Effect of APOE ε Genotype on Lipoprotein(a) and the Associated Risk of Myocardial Infarction and Aortic Valve Stenosis

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Standard

Effect of APOE ε Genotype on Lipoprotein(a) and the Associated Risk of Myocardial Infarction and Aortic Valve Stenosis. / Kritharides, Leonard; Nordestgaard, Børge G; Tybjærg-Hansen, Anne; Kamstrup, Pia R; Afzal, Shoaib.

I: Journal of Clinical Endocrinology and Metabolism, Bind 102, Nr. 9, 01.09.2017, s. 3390-3399.

Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt

Harvard

Kritharides, L, Nordestgaard, BG, Tybjærg-Hansen, A, Kamstrup, PR & Afzal, S 2017, 'Effect of APOE ε Genotype on Lipoprotein(a) and the Associated Risk of Myocardial Infarction and Aortic Valve Stenosis', Journal of Clinical Endocrinology and Metabolism, bind 102, nr. 9, s. 3390-3399. https://doi.org/10.1210/jc.2017-01049

APA

Kritharides, L., Nordestgaard, B. G., Tybjærg-Hansen, A., Kamstrup, P. R., & Afzal, S. (2017). Effect of APOE ε Genotype on Lipoprotein(a) and the Associated Risk of Myocardial Infarction and Aortic Valve Stenosis. Journal of Clinical Endocrinology and Metabolism, 102(9), 3390-3399. https://doi.org/10.1210/jc.2017-01049

Vancouver

Kritharides L, Nordestgaard BG, