ischemic stroke for the minor allele in the combined sample was 1.02 (95% CI, 0.93 to 1.13). Conclusions— The single-nucleotide polymorphism rs12425791 does not confer a substantial risk for ischemic stroke in our population. Our results support a recent large study including other European populations.
Published: 2010

39. Vanin-1 T26I polymorphism, hypertension and cardiovascular events in two large urban-based prospective studies in Swedes

Author: Elisa Danese, Gunnar Engström, Martina Montagnana, P. Minuz, Marketa Sjögren, Peter Almgren, Gian Cesare Guidi, Cristiano Fava, Bo Hedblad, and Olle Melander
Subjects: Male, medicine.medical_specialty, Heterozygote, Genotype, Urban Population, Vanin-1 I26T polymorphism, hypertension, cardiovascular events, Endocrinology, Diabetes and Metabolism, Diastole, Medicine (miscellaneous), GPI-Linked Proteins, Polymorphism, Single Nucleotide, Amidohydrolases, Diet and cancer, Internal medicine, medicine, Humans, Cardiac and Cardiovascular Systems, Prospective Studies, Prospective cohort study, Aged, Proportional Hazards Models, Sweden, Nutrition and Dietetics, Proportional hazards model, business.industry, Hazard ratio, Middle Aged, Surgery, Stroke, Blood pressure, Phenotype, Cardiovascular Diseases, Cohort, Hypertension, Female, Cardiology and Cardiovascular Medicine, business
Abstract: BACKGROUND AND AIMS: Vanin-1 (gene name VNN1) is an enzyme with pantetheinase activity generating the amino-thiol cysteamine which is implicated in the regulation of red-ox status through its effect on glutathione. We tested the hypothesis that the rs2294757 VNN1 T26I polymorphism could affect blood pressure (BP) levels, hypertension prevalence, and risk of incident cardiovascular events. METHODS AND RESULTS: The VNN1 T26I polymorphism was genotyped in 5664 participants of the cardiovascular cohort of the "Malmö Diet and Cancer" (MDC-CVA) study and successively in 17874 participants of the "Malmö Preventive project"(MPP). The incidence of cardiovascular events was monitored for an average of nearly 12 years of follow-up in the MDC-CVA and for 25 years in the MPP. Both before and after adjustment for sex, age and BMI in the MDC-CVA the polymorphism had a mild lowering effect on diastolic BP and hypertension, especially in females. However in MPP no effect on BP phenotypes was detectable. Before and after adjustment for major cardiovascular risk factors, the hazard ratio for incident ischemic stroke and coronary events in the MDC-CVA was not significantly different in carriers of different genotypes. CONCLUSIONS: Our data do not support a major role for the VNN1 T26I variant in determining BP level and incident ischemic events.
Published: 2010

