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The -629C>A polymorphism in the CETP gene does not explain the association of TaqIB polymorphism with risk and age of myocardial infarction in Icelandic men.

https://arctichealth.org/en/permalink/ahliterature53840
Source
Atherosclerosis. 2001 Nov;159(1):187-92
Publication Type
Article
Date
Nov-2001
Author
G. Eiriksdottir
M K Bolla
B. Thorsson
G. Sigurdsson
S E Humphries
V. Gudnason
Author Affiliation
Molecular Genetics Laboratory, Hjartavernd, Icelandic Heart Association, Lagmuli 9, 108, Reykjavik, Iceland. gudny@hjarta.is
Source
Atherosclerosis. 2001 Nov;159(1):187-92
Date
Nov-2001
Language
English
Publication Type
Article
Keywords
Aged
Carrier Proteins - genetics
Gene Frequency
Genotype
Glycoproteins
Homozygote
Humans
Iceland
Linkage Disequilibrium
Lipids - blood
Lipoproteins, HDL Cholesterol - blood
Male
Myocardial Infarction - blood - genetics
Polymerase Chain Reaction
Polymorphism, Genetic
Promoter Regions (Genetics) - genetics
Prospective Studies
Research Support, Non-U.S. Gov't
Risk factors
Abstract
The aim of this study was to examine whether the well-established effect of the common TaqIB polymorphism in intron 1 of the gene for cholesterol ester transfer protein (CETP) on high density lipoprotein cholesterol (HDL-C) concentration and increased risk of myocardial infarction (MI), could be explained by the recently identified -629C>A functional polymorphism in the promoter. Non-fatal MI cases (388 male) and a control group of 794 healthy men were recruited from the 30 year long prospective Reykjavik Study. In the healthy men the frequency of the TaqIB B2 allele was 0.47 (95% CI: 0.44-0.50) and there was a strong allelic association with the -629A allele (D=-0.21, P
PubMed ID
11689220 View in PubMed
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Aggregation of lipoprotein and inflammatory parameters in families with a history of premature myocardial infarction: the Tallinn myocardial infarction study.

https://arctichealth.org/en/permalink/ahliterature154200
Source
Clin Chem Lab Med. 2008;46(11):1602-8
Publication Type
Article
Date
2008
Author
Katrin Aasvee
Elvira Kurvinen
Jouko Sundvall
Matti Jauhiainen
Inna Tur
Author Affiliation
Department of Chronic Disease Prevention, National Institute for Health Development, Tallinn, Estonia. katrin.aasvee@tai.ee
Source
Clin Chem Lab Med. 2008;46(11):1602-8
Date
2008
Language
English
Publication Type
Article
Keywords
Acute-Phase Proteins - metabolism
Adolescent
Adult
Age Factors
Apolipoprotein A-I - blood
Apolipoproteins B - blood
Apolipoproteins E - genetics
C-Reactive Protein - metabolism
Child
Cholesterol - blood
Cholesterol, HDL - blood
Cholesterol, LDL - blood
Family Health
Female
Finland
Humans
Lipoprotein(a) - blood
Lipoproteins - blood
Male
Middle Aged
Myocardial Infarction - blood - genetics
Polymorphism, Genetic
Risk factors
Sex Factors
Triglycerides - blood
Abstract
The offspring of individuals with a history of premature myocardial infarction are at increased risk of premature coronary attacks. The aim of this study was to determine parent/offspring associations of coronary risk factors in families affected by premature myocardial infarction and to compare these to corresponding control families.
The cohort of cases consisted of 71 male survivors of myocardial infarction and their 128 descendants (aged 7-18 years). As control families, 85 randomly selected healthy males with their 66 descendants were investigated. Besides traditional risk factors, serum high sensitive C-reactive protein (hsCRP), apolipoprotein (apo) E phenotypes and lipoprotein(a) were analyzed.
In the offspring of the patients, fibrinogen and atherogenic lipoprotein parameters were higher than in the corresponding controls, but hsCRP, lipoprotein(a) and anthropometric data did not differ between the groups. The adult-offspring positive correlations were detected in fibrinogen and in almost all measured lipoprotein fractions in the affected families; amongst the controls, the association was observed only for triglyceride levels. Multiple logistic regression analysis demonstrated independent association of offspring apoB, apoA-I and fibrinogen levels with a family history of premature myocardial infarction.
