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The -1C to T polymorphism in the annexin A5 gene is not associated with the risk of acute myocardial infarction or sudden cardiac death in middle-aged Finnish males.

https://arctichealth.org/en/permalink/ahliterature53135
Source
Scand J Clin Lab Invest. 2005;65(2):133-40
Publication Type
Article
Date
2005
Author
K S Kaikkonen
S. Kakko
M L Kortelainen
J M Tapanainen
M J Savolainen
Y. Antero Kesäniemi
H V Huikuri
E R Savolainen
Author Affiliation
Division of Cardiology, Department of Internal Medicine, University of Oulu, Finland.
Source
Scand J Clin Lab Invest. 2005;65(2):133-40
Date
2005
Language
English
Publication Type
Article
Keywords
5' Untranslated Regions - genetics
Adult
Aged
Annexin A5 - genetics
Death, Sudden, Cardiac - epidemiology - etiology
Finland - epidemiology
Genetic markers
Genetic Predisposition to Disease
Genetic Screening
Humans
Male
Middle Aged
Myocardial Infarction - epidemiology - genetics
Polymorphism, Genetic
Research Support, Non-U.S. Gov't
Risk factors
Abstract
OBJECTIVE: A common polymorphism (-1C to T) in the translation initiation sequence of annexin A5 (ANV) gene has recently been associated with a decreased risk of acute myocardial infarction (AMI). The aim of the present study was to analyze the association between the ANV genepolymorphism and the risk of AMI and ischemic sudden cardiac death (SCD) in middle-aged Finnish males. MATERIAL AND METHODS: A case-control study involving three distinct groups of subjects was carried out: (1) victims of SCD (n=98), (2) survivors of AMI (n=212), and (3) randomly selected control subjects without any history of coronary heart disease (n=243). The ANV polymorphism was genotyped in each study group. RESULTS: Among the control group of healthy Finnish males the prevalence rates of the CC, CT, and TT genotypes were 83.1%, 15.2%, and 1.6%, respectively. Among the survivors of AMI, the prevalence rates of CC, CT, and TT were 79.7%, 20.3%, and 0%, respectively, and among the victims of SCD 83.7%, 16.3%, and 0%, respectively. No significant differences in the genotype or allele distributions were observed between the study groups. CONCLUSION: The -1C to T polymorphism in the ANV gene is not associated with the risk of AMI or SCD in middle-aged Finnish males.
PubMed ID
16025836 View in PubMed
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Age as a risk factor for myocardial infarction in Leiden mutation carriers.

https://arctichealth.org/en/permalink/ahliterature204822
Source
Mol Genet Metab. 1998 Jun;64(2):155-7
Publication Type
Article
Date
Jun-1998
Author
S. Baranovskaya
S. Kudinov
E. Fomicheva
V. Vasina
D. Solovieva
V. Khavinson
E. Schwartz
Author Affiliation
Laboratory of Human Molecular Genetics, Petersburg Nuclear Physics Institute, St.Petersburg Area, 188350, Russia.
Source
Mol Genet Metab. 1998 Jun;64(2):155-7
Date
Jun-1998
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Age Factors
Aged
Aged, 80 and over
Aging - genetics - pathology
Alleles
Child
Data Interpretation, Statistical
Drug resistance
Factor V - genetics
Gene Frequency
Heterozygote
Homozygote
Humans
Middle Aged
Mutation - genetics
Myocardial Infarction - epidemiology - genetics
Protein C - pharmacology
Risk factors
Russia - epidemiology
Abstract
A single factor V gene G-A mutation (Arg506Gln) underlying activated protein C (APC) resistance is a common risk factor for venous thromboembolism. It is still unclear whether the factor V Leiden predisposes patients to arterial thrombosis and myocardial infarction (MI). To determine a correlation between the factor V Leiden mutation and MI in different age categories, DNA samples from 287 patients with "early" and "late" MI were investigated. As control groups 373 young subjects (mean age 11 years) and 110 elderly ones (mean age 80 years) were studied. We found a significant difference in mutant allele distribution in the "late" MI group compared to the "early" MI group (chi2 = 9.86, OR = 13,7, P
PubMed ID
9705241 View in PubMed
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Age-dependent association between hepatic lipase gene C-480T polymorphism and the risk of pre-hospital sudden cardiac death: the Helsinki Sudden Death Study.

https://arctichealth.org/en/permalink/ahliterature168688
Source
Atherosclerosis. 2007 Jun;192(2):421-7
Publication Type
Article
Date
Jun-2007
Author
Yue-Mei Fan
Terho Lehtimäki
Riikka Rontu
Erkki Ilveskoski
Sirkka Goebeler
Olli Kajander
Jussi Mikkelsson
Markus Perola
Pekka J Karhunen
Author Affiliation
Laboratory of Atherosclerosis Genetics, Centre for Laboratory Medicine, Tampere University Hospital, Tampere, Finland. loyufa@uta.fi
Source
Atherosclerosis. 2007 Jun;192(2):421-7
Date
Jun-2007
Language
English
Publication Type
Article
Keywords
Adult
Aged
Autopsy
Death, Sudden, Cardiac - epidemiology - etiology
Finland - epidemiology
Humans
Lipase - genetics
Male
Middle Aged
Myocardial Infarction - epidemiology - genetics
Polymorphism, Genetic
Risk factors
Abstract
We investigated the association between hepatic lipase (HL) C-480T polymorphism and the risk of acute myocardial infarction (AMI) as well as pre-hospital sudden cardiac death (SCD).
Seven hundred sudden or unnatural pre-hospital deaths of middle-aged (33-70 years, mean 53 years) Caucasian Finnish men were subjected to detailed autopsy (Helsinki Sudden Death Study). Genotype data were obtained for 682 men.
In logistic regression analysis with age, body mass index, hypertension, diabetes, smoking and alcohol consumption as covariates, men with the TT genotype had an increased risk for SCD and AMI compared to CC carriers (OR=3.0, P=0.011; and OR=3.7, P=0.003). There was a significant age-by-genotype interaction (P or =50%) than men with the CT or CC genotype (P=0.019).
The results suggest that HL C-480T polymorphism is a strong age-dependent risk factor of SCD in early middle-aged men.
PubMed ID
16793047 View in PubMed
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Array-based multiplex analysis of candidate genes reveals two independent and additive genetic risk factors for myocardial infarction in the Finnish population.

https://arctichealth.org/en/permalink/ahliterature204871
Source
Hum Mol Genet. 1998 Sep;7(9):1453-62
Publication Type
Article
Date
Sep-1998
Author
T. Pastinen
M. Perola
P. Niini
J. Terwilliger
V. Salomaa
E. Vartiainen
L. Peltonen
A. Syvänen
Author Affiliation
Department of Human Molecular Genetics, National Public Health Institute, Mannerheimintie 166, FIN 00300, Helsinki, Finland. tomi.pastinen@ktl.fi
Source
Hum Mol Genet. 1998 Sep;7(9):1453-62
Date
Sep-1998
Language
English
Publication Type
Article
Keywords
Adult
Alleles
Base Sequence
Case-Control Studies
Coronary Disease - epidemiology - genetics
Cross-Sectional Studies
DNA - genetics
DNA Primers - genetics
Female
Finland - epidemiology
Genetic Variation
Genotype
Humans
Male
Middle Aged
Myocardial Infarction - epidemiology - genetics
Plasminogen Inactivators - genetics
Platelet Glycoprotein GPIIb-IIIa Complex - genetics
Polymerase Chain Reaction
Receptors, LDL - genetics
Risk factors
Abstract
We analysed common variants of eight genes implicated previously as risk factors for coronary heart disease or myocardial infarction (MI) in a cross-sectional study on patients with a history of MI and in carefully matched controls from the Finnish population. The most common low density lipoprotein receptor mutations in Finland were also included in our analysis. Multiplex genotyping of the target genes was performed using a specific and efficient array-based minisequencing system. The 4G allele of the plasminogen activator inhibitor gene (P
PubMed ID
9700201 View in PubMed
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Association of FXIII Val34Leu with decreased risk of myocardial infarction in Finnish males.