40. Variation in GYS1 interacts with exercise and gender to predict cardiovascular mortality

Author: Marketa Sjögren, Marju Orho-Melander, Jenny Fredriksson, Joyce Carlson, Valeriya Lyssenko, Bo Isomaa, Leif Groop, Peter Almgren, Marja-Riitta Taskinen, Dragi Anevski, and Kardiologian yksikkö
Subjects: Male, Apolipoprotein E, Type 2 diabetes, chemistry.chemical_compound, 0302 clinical medicine, Risk Factors, Polymorphism (computer science), Metabolic Syndrome, 2. Zero hunger, Sex Characteristics, 0303 health sciences, education.field_of_study, Multidisciplinary, Hazard ratio, Middle Aged, Diabetes and Endocrinology, Glycogen Synthase, Cardiovascular Diseases, Medicine, Female, Research Article, medicine.medical_specialty, Science, Population, 030209 endocrinology & metabolism, Physical exercise, Endocrinology and Diabetes, Polymorphism, Single Nucleotide, 03 medical and health sciences, Apolipoproteins E, Predictive Value of Tests, Internal medicine, medicine, Humans, education, Exercise, Aged, 030304 developmental biology, Polymorphism, Genetic, Cholesterol, business.industry, Genetics and Genomics/Gene Therapy, Genetic Variation, medicine.disease, Endocrinology, Diabetes Mellitus, Type 2, chemistry, Multivariate Analysis, Medicinal Chemistry, Metabolic syndrome, business
Abstract: "Background. The muscle glycogen synthase gene (GYS1) has been associated with type 2 diabetes (T2D), the metabolic syndrome (MetS), male myocardial infarction and a defective increase in muscle glycogen synthase protein in response to exercise. We addressed the questions whether polymorphism in GYS1 can predict cardiovascular (CV) mortality in a high-risk population, if this risk is influenced by gender or physical activity, and if the association is independent of genetic variation in nearby apolipoprotein E gene (APOE). Methodology/Principal Findings. Polymorphisms in GYS1 (XbaIC>T) and APOE (-219G>T, epsilon 2/epsilon 3/epsilon 4) were genotyped in 4,654 subjects participating in the Botnia T2D-family study and followed for a median of eight years. Mortality analyses were performed using Cox proportional-hazards regression. During the follow-up period, 749 individuals died, 409 due to CV causes. In males the GYS1 XbaI T-allele (hazard ratio (HR) 1.9 [1.2-2.9]), T2D (2.5 [1.7-3.8]), earlier CV events (1.7 [1.2-2.5]), physical inactivity (1.9 [1.2-2.9]) and smoking (1.5 [1.0-2.3]) predicted CV mortality. The GYS1 XbaI T-allele predicted CV mortality particularly in physically active males (HR 1.7 [1.3-2.0]). Association of GYS1 with CV mortality was independent of APOE (219TT/epsilon 4), which by its own exerted an effect on CV mortality risk in females (2.9 [1.9-4.4]). Other independent predictors of CV mortality in females were fasting plasma glucose (1.2 [1.1-1.2]), high body mass index (BMI) (1.0 [1.0-1.1]), hypertension (1.9 [1.2-3.1]), earlier CV events (1.9 [1.3-2.8]) and physical inactivity (1.9 [1.2-2.8]). Conclusions/Significance. Polymorphisms in GYS1 and APOE predict CV mortality in T2D families in a gender-specific fashion and independently of each other. Physical exercise seems to unmask the effect associated with the GYS1 polymorphism, rendering carriers of the variant allele less susceptible to the protective effect of exercise on the risk of CV death, which finding could be compatible with a previous demonstration of defective increase in the glycogen synthase protein in carriers of this polymorphism." "Background. The muscle glycogen synthase gene (GYS1) has been associated with type 2 diabetes (T2D), the metabolic syndrome (MetS), male myocardial infarction and a defective increase in muscle glycogen synthase protein in response to exercise. We addressed the questions whether polymorphism in GYS1 can predict cardiovascular (CV) mortality in a high-risk population, if this risk is influenced by gender or physical activity, and if