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Advanced age, low left atrial appendage velocity, and factor V promoter sequence variation as predictors of left atrial thrombosis in patients with nonvalvular atrial fibrillation.

https://arctichealth.org/en/permalink/ahliterature146014
Source
J Thromb Thrombolysis. 2010 Aug;30(2):192-9
Publication Type
Article
Date
Aug-2010
Author
Dmitry A Zateyshchikov
Alexey N Brovkin
Dimitry A Chistiakov
Valery V Nosikov
Author Affiliation
Scientific-Educational Medical Center of the Department of General Management of Russian President, Moscow, Russia.
Source
J Thromb Thrombolysis. 2010 Aug;30(2):192-9
Date
Aug-2010
Language
English
Publication Type
Article
Keywords
Age Factors
Aged
Atrial Appendage - physiopathology - ultrasonography
Atrial Fibrillation - complications - physiopathology - ultrasonography
Atrial Function, Left
Chi-Square Distribution
Cross-Sectional Studies
Echocardiography, Transesophageal
Factor V - genetics
Female
Genetic Predisposition to Disease
Humans
Logistic Models
Male
Middle Aged
Odds Ratio
Polymerase Chain Reaction
Polymorphism, Genetic
Polymorphism, Restriction Fragment Length
Promoter Regions, Genetic
Risk assessment
Risk factors
Russia
Stroke Volume
Thrombosis - etiology - genetics - physiopathology
Ventricular Function, Left
Abstract
Atrial fibrillation (AF) renders individual patients at risk for development of an atrial thrombus. The aim of this study was to determine clinical and echocardiographic factors influencing the risk of left atrial thrombosis (LAT) in patients with persistent nonvalvular AF. Genetic variants encoding haemostatic factors have been also assessed for putative association with LAT. In the cross-sectional study, a total of 212 patients (132 males and 80 females) with nonvalvular persistent AF (duration range 48 h-90 days) have been selected. LAT was visualized by transesophageal echocardiography. The FGB G(-455)A, PAI-1 4G/5G, F5 C(-224)T, and F5 R506Q genetic markers were tested using the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) approach. To reveal independent factors contributing to the thromboembolic risk in AF, a multivariate logistic model was applied. LA thrombi were found in 44 out of 212 subjects (21%). LAT was more frequently observed in patients at age >75 years (P 75 years, LVEF
PubMed ID
20082208 View in PubMed
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An association between the common hereditary hemochromatosis mutation and the factor V Leiden allele in a population with thrombosis.

https://arctichealth.org/en/permalink/ahliterature204897
Source
Blood. 1998 Aug 15;92(4):1461-2
Publication Type
Article
Date
Aug-15-1998

Congenital disorder of oxygen sensing: association of the homozygous Chuvash polycythemia VHL mutation with thrombosis and vascular abnormalities but not tumors.

https://arctichealth.org/en/permalink/ahliterature181962
Source
Blood. 2004 May 15;103(10):3924-32
Publication Type
Article
Date
May-15-2004
Author
Victor R Gordeuk
Adelina I Sergueeva
Galina Y Miasnikova
Daniel Okhotin
Yaroslav Voloshin
Peter L Choyke
John A Butman
Katerina Jedlickova
Josef T Prchal
Lydia A Polyakova
Author Affiliation
Center for Sickle Cell Disease, Department of Medicine, Howard University, Washington, DC 20059, USA. vgordeuk@howard.edu
Source
Blood. 2004 May 15;103(10):3924-32
Date
May-15-2004
Language
English
Publication Type
Article
Keywords
Adaptation, Physiological - genetics
Adolescent
Adult
Anoxia - congenital - genetics
Child
Cross-Sectional Studies
Female
Homozygote
Humans
Hypoxia-Inducible Factor 1, alpha Subunit
Male
Mutation
Neoplasms - genetics
Polycythemia - complications - epidemiology - genetics - mortality
Retrospective Studies
Russia - epidemiology
Survival Rate
Syndrome
Thrombosis - etiology - genetics
Transcription Factors - blood
Tumor Suppressor Proteins - genetics
Ubiquitin-Protein Ligases - genetics
Vascular Diseases - etiology - genetics
Vascular Endothelial Growth Factor A - blood
Von Hippel-Lindau Tumor Suppressor Protein
Abstract
Adaptation to hypoxia is critical for survival and regulates multiple processes, including erythropoiesis and vasculogenesis. Chuvash polycythemia is a hypoxia-sensing disorder characterized by homozygous mutation (598C>T) of von Hippel-Lindau gene (VHL), a negative regulator of hypoxia sensing. Although endemic to the Chuvash population of Russia, this mutation occurs worldwide and originates from a single ancient event. That VHL 598C>T homozygosity causes elevated normoxic levels of the transcription factor hypoxia inducible factor-1alpha (HIF-1alpha), serum erythropoietin and hemoglobin is known, but the disease phenotype has not been documented in a controlled manner. In this matched cohort study, VHL 598C>T homozygosity was associated with vertebral hemangiomas, varicose veins, lower blood pressures, and elevated serum vascular endothelial growth factor (VEGF) concentrations (P T homozygotes than in controls, erythropoietin response to hypoxia was identical. Thus, Chuvash polycythemia is a distinct VHL syndrome manifested by thrombosis, vascular abnormalities, and intact hypoxic regulation despite increased basal expression of hypoxia-regulated genes.
PubMed ID
14726398 View in PubMed
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Risk factors for venous thrombosis in Swedish children and adolescents.

https://arctichealth.org/en/permalink/ahliterature29449
Source
Acta Paediatr. 2005 Jun;94(6):717-22
Publication Type
Article
Date
Jun-2005
Author
Olof Rask
Erik Berntorp
Rolf Ljung
Author Affiliation
Department of Paediatrics, University Hospital, Malmö, Sweden. olof.rask@pediatrik.mas.lu.se
Source
Acta Paediatr. 2005 Jun;94(6):717-22
Date
Jun-2005
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Child
Child, Preschool
Female
Humans
Infant
Infant, Newborn
Male
Research Support, Non-U.S. Gov't
Retrospective Studies
Risk factors
Sweden - epidemiology
Venous Thrombosis - etiology - genetics
Abstract
AIM: To identify prothrombotic risk profiles in children and adolescents referred to a regional coagulation centre in southern Sweden for a first thrombotic event. METHODS: One hundred and twenty-eight consecutive children and adolescents (newborn to 20 y) referred for evaluations of a first episode of venous thrombosis were investigated. Clinical data were collected retrospectively, and the following variables were investigated: protein C, protein S, antithrombin; resistance to activated protein C; the genotypes FV-G1691A, F II-G20210A, MTHFR-C677T, MTHFR- A1298C; coagulation factors VIII and XI. RESULTS: 104/128 subjects (81%) had identifiable acquired risk factors, most often indwelling catheters and hormone therapy. Predisposing genetic factors related to thromboembolic events were revealed in 53/83 (64%) of subjects who agreed to follow-up blood sampling, and 17/83 (20%) had two or more inherited risk factors. Combinations of genetic and acquired risk factors were identified in 45/83 (54%) of the subjects, and 77/83 (93%) had at least one such risk factor. Both sexes had one peak in frequency at less than 1 y of age and then an increase during adolescence, more in females than in males. Plasma values for coagulation factors VIII and XI were age appropriate and showed a normal Gaussian distribution. CONCLUSION: This study identified prothrombotic risk profiles in almost all children and adolescents with venous thrombosis, which underlines the importance of careful evaluation of genetic and acquired risk factors.
PubMed ID
16188774 View in PubMed
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