https://arctichealth.org/en/permalink/ahliterature203068
Source
Atherosclerosis. 1999 Feb;142(2):295-300
Publication Type
Article
Date
Feb-1999
Author
U. Wartiovaara
M. Perola
H. Mikkola
K. Tötterman
V. Savolainen
A. Penttilä
P J Grant
M J Tikkanen
E. Vartiainen
P J Karhunen
L. Peltonen
A. Palotie
Author Affiliation
Department of Clinical Chemistry and Biomedicine, Helsinki University Central Hospital, Finland.
Source
Atherosclerosis. 1999 Feb;142(2):295-300
Date
Feb-1999
Language
English
Publication Type
Article
Keywords
Alleles
DNA - analysis
DNA Primers - chemistry
Factor XIII - genetics
Fibrinolysis - genetics
Finland - epidemiology
Genetic markers
Genotype
Humans
Incidence
Male
Middle Aged
Myocardial Infarction - epidemiology - genetics
Plasminogen Activator Inhibitor 1 - genetics
Polymorphism, Genetic
Prevalence
Risk factors
Abstract
Factor XIII is a transglutaminase that crosslinks fibrin in the last steps of the coagulation process. A few polymorphic sites have been identified in this gene, one of them being a point mutation (FXIII Val34Leu), leading to an amino acid change of valine to leucine. Recently, in British patients, FXIII 34Leu allele was suggested to be associated with a decreased incidence of myocardial infarction (MI). PAI-1 4G/4G genotype seemed to lessen the beneficial effect of FXIII 34Leu allele. The aim of our study was to further investigate the possible protective role of the FXIII 34Leu allele against MI and its suggested interaction with the PAI-1 4G/5G polymorphism. We carried out genotype analyses for FXIII Val34Leu using solid-phase minisequencing in two independent Finnish study groups. In our study, the FXIII 34Leu allele was associated with a lower risk of MI (P = 0.009), however, the PAI-1 4G allele showed no interaction with this polymorphism. To establish the population frequency of the FXIII 34Leu allele and to study the possible variations in Finland four DNA pools from different geographical areas of Finland were genotyped. No significant differences in the allele frequencies were observed (21-28%) except in the Eastern Kainuu area (13%), an area with an increased risk of mortality from coronary artery disease (CAD), supporting the results presented above. The association of FXIII 34Leu variant with a lower incidence of myocardial infarction suggests a new role for FXIII in a polygenic thrombotic disease.
PubMed ID
10030380 View in PubMed
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Association of interleukin 8 with myocardial infarction: results from the Stockholm Heart Epidemiology Program.

https://arctichealth.org/en/permalink/ahliterature258580
Source
Int J Cardiol. 2014 Mar 1;172(1):173-8
Publication Type
Article
Date
Mar-1-2014
Author
Ilais Moreno Velásquez
Paolo Frumento
Katarina Johansson
Anita Berglund
Ulf de Faire
Karin Leander
Bruna Gigante
Source
Int J Cardiol. 2014 Mar 1;172(1):173-8
Date
Mar-1-2014
Language
English
Publication Type
Article
Keywords
Aged
Case-Control Studies
Coronary Artery Disease - epidemiology - genetics - metabolism
Female
Genetic Predisposition to Disease - epidemiology - genetics
HapMap Project
Humans
Interleukin-8 - blood - genetics
Logistic Models
Male
Middle Aged
Myocardial Infarction - epidemiology - genetics - metabolism
Odds Ratio
Polymorphism, Single Nucleotide
Receptors, Interleukin-8A - genetics - metabolism
Receptors, Interleukin-8B - genetics - metabolism
Risk factors
Sweden - epidemiology
Abstract
Interleukin 8 (IL8) has been contradictorily associated with the risk of myocardial infarction (MI).
To investigate the association of IL8 serum levels with the risk of MI and the association of the IL8 (IL8) and IL8 receptors (CXCR1 and CXCR2) genetic variants with IL8 levels and MI risk in a large case control study, the Stockholm Heart Epidemiology Program.
IL8 levels (pg/mL) were divided into quartiles and the MI risk was calculated by logistic regression and expressed as odds ratio (OR) and 95% CI. Two IL8 SNPs (rs4073A/T, rs2227306C/T) and three SNPs tagging CXCR1 and CXCR2 (rs4674258C/T, rs1008563C/T, rs6723449T/C) were analyzed for association with IL8 levels and with MI risk. Multivariate adjusted ORs for MI risk by IL8 levels in the highest quartiles indicated reduced point estimates in both women (OR 0.37; 95% CI 0.2-0.8) and men when compared to the lowest quartile. In female cases, IL8 levels decreased progressively in the six months after MI (p=0.03). IL8, CXCR1 and CXCR2 genetic variants were not associated with IL8 levels. In men, the T allele at the IL8 SNP rs4073 was associated with a slight increase in the MI risk under an additive and a recessive model of inheritance.
IL8 serum levels were associated with a reduced occurrence of MI among women, whereas IL8 was associated with a slightly increased risk among men, possibly through different mechanisms. These data suggest that the biological effects of IL8 on MI risk may vary over time and warrant further cohort studies with repetitive IL8 measurements.
PubMed ID
24462138 View in PubMed
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C4 null alleles and myocardial infarction.

https://arctichealth.org/en/permalink/ahliterature47995
Source
Atherosclerosis. 1999 Apr;143(2):377-81
Publication Type
Article
Date
Apr-1999
Author
S. Nityanand
A. Hamsten
H. Lithell
G. Holm
A K Lefvert
Author Affiliation
Immunological Research Unit, Center for Molecular Medicine Karolinska Hospital, Stockholm, Sweden.
Source
Atherosclerosis. 1999 Apr;143(2):377-81
Date
Apr-1999
Language
English
Publication Type
Article
Keywords
Adult
Age Distribution
Aged
Alleles
Case-Control Studies
Comparative Study
Complement C4 - analysis - genetics
Cross-Sectional Studies
Genetics, Population
Humans
Incidence
Logistic Models
Male
Middle Aged
Myocardial Infarction - epidemiology - genetics
Reference Values
Research Support, Non-U.S. Gov't
Risk factors
Sampling Studies
Sex Distribution
Survival Rate
Sweden - epidemiology
Abstract
The classical risk factors, hypercholesterolemia, smoking, hypertension and diabetes, explain only a part of the epidemiological features of atherosclerotic coronary heart disease. Investigations in the past few years have shown involvement of immunological mechanisms in atherosclerosis. Circulating immune complexes accelerate atherosclerosis both in experimental animal models and in humans. The fourth component of complement (C4) plays an important role in the solubilisation and elimination of immune complexes. C4 consists of two allotypes, C4A and C4B. An earlier report showed an association between C4B null alleles (C4B*Q0) and myocardial infarction and to infarction related mortality. In the present investigation, C4A*Q0 and C4B*Q0 were studied in two population samples. The first (Group I) was a cross sectional study of 100 consecutive males with myocardial infarction before the age of 45 years and 164 population based healthy controls, age and sex matched. The second (Group II) was a nested case control study in which a cohort of 50 year-old males were followed for 20 years for development of myocardial infarction between 50-60 and 60-70 years, and the results compared with those who did not develop MI. We observed no association of homozygous and/or heterozygous C4A*Q0 or C4B*Q0 with myocardial infarction occurring in the age groups 0.05). The prevalence/frequency of C4A*Q0 and C4B*Q0 was not related to the age at which MI occurred. The prevalence of C4A*Q0 was not affected by age. We thus conclude that partial deficiency of C4 does not appear to be a major risk factor for myocardial infarction.
PubMed ID
10217367 View in PubMed
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Coronary heart disease risk factors in subjects whose brothers, sisters or husbands developed premature myocardial infarction during 12 years of follow-up. The Finnmark Study (1977-1989).

https://arctichealth.org/en/permalink/ahliterature203322
Source
J Cardiovasc Risk. 1998 Oct-Dec;5(5-6):325-30
Publication Type
Article
Author
T. Brenn
I. Njølstad
Author Affiliation
Institute of Community Medicine, University of Tromsø, Norway. Tormod.Brenn@ism.uit.no
Source
J Cardiovasc Risk. 1998 Oct-Dec;5(5-6):325-30
Language
English
Publication Type
Article
Keywords
Adult
Coronary Disease - epidemiology - genetics - prevention & control
Female
Finland - epidemiology
Follow-Up Studies
Humans
Hypertension - complications
Life Style
Lipids - blood
Male
Middle Aged
Myocardial Infarction - epidemiology - genetics - prevention & control
Pedigree
Risk assessment
Sex Factors
Smoking - adverse effects
Abstract
In individuals whose relatives have experienced heart disease, levels of classic risk factors may have been underestimated because of life style changes after serious family disease or inaccurate disease reports.
To overcome pitfalls noted in previous research, risk factors were measured at a screening of the general population aged 20-52 years in four Norwegian municipalities. After 12 years of follow-up, a first myocardial infarction was evident in 51 of 753 sibships and in 68 of 1518 spouse pairs.
Multiple adjusted means were higher in men with than in men without a brother or sister who became affected: 7.17 versus 6.84 mmol/l (P=0.07) for serum total cholesterol, 140.8 versus 135.6 mmHg (P=0.02) and 85.7 versus 82.5 mmHg (P=0.04) for systolic and diastolic blood pressure. Total cholesterol readings were higher the younger (P
PubMed ID
9920004 View in PubMed
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A detailed family history of myocardial infarction and risk of myocardial infarction--a nationwide cohort study.

https://arctichealth.org/en/permalink/ahliterature269546
Source
PLoS One. 2015;10(5):e0125896
Publication Type
Article
Date
2015
Author
Mattis Flyvholm Ranthe
Jonathan Aavang Petersen
Henning Bundgaard
Jan Wohlfahrt
Mads Melbye
Heather A Boyd
Source
PLoS One. 2015;10(5):e0125896
Date
2015
Language
English
Publication Type
Article
Keywords
Adult
Cohort Studies
Denmark
Diabetes Mellitus - epidemiology - genetics - pathology
Family
Female
Humans
Hypertension - epidemiology - genetics - pathology
Male
Middle Aged
Myocardial Infarction - epidemiology - genetics - pathology
Risk factors
Abstract
Family history of myocardial infarction (MI) is an independent risk factor for MI. Several genetic variants are associated with increased risk of MI and family history of MI in a first-degree relative doubles MI risk. However, although family history of MI is not a simple dichotomous risk factor, the impact of specific, detailed family histories has not received much attention, despite its high clinical relevance. We examined risk of MI by MIs in first- and second-degree relatives and by number and age of affected relatives.
Using Danish national registers, we established a nationwide cohort of persons born between 1930 and 1992 with identifiable first- or second-degree relatives. Incident MIs in both cohort members and relatives aged =20 years were identified. We calculated incidence rate ratios (IRRs) for MI by family history of MI, by Poisson regression. In 4.4 million persons followed for 104 million person-years, we identified 128,384 incident MIs. IRRs with 95% confidence intervals [CIs] for MI by history of MI in 1, 2 or =3 first-degree relatives were 1.46 (1.42-1.49), 2.38 (2.22-2.56) and 3.58 (2.66-4.81), respectively. Corresponding estimates for second-degree relatives were 1.17 (1.05-1.30), 1.87 (1.46-2.38) and 2.18 (1.09-4.36). A history of MI in combinations of first- and second-degree relatives increased risks 1.8- to 7-fold in middle-aged persons (36 to 55 years). Estimates were robust to adjustment for diabetes, hypertension, dyslipidemia and use of cardiovascular medications.
A detailed family history, particularly number of affected first- and second-degree relatives, contributes meaningfully to risk assessment, especially in middle-aged persons. Future studies should test for potential improvement of risk algorithm prediction using detailed family histories.
Notes
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PubMed ID
26011129 View in PubMed
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Elevated Lipoprotein(a) Levels, LPA Risk Genotypes, and Increased Risk of Heart Failure in the General Population.

https://arctichealth.org/en/permalink/ahliterature277021
Source
JACC Heart Fail. 2016 Jan;4(1):78-87
Publication Type
Article
Date
Jan-2016
Author
Pia R Kamstrup
Børge G Nordestgaard
Source
JACC Heart Fail. 2016 Jan;4(1):78-87
Date
Jan-2016
Language
English
Publication Type
Article
Keywords
Aged
Aortic Valve Stenosis - epidemiology - genetics
Denmark - epidemiology
Exons
Female
Genotype
Heart Failure - epidemiology - genetics
Humans
Kringles - genetics
Lipoprotein(a) - genetics - metabolism
Male
Mendelian Randomization Analysis
Middle Aged
Myocardial Infarction - epidemiology - genetics
Polymorphism, Single Nucleotide - genetics
Prospective Studies
Risk assessment
Risk factors
Abstract
This study sough to test whether elevated lipoprotein(a) levels and corresponding LPA risk genotypes (low number of kringle IV type 2 repeats, rs3798220 and rs10455872, minor allele carriers) are associated with an increased risk of heart failure (HF).
Elevated lipoprotein(a) levels represent a genetically determined risk factor for myocardial infarction (MI) and aortic valve stenosis (AVS). It is presently unknown whether elevated lipoprotein(a) levels also cause heart failure (HF).
We combined 2 general population studies, the Copenhagen City Heart Study (n = 10,855) and the Copenhagen General Population Study (n = 87,242), which totaled 98,097 Danish participants, of whom 4,122 were diagnosed with HF (1976 to 2013). We conducted observational and genetic instrumental variable analyses in a Mendelian randomization study design, assessing evidence of causality, and we performed mediation analyses.
Elevated lipoprotein(a) levels were associated with multivariable adjusted hazard ratios for HF of 1.10 (95% CI: 0.97 to 1.25) for the 34th to 66th percentiles (8 to 19 mg/dl), 1.24 (95% CI: 1.08 to 1.42) for the 67th to 90th percentiles (20 to 67 mg/dl), 1.57 (95% CI: 1.32 to 1.87) for the 91st to 99th percentiles (68 to 153 mg/dl), and 1.79 (95% CI: 1.18 to 2.73) for levels >99th percentile (>153 mg/dl) versus levels 
Notes
Comment In: JACC Heart Fail. 2016 Jan;4(1):88-926738954
PubMed ID
26656145 View in PubMed
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35 records – page 1 of 4.