The most informative predictors of future coronary attacks during childhood are apoB-100 and apoB/apoA-I ratio; serum hsCRP and lipoprotein(a) do not have predictive value in childhood.
PubMed ID
19012525 View in PubMed
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Associations between lipoprotein lipase gene polymorphisms and plasma correlations of lipids, lipoproteins and lipase activities in young myocardial infarction survivors and age-matched healthy individuals from Sweden.

https://arctichealth.org/en/permalink/ahliterature55071
Source
Atherosclerosis. 1992 Dec;97(2-3):171-85
Publication Type
Article
Date
Dec-1992
Author
R E Peacock
A. Hamsten
P. Nilsson-Ehle
S E Humphries
Author Affiliation
University College and Middlesex School of Medicine, Department of Medicine, Rayne Institute, London, UK.
Source
Atherosclerosis. 1992 Dec;97(2-3):171-85
Date
Dec-1992
Language
English
Publication Type
Article
Keywords
Adult
Age Factors
Alleles
Genotype
Humans
Lipase - blood
Lipids - blood
Lipoprotein Lipase - blood - genetics
Lipoproteins - blood
Male
Middle Aged
Myocardial Infarction - blood - genetics
Polymorphism, Genetic
Research Support, Non-U.S. Gov't
Abstract
Association studies were carried out on a sample of 87 patients from Sweden who had survived a myocardial infarction (MI) at a young age and 93 age-matched healthy individuals, to compare the impact of polymorphisms (PvuII, HindIII and Serine447-Stop) at the lipoprotein lipase (LPL) gene locus on among-individual differences in plasma lipid traits and progression of atherosclerosis. Significant linkage disequilibrium was detected between any two of these polymorphisms, with the Stop447 allele being only found on the same chromosome as the rare alleles (no cutting sites) of the PvuII and HindIII polymorphisms. In the healthy individuals, weak associations were found between genotypes of the HindIII polymorphism and triglycerides and the PvuII polymorphism and high density lipoprotein cholesterol explaining 7.4% and 5.6% of sample variance (P = 0.03 and 0.09), respectively. No associations were found between these traits and genotypes of the Serine447-Stop substitution, and thus it is unlikely to be the cause of the associations seen with the PvuII and HindIII polymorphisms even though it truncates the enzyme amino acid sequence. The presence of the rare allele, H-, of the HindIII polymorphism was associated with a smaller variance in triglycerides and both cholesterol and triglycerides in the very low density lipoprotein fraction, and with larger interdependent variation between these lipid traits, and also between LPL activity and these lipid traits. This implies that the H- allele, rather than the Stop447 allele, has the major impact on interdependence between traits which are directly or indirectly influenced by LPL activity. In the healthy individuals who were carriers of the apolipoprotein E2 allele, the inter-dependence between LPL activity and lipid traits was significantly smaller, and that between high density lipoprotein cholesterol and both cholesterol and triglycerides in the very low density lipoprotein fraction was much larger compared with non-carriers (P
PubMed ID
1466662 View in PubMed
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CARD8 gene encoding a protein of innate immunity is expressed in human atherosclerosis and associated with markers of inflammation.

https://arctichealth.org/en/permalink/ahliterature114521
Source
Clin Sci (Lond). 2013 Oct;125(8):401-7
Publication Type
Article
Date
Oct-2013
Author
Geena Varghese Paramel
Lasse Folkersen
Rona J Strawbridge
Ali Ateia Elmabsout
Eva Särndahl
Pia Lundman
Jan-Håkan Jansson
Göran K Hansson
Allan Sirsjö
Karin Fransén
Author Affiliation
Department of Clinical Medicine, School of Health and Medical Sciences, Örebro University, Örebro, Sweden.