the association is independent of genetic variation in nearby apolipoprotein E gene (APOE). Methodology/Principal Findings. Polymorphisms in GYS1 (XbaIC>T) and APOE (-219G>T, epsilon 2/epsilon 3/epsilon 4) were genotyped in 4,654 subjects participating in the Botnia T2D-family study and followed for a median of eight years. Mortality analyses were performed using Cox proportional-hazards regression. During the follow-up period, 749 individuals died, 409 due to CV causes. In males the GYS1 XbaI T-allele (hazard ratio (HR) 1.9 [1.2-2.9]), T2D (2.5 [1.7-3.8]), earlier CV events (1.7 [1.2-2.5]), physical inactivity (1.9 [1.2-2.9]) and smoking (1.5 [1.0-2.3]) predicted CV mortality. The GYS1 XbaI T-allele predicted CV mortality particularly in physically active males (HR 1.7 [1.3-2.0]). Association of GYS1 with CV mortality was independent of APOE (219TT/epsilon 4), which by its own exerted an effect on CV mortality risk in females (2.9 [1.9-4.4]). Other independent predictors of CV mortality in females were fasting plasma glucose (1.2 [1.1-1.2]), high body mass index (BMI) (1.0 [1.0-1.1]), hypertension (1.9 [1.2-3.1]), earlier CV events (1.9 [1.3-2.8]) and physical inactivity (1.9 [1.2-2.8]). Conclusions/Significance. Polymorphisms in GYS1 and APOE predict CV mortality in T2D families in a gender-specific fashion and independently of each other. Physical exercise seems to unmask the effect associated with the GYS1 polymorphism, rendering carriers of the variant allele less susceptible to the protective effect of exercise on the risk of CV death, which finding could be compatible with a previous demonstration of defective increase in the glycogen synthase protein in carriers of this polymorphism." "Background. The muscle glycogen synthase gene (GYS1) has been associated with type 2 diabetes (T2D), the metabolic syndrome (MetS), male myocardial infarction and a defective increase in muscle glycogen synthase protein in response to exercise. We addressed the questions whether polymorphism in GYS1 can predict cardiovascular (CV) mortality in a high-risk population, if this risk is influenced by gender or physical activity, and if the association is independent of genetic variation in nearby apolipoprotein E gene (APOE). Methodology/Principal Findings. Polymorphisms in GYS1 (XbaIC>T) and APOE (-219G>T, epsilon 2/epsilon 3/epsilon 4) were genotyped in 4,654 subjects participating in the Botnia T2D-family study and followed for a median of eight years. Mortality analyses were performed using Cox proportional-hazards regression. During the follow-up period, 749 individuals died, 409 due to CV causes. In males the GYS1 XbaI T-allele (hazard ratio (HR) 1.9 [1.2-2.9]), T2D (2.5 [1.7-3.8]), earlier CV events (1.7 [1.2-2.5]), physical inactivity (1.9 [1.2-2.9]) and smoking (1.5 [1.0-2.3]) predicted CV mortality. The GYS1 XbaI T-allele predicted CV mortality particularly in physically active males (HR 1.7 [1.3-2.0]). Association of GYS1 with CV mortality was independent of APOE (219TT/epsilon 4), which by its own exerted an effect on CV mortality risk in females (2.9 [1.9-4.4]). Other independent predictors of CV mortality in females were fasting plasma glucose (1.2 [1.1-1.2]), high body mass index (BMI) (1.0 [1.0-1.1]), hypertension (1.9 [1.2-3.1]), earlier CV events (1.9 [1.3-2.8]) and physical inactivity (1.9 [1.2-2.8]). Conclusions/Significance. Polymorphisms in GYS1 and APOE predict CV mortality in T2D families in a gender-specific fashion and independently of each other. Physical exercise seems to unmask the effect associated with the GYS1 polymorphism, rendering carriers of the variant allele less susceptible to the protective effect of exercise on the risk of CV death, which finding could be compatible with a previous demonstration of defective increase in the glycogen synthase protein in carriers of this polymorphism."
Published: 2007

41. 1A.10

Author: Katarzyna Polonis, K. Narkiewicz, Marcin Wirtwein, Marketa Sjögren, M. Hoffman, D. Jarosz, Marcin Gruchała, Wojciech Sobiczewski, Olle Melander, and Thomas Hedner
Subjects: medicine.medical_specialty, Framingham Risk Score, Physiology, business.industry, Coronary heart disease, stomatognathic diseases, Internal medicine, Internal Medicine, medicine, Cardiology, In patient, Cardiology and Cardiovascular Medicine, business, Gene
Abstract: Coronary heart disease (CHD) development is associated to a combination of lifestyle and genetic factors. A number of lifestyle risk factors is well defined, while genetic factors have not yet been well determined.
Published: 2015
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42. The -374 T/A polymorphism in the gene encoding RAGE is associated with diabetic nephropathy and retinopathy in type 1 diabetic patients

Author: Marketa Sjögren, Leif Groop, Elisabet Agardh, Ekaterine Bakhtadze, Eero Lindholm, Carl-David Agardh, and Corrado M. Cilio
Subjects: medicine.medical_specialty, endocrine system diseases, Endocrinology, Diabetes and Metabolism, Receptor for Advanced Glycation End Products, Type 2 diabetes, Polymorphism, Single Nucleotide, Diabetic nephropathy, Reference Values, Diabetes mellitus, Internal medicine, Immunopathology, HLA-DQ Antigens, Internal Medicine, medicine, HLA-DQ beta-Chains, Humans, Diabetic Nephropathies, Receptors, Immunologic, Autoimmune disease, Glycated Hemoglobin, Type 1 diabetes, HLA-DQB1, Diabetic Retinopathy, business.industry, medicine.disease, Endocrinology, Diabetes Mellitus, Type 1, Phenotype, Diabetes Mellitus, Type 2, cardiovascular system, business, Retinopathy
Abstract: The receptor for AGE (RAGE) is considered to be mainly an intracellular signal-transducer or pro-inflammatory peptide of possible importance for inflammation and autoimmune diseases. Our aim was to study whether the -374 T/A polymorphism in the gene encoding RAGE (AGER) is associated with diabetes type and presence of diabetic complications.The AGER -374 T/A polymorphism was genotyped in 867 type 1 diabetic patients, 2,467 type 2 diabetic patients and 205 non-diabetic control subjects of Scandinavian origin.AGER polymorphism was related to different HLA-DQB1 genotypes and the presence of diabetic complications. Type 1 diabetic patients had a higher frequency of the AGER -374 A/A or T/A genotypes than type 2 diabetic patients (51.1 vs 44.9%, p=0.002) and control subjects (51.1 vs 47.6%, p=0.0006). The RAGE -374 T/A polymorphism was associated with HLA-DQB1 genotypes; patients with HLA risk genotypes had a higher frequency of the A/A or T/A genotypes than patients with other HLA-DQB1 genotypes (60.3 vs 40.3%, p0.000001). In type 1 diabetic patients, the frequency of the A/A or T/A genotypes was higher in patients with diabetic nephropathy than without (61.1 vs 46.8%, p=0.006) and with sight-threatening retinopathy than without (56.1 vs 47.6%, p=0.03). In type 2 diabetic patients with HbA(1c) values below the median, the T/T genotype was more frequent in patients with diabetic nephropathy than without (54.3 vs 38.2%, p=0.02).Our results show an association between the AGER -374 T/A polymorphism and type 1 diabetes. This association was HLA-DQB1-dependent. The polymorphism was associated with diabetic nephropathy in both type 1 and type 2 diabetes, in an HbA(1c)-dependent manner in the latter group, and also with sight-threatening retinopathy in type 1 diabetic patients.
Published: 2005

43. Genetic prediction of future type 2 diabetes

Author: Peter Almgren, Marju Orho-Melander, Carola Saloranta, Valeriya Lyssenko, Tiinamaija Tuomi, Dragi Anevski, Leif Groop, and Marketa Sjögren
Subjects: Blood Glucose, Male, endocrine system diseases, Type 2 diabetes, Body Mass Index, Endocrinology, 0302 clinical medicine, Risk Factors, Genotype, Diabetes/Endocrinology/Metabolism, Prospective Studies, Finland, 2. Zero hunger, 0303 health sciences, Diabetes, Hazard ratio, General Medicine, Middle Aged, 3. Good health, Medicine, Female, Research Article, Adult, Peroxisome proliferator-activated receptor gamma, medicine.medical_specialty, Adolescent, 030209 endocrinology & metabolism, Endocrinology and Diabetes, Genetics/Genomics/Gene Therapy, Polymorphism, Single Nucleotide, 03 medical and health sciences, Insulin resistance, Predictive Value of Tests, Diabetes mellitus, Internal medicine, Genetics, medicine, Humans, Genetic Predisposition to Disease, Aged, 030304 developmental biology, Proportional hazards model, business.industry, nutritional and metabolic diseases, medicine.disease, Diabetes Mellitus, Type 2, business, Body mass index
Abstract: Background Type 2 diabetes (T2D) is a multifactorial disease in which environmental triggers interact with genetic variants in the predisposition to the disease. A number of common variants have been associated with T2D but our knowledge of their ability to predict T2D prospectively is limited. Methods and Findings By using a Cox proportional hazard model, common variants in the PPARG (P12A), CAPN10 (SNP43 and 44), KCNJ11 (E23K), UCP2 (−866G>A), and IRS1 (G972R) genes were studied for their ability to predict T2D in 2,293 individuals participating in the Botnia study in Finland. After a median follow-up of 6 y, 132 (6%) persons developed T2D. The hazard ratio for risk of developing T2D was 1.7 (95% confidence interval [CI] 1.1–2.7) for the PPARG PP genotype, 1.5 (95% CI 1.0–2.2) for the CAPN10 SNP44 TT genotype, and 2.6 (95% CI 1.5–4.5) for the combination of PPARG and CAPN10 risk genotypes. In individuals with fasting plasma glucose ≥ 5.6 mmol/l and body mass index ≥ 30 kg/m2, the hazard ratio increased to 21.2 (95% CI 8.7–51.4) for the combination of the PPARG PP and CAPN10 SNP43/44 GG/TT genotypes as compared to those with the low-risk genotypes with normal fasting plasma glucose and body mass index < 30 kg/m2. Conclusion We demonstrate in a large prospective study that variants in the PPARG and CAPN10 genes predict future T2D. Genetic testing might become a future approach to identify individuals at risk of developing T2D., In a large prospective study, Lyssenko and colleagues show that variants in the PPARG and CAPN10 genes can help predict whether a person will develop Type 2 diabetes.
Published: 2005

44. 40(th) EASD Annual Meeting of the European Association for the Study of Diabetes : Munich, Germany, 5-9 September 2004

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Butler, Francisco Javier Ampudia-Blasco, O N Kong, Attali J-R., C A Hedman, K Oshinyemi, Nicolle Müller, I C Cranston, N Okumus, M V Vlaiculescu, Balasubramanian Ravikumar, W W Cheatham, K Mukasa, K B Biswas, Annunziata Lapolla, Phil McEwan, G Mader, Gilles Chassot, Dragi Anevski, Werner A. Scherbaum, M Donath, C Hesselmann, R A Gandhi, David E. Moller, Ezio Bonifacio, C Garcia, V Ifandi, P Hornnes, Nieuwenhoven Fav., C Puech, S Pérez-Del-Pulgar, Kim S-R., G Hines, C Rubio Terrés, Michael Gaster, N. Hosszufalusi, A Scholze, Andrew A. Young, Stavros Liatis, F Hariri, S Tan, Paul Valensi, Allan E. Karlsen, J Kim, E. Moberg, J Kaiser, L Berman, G Nelson, A Altkrüger, P Kothare, D B Cook, S Doran, G. van Dijk, Shahnaz Shahinfar, Kim C-S., P Stahl, M Manousaki, S Sigrist, S K Lim, M. P. Stern, A Guberti, C Rezzani, J McKenney, Karl Thomaseth, Sofia Carlsson, M Julia, R Brillante, I Rubesova, T Darkow, E Matsumoto, Wendy M. 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D, Torjesen, P, Kilhovd, B, Berg, T, Sandvik, L, Hanssen, K, Mentink, C, Donchenko, G, Stepanenko, S, Maingrette, F, Deng, H, Lindenmair, A, Freudenthaler, A, Baumgartner parzer, S, Nizheradze, K, Khoruzhenko, A, Tronko, N, Sheu, W, Ou, H, Shen, H, Lin, T, Wu, H, Yang, C, Mogylnytska, L, Schmoelzer, I, Davies, J, Band, M, Struthers, A, Prázný, M, Škrha, J, Kasalová, Z, Neelotpol, S, Jahan, P, Kauschke, S, Harrop, C, Schäfer, A, Widder, J, Eigenthaler, M, Walter, U, Uchimura, I, Ikebukuro, M, Kaibara, M, Hirata, M, Helal, R, Pervin, F, Yang, X, Jansson, P, Nagaev, I, Jack, M, Carvalho, E, Sunnerhagen, K, Cam, M, Cushman, S, Smith, U, Creely, S, Farmer, J, Gustafson, B, Kusminski, C, Krusinova, E, Wohl, P, Klementova, M, Lanska, V, Mcdougall, C, Kelly, I, Abbas, Z, Lutale, J, Archibald, L, Karunajeewa, H, Stingemore, N, Stuccio, G, Mcgechie, D, Muller, L, Hak, E, Goudzwaard, W, Montorsi, F, Homering, M, Sprenger, K, Goldstein, I, Asnaghi, V, Ferrari, G, Rastaldi, M, Gabellini, D, Dell'Antonio, G, Maestroni, A, Ruggieri, D, Luzi, L, Piemonti, L, Zerbini, G, Anafaroglu, I, Tutuncu, N, Sultana, M, Siddiqua, N, Iwasaki, T, Nakajima, A, Yoneda, M, Mukasa, K, Tanaka, S, and Sekihara, H
Subjects: 0303 health sciences, medicine.medical_specialty, business.industry, EASD, Endocrinology, Diabetes and Metabolism, Human physiology, medicine.disease, 03 medical and health sciences, 0302 clinical medicine, Diabetes mellitus, Family medicine, Internal Medicine, Medicine, business, 030217 neurology & neurosurgery, 030304 developmental biology
Published: 2004

45. A MYOCARDIAL INFARCTION GENETIC RISK SCORE ASSOCIATES WITH CAROTID ATHEROSCLEROSIS

Author: B. Hedblad, Peter Almgren, Olle Melander, Viktor Hamrefors, Marketa Sjögren, and Gunnar Engström
Subjects: Carotid atherosclerosis, medicine.medical_specialty, Physiology, business.industry, Internal medicine, Internal Medicine, Cardiology, Medicine, Myocardial infarction, Genetic risk, Cardiology and Cardiovascular Medicine, business, medicine.disease
Published: 2011
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46. SMOKING AND OBESITY ASSOCIATED BDNF GENE VARIANCE PREDICTS TOTAL AND CARDIOVASCULAR MORTALITY IN SMOKERS (THE CARENORTH CONSORTIUM)

Author: B. Wahlstrand, Marketa Sjögren, Gunnar Engström, Thomas Hedner, S. Halldén, B. Hedblad, Michal Hoffmann, K. Narkiewicz, and Olle Melander
Subjects: medicine.medical_specialty, Physiology, business.industry, Variance (accounting), medicine.disease, Obesity, Bdnf gene, Internal medicine, Internal Medicine, Medicine, Cardiology and Cardiovascular Medicine, business, Psychiatry, Cardiovascular mortality
Published: 2011
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47. Clinical Evaluation of the Polygenetic Background of Blood Pressure in the Population-Based Setting

Author: Olle Melander, John D. Overton, Luca A. Lotta, Pietro Minuz, Aris Baras, Alice Giontella, Cristiano Fava, and Marketa Sjögren
Subjects: 0301 basic medicine, Male, medicine.medical_specialty, Multifactorial Inheritance, hypertension, genotype, Population based, 030204 cardiovascular system & hematology, Polymorphism, Single Nucleotide, genetic risk score, Article, Body Mass Index, Coronary artery disease, 03 medical and health sciences, 0302 clinical medicine, Internal medicine, Genotype, Epidemiology, Internal Medicine, medicine, Humans, Prospective Studies, Genetic risk, Aged, business.industry, blood pressure, Atrial fibrillation, Middle Aged, medicine.disease, 030104 developmental biology, Blood pressure, Cardiology, Female, epidemiology, business, Clinical evaluation, Genome-Wide Association Study
Abstract: The clinical value of the polygenetic component of blood pressure (BP) is commonly questioned. We evaluated a genetic risk score for BP (BP-GRS 858 ), based on the most recently published genome-wide association studies variants that were significantly associated with either systolic BP or diastolic BP, for prediction of hypertension and cardiovascular end points. The genotyping was performed in 2 urban-based prospective cohorts: the Malmö Diet and Cancer (n=29 295) and the Malmö Preventive Project (n=9367) and a weighted BP-GRS 858 based on 858 SNPs was calculated. At baseline, we found a difference of 9.0 mm Hg (systolic BP) and 4.8 mm Hg (diastolic BP) between the top and the bottom quartile of BP-GRS 858 . In Malmö Preventive Project, the top versus bottom quartile of BP-GRS 858 was associated with a doubled risk of incident hypertension (odds ratio, 2.05 [95% CI, 1.75–2.39], P =1.4×10 −21 ), a risk higher than that of body mass index, as evaluated in quartiles. In Malmö Diet and Cancer, significant association was found between the age and sex-adjusted BP-GRS 858 and the incidence of total cardiovascular events, stroke, coronary artery disease, heart failure, atrial fibrillation, and total mortality. Most of these associations remained significant after adjusting for traditional risk factors, including hypertension. BP-GRS 858 could contribute predictive information regarding future hypertension, with an effect size comparable to other well-known risk factors such as obesity, and predicts cardiovascular events. Given that the exposure to high polygenetic risk starts at birth, we suggest that the BP-GRS 858 might be useful to identify children or adolescents who would benefit from early hypertension screening and treatment.
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