Source
Clin Sci (Lond). 2013 Oct;125(8):401-7
Date
Oct-2013
Language
English
Publication Type
Article
Keywords
Atherosclerosis - blood - genetics
Biological Markers - blood
C-Reactive Protein - metabolism
CARD Signaling Adaptor Proteins - genetics
Chemokine CCL2 - blood
Cohort Studies
Cytokines - blood
Gene Expression Profiling
Gene Frequency
Genotype
Humans
Immunity, Innate - genetics
Inflammation - blood - genetics
Inflammation Mediators - blood
Myocardial Infarction - blood - genetics
Neoplasm Proteins - genetics
Oligonucleotide Array Sequence Analysis
Plaque, Atherosclerotic - blood - genetics
Polymorphism, Single Nucleotide
Risk factors
Sweden
Abstract
Inflammation is a key factor in the development of atherosclerotic coronary artery disease. It is promoted through the inflammasome, a molecular machine that produces IL (interleukin)-1? in response to cholesterol crystal accumulation in macrophages. The CARD8 (caspase recruitment domain 8) protein modulates this process by suppressing caspase 1 and the transcription factor NF-?B (nuclear factor ?B). The expression of CARD8 mRNA was examined in atherosclerotic vascular tissue and the impact on MI (myocardial infarction) of a polymorphism in the CARD8 gene determined. CARD8 mRNA was analysed by microarray of human atherosclerotic tissue and compared with transplant donor arterial tissue. Microarray analysis was performed for proximal genes associated with the rs2043211 locus in plaque. The CARD8 rs2043211 polymorphism was analysed by genotyping of two Swedish MI cohorts, FIA (First Myocardial Infarction in Northern Sweden) and SCARF (Stockholm Coronary Atherosclerosis Risk Factor). The CRP (C-reactive protein) level was measured in both cohorts, but the levels of the pro-inflammatory cytokines IL-1?, IL-18, TNF (tumour necrosis factor) and MCP-1 (monocyte chemoattractant protein) were measured in sera available from the SCARF cohort. CARD8 mRNA was highly expressed in atherosclerotic plaques compared with the expression in transplant donor vessel (P
PubMed ID
23611467 View in PubMed
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hTERT (-1327)T/C polymorphism is not associated with age-related telomere attrition in peripheral blood.

https://arctichealth.org/en/permalink/ahliterature77126
Source
Biochem Biophys Res Commun. 2007 Jun 22;358(1):215-8
Publication Type
Article
Date
Jun-22-2007
Author
Nordfjäll Katarina
Osterman Pia
Melander Olle
Nilsson Peter
Roos Göran
Author Affiliation
Department of Medical Biosciences, Pathology, By 6M, 2nd floor, Umeå University, SE-90187 Umeå, Sweden.
Source
Biochem Biophys Res Commun. 2007 Jun 22;358(1):215-8
Date
Jun-22-2007
Language
English
Publication Type
Article
Keywords
Aged
Aging - genetics
Female
Genomic Instability
Genotype
Humans
Male
Middle Aged
Myocardial Infarction - blood - genetics
Polymorphism, Genetic
Sweden
Telomerase - blood - genetics
Telomere - genetics - ultrastructure
Abstract
Regulation of the telomerase catalytic subunit, hTERT, is a complex process accomplished on many levels. Transcription of the hTERT gene has been widely studied but less is known about the implication of genetic variations. Recently, a functional T to C transition polymorphism was indicated 1327 bp upstream the hTERT transcription starting site. The (-1327)C/C genotype was associated with shorter telomere length compared to the alternative genotypes in healthy individuals and in coronary artery disease patients. We tested this observation and analysed telomere length and the (-1327)T/C polymorphism in 226 myocardial infarction patients and 444 controls from southern Sweden. No significant difference in telomere length was found among the genotypes after age adjustments in the control group (p=0.794) or in the MI group (p=0.339). Moreover, no increased age-related attrition was observed for the (-1327)C/C genotype as previously indicated, rather a telomere elongation in the control group (p=0.021) not seen in the MI group (p=0.249).
PubMed ID
17481586 View in PubMed
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Influence of eotaxin 67G>A polymorphism on plasma eotaxin concentrations in myocardial infarction survivors and healthy controls.

https://arctichealth.org/en/permalink/ahliterature82702
Source
Atherosclerosis. 2006 Dec;189(2):458-63
Publication Type
Article
Date
Dec-2006
Author
Sheikine Yuri
Olsen Birgitta
Gharizadeh Baback
Jatta Ken
Tornvall Per
Ghaderi Mehran
Author Affiliation
Experimental Cardiovascular Research Unit, Center for Molecular Medicine L8:03, Karolinska University Hospital, SE-17176, Stockholm, Sweden. yuri.sheikine@cmm.ki.se
Source
Atherosclerosis. 2006 Dec;189(2):458-63
Date
Dec-2006
Language
English
Publication Type
Article
Keywords
Chemokines, CC - blood - genetics
Chemotactic Factors, Eosinophil
DNA - genetics
Female
Follow-Up Studies
Gene Frequency
Humans
Male
Middle Aged
Myocardial Infarction - blood - genetics - mortality
Polymerase Chain Reaction
Polymorphism, Genetic
Prognosis
Retrospective Studies
Severity of Illness Index
Survival Rate
Sweden - epidemiology
Abstract
Eotaxin (CCL11) is a CC chemokine, whose systemic levels might be associated with coronary artery disease (CAD) and genetic variants predispose to the myocardial infarction (MI). However, the relationship between eotaxin genetic variants and plasma concentrations in CAD patients is still incompletely characterized. We genotyped 311 patients, who survived first MI and 338 controls for a 67G>A single nucleotide polymorphism in the eotaxin gene. By measuring plasma eotaxin concentrations in those subjects we related the former to the presence of 67G>A SNP. There were no differences in eotaxin genotype frequencies between patients and controls. Patient G/G carriers had higher circulating eotaxin levels compared both to G/A and A/A patients (P=0.046) and G/G controls (P=0.028), which might indicate the influence of additional factors (e.g. inflammatory mediators) on eotaxin secretion in those patients. At the same time, eotaxin levels did not differ between patients and controls irrespective of the 67G>A SNP variants they carried. There were no associations between plasma eotaxin levels, biochemical indicators of CAD and the degree of coronary artery stenosis in post-MI patients. Interestingly, some medications taken by the patients (e.g. diuretics and short-acting nitrates) might affect plasma eotaxin levels. In conclusion, our results show that there is no clear association between the presence of eotaxin 67G>A SNP, its plasma levels and CAD parameters in post-MI patients and that circulating eotaxin levels do not differ between subjects with clinical manifestations of coronary atherosclerosis and healthy controls.
PubMed ID
16510147 View in PubMed
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Insertion/deletion (I/D) polymorphism at the locus for angiotensin I-converting enzyme and myocardial infarction.

https://arctichealth.org/en/permalink/ahliterature54964
Source
Clin Genet. 1993 Dec;44(6):292-7
Publication Type
Article
Date
Dec-1993
Author
M. Bøhn
K E Berge
A. Bakken
J. Erikssen
K. Berg
Author Affiliation
Institute of Medical Genetics, University of Oslo, Norway.
Source
Clin Genet. 1993 Dec;44(6):292-7
Date
Dec-1993
Language
English
Publication Type
Article
Keywords
Apolipoproteins B - analysis
Body mass index
Case-Control Studies
DNA - blood
Female
Follow-Up Studies
Gene Deletion
Gene Frequency
Genotype
Humans
Lipids - blood
Male
Middle Aged
Myocardial Infarction - blood - genetics
Norway
Peptidyl-Dipeptidase A - genetics
Polymerase Chain Reaction
Polymorphism, Genetic - genetics
Research Support, Non-U.S. Gov't
Risk factors
Sex Factors
Abstract
Male (n = 185) and female (n = 49) survivors of myocardial infarction (MI) below 56 and 61 years of age, respectively, were compared to 366 controls with respect to distribution of genotypes in an insertion/deletion (ID) polymorphism at the angiotensin I-converting enzyme (ACE) locus. The frequency of the DD genotype (homozygosity for the deletion allele) was significantly lower among male patients than controls (22.7% versus 34.9%, p = 0.011). In a "low-risk" group, defined as having less than the sex-specific, age-adjusted median values of body mass index (BMI) and apolipoprotein B (apoB), respectively, and absence of treatment with lipid-lowering drugs, the prevalence of the DD genotype was not statistically different between male patients and controls. In a male "high-risk" group (those individuals who had not been defined as "low-risk" subjects), the prevalence of the DD genotype was 20.9% in patients and 38.3% in controls (p = 0.002). In women, no significant differences in genotype frequencies between patients and controls were found in the whole sample or in any subgroup. These results appear to be at variance with data reported recently by Cambien et al. (1992). The difference may be due to chance, undetected selection biases, different gene-environment interactions between Norway and France or Ireland, or to preferential loss of DD individuals in our male "high-risk" group.
PubMed ID
8131299 View in PubMed
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Insight into the nature of the CRP-coronary event association using Mendelian randomization.

https://arctichealth.org/en/permalink/ahliterature170062
Source
Int J Epidemiol. 2006 Aug;35(4):922-31
Publication Type
Article
Date
Aug-2006
Author
Juan P Casas
Tina Shah
Jackie Cooper
Emma Hawe
Alex D McMahon
Dairena Gaffney
Christopher J Packard
Denis S O'Reilly
Irene Juhan-Vague
John S Yudkin
Elena Tremoli
Maurizio Margaglione
Giovanni Di Minno
Anders Hamsten
Teake Kooistra
Jeffrey W Stephens
Steven J Hurel
Shona Livingstone
Helen M Colhoun
George J Miller
Leonelo E Bautista
Tom Meade
Naveed Sattar
Steve E Humphries
Aroon D Hingorani
Author Affiliation
Centre for Clinical Pharmacology, Department of Medicine, BHF Laboratories at University College London, UCL, London, UK.
Source
Int J Epidemiol. 2006 Aug;35(4):922-31
Date
Aug-2006
Language
English
Publication Type
Article
Keywords
C-Reactive Protein - analysis - genetics
Gene Frequency
Genetic Predisposition to Disease
Genotype
Homozygote
Humans
Linkage Disequilibrium
Male
Myocardial Infarction - blood - genetics
Odds Ratio
Phenotype
Polymorphism, Genetic
Risk Assessment - methods
Abstract
It is unclear wheather the association between C-reactive protein (CRP) and incident coronary events is free from bias and confounding. Individuals homozygous for a +1444C>T polymorphism in the CRP gene have higher circulating concentrations of CRP. Since the distribution of this polymorphism occurs at random during gamete formation, its association with coronary events should not be biased or confounded.
We calculated the weighted mean difference in CRP between individuals with variants of the +1444C>T polymorphism in the CRP gene among 4,659 European men from six studies (genotype-intermediate phenotype studies). We used this difference together with data from previous observational studies to compute an expected odds ratio (OR) for non-fatal myocardial infarction (MI) among individuals homozygous for the T allele. We then performed four new genetic association studies (6,201 European men) to obtain a summary OR for the association between the +1444C>T polymorphism and non-fatal MI (genotype-disease studies).
CRP was 0.68 mg/l [95% confidence interval (95% CI) 0.31-1.10; P = 0.0001] higher among subjects homozygous for the +1444-T allele, with no confounding by a range of covariates. The expected ORs among TT subjects for non-fatal MI corresponding to this difference in CRP was 1.20 (95% CI 1.07-1.38) using the Reykjavik Heart study data and 1.25 (1.09-1.43) for all observational studies to 2004. The estimate for the observed adjusted-OR for non-fatal MI among TT subjects was 1.01 (95% CI 0.74-1.38), lower than both expected ORs.
A common CRP gene polymorphism is associated with important differences in CRP concentrations, free from confounding. The null association of this variant with coronary events suggests possible residual confounding (or reverse causation) in the CRP-coronary event association in observational studies, though the confidence limits are still compatible with a modest causal effect. Additional studies of genotype (or haplotype) and coronary events would help clarify whether or not the link between CRP and coronary events in observational studies is causal.
Notes
Comment In: Int J Epidemiol. 2006 Aug;35(4):932-416854935
PubMed ID
16565153 View in PubMed
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Interaction of the lipoprotein lipase asparagine 291-->serine mutation with body mass index determines elevated plasma triacylglycerol concentrations: a study in hyperlipidemic subjects, myocardial infarction survivors, and healthy adults.

https://arctichealth.org/en/permalink/ahliterature54731
Source
J Lipid Res. 1995 Oct;36(10):2104-12
Publication Type
Article
Date
Oct-1995
Author
R M Fisher
F. Mailly
R E Peacock
A. Hamsten
M. Seed
J S Yudkin
U. Beisiegel
G. Feussner
G. Miller
S E Humphries
Author Affiliation
Department of Medicine, University College London Medical School, Rayne Institute, UK.
Source
J Lipid Res. 1995 Oct;36(10):2104-12
Date
Oct-1995
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Aged
Amino Acid Sequence
Arginine - chemistry
Base Sequence
Body mass index
Case-Control Studies
Female
Humans
Hyperlipidemia - blood - genetics
Lipoprotein Lipase - chemistry - genetics
Male
Middle Aged
Molecular Sequence Data
Mutation
Myocardial Infarction - blood - genetics - mortality
Research Support, Non-U.S. Gov't
Serine - chemistry
Survivors
Triglycerides - blood
Variation (Genetics)
Abstract
A mutation in the lipoprotein lipase (LPL) gene, resulting in the substitution of asparagine by serine at residue 291 (LPL-S291), was found to occur in young survivors of a myocardial infarction from Sweden, combined hyperlipidemic subjects from the United Kingdom, and type III hyperlipidemic subjects from Germany at allelic carrier frequencies no different from those found in companion healthy control subjects (3.63 vs. 3.37; 1.85 vs. 1.60; and 2.00 vs. 1.56%, respectively). In a group of 620 healthy middle-aged men from the United Kingdom with baseline and three subsequent annual lipid measurements, mean plasma triacylglycerol (TG), (but not plasma cholesterol) concentrations in carriers of the mutation were significantly elevated over non-carriers (1.95 vs. 1.61 mmol/l, P = 0.05, and 5.83 vs. 5.65 mmol/l, P = 0.29, respectively). When these healthy control subjects were divided according to tertiles of body mass index (BMI), as expected, non-carriers whose BMI was in the upper two tertiles (BMI > or = 25.0 kg/m2) had higher plasma TG concentrations than those in the lowest tertile (1.90 vs. 1.54 mmol/l), but this difference was much greater in LPL-S291 carriers (2.33 vs. 1.36 mmol/l, P = 0.01, BMI x genotype interaction, P = 0.02). To confirm this effect, a second group of 319 healthy subjects from the United Kingdom was screened for LPL-S291. The allelic frequency of the mutation was found to be 1.88% and the effect on plasma lipid concentrations was very similar to that observed in the first control group (plasma TG, 2.31 vs. 1.27 mmol/l, P or = 23.3 kg/m2) had higher plasma TG concentrations than non-carriers (2.31 vs. 1.42 mmol/l). Thus, the LPL-S291 variant may predispose individuals to elevated plasma TG concentrations under conditions such as increased BMI.
PubMed ID
8576637 View in PubMed
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Lipoprotein (a) as a risk factor for atherosclerotic diseases.

https://arctichealth.org/en/permalink/ahliterature55539
Source
Pages 458-461 in H. Linderholm et al., eds. Circumpolar Health 87. Proceedings of the Seventh International Congress on Circumpolar Health, Umeå, Sweden, 1987. Arctic Medical Research. 1988;47 Supp 1.
Publication Type
Article
Date
1988
  1 document  
Author
Dahlén, D.H.
Dahlen, G.H.
Author Affiliation
Department of Clinical Chemistry, University of Umeå, Umeå, Sweden
Source
Pages 458-461 in H. Linderholm et al., eds. Circumpolar Health 87. Proceedings of the Seventh International Congress on Circumpolar Health, Umeå, Sweden, 1987. Arctic Medical Research. 1988;47 Supp 1.
Date
1988
Language
English
Geographic Location
Sweden
Publication Type
Article
Digital File Format
Text - PDF
Physical Holding
Alaska Medical Library
Keywords
Adult
Coronary Arteriosclerosis - blood - genetics
Genes, Dominant
Humans
Lipoprotein(a)
Lipoproteins - blood - genetics
Male
Myocardial Infarction - blood - genetics
Risk factors
Sweden
PubMed ID
2978804 View in PubMed
Documents
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17 records – page 1 of 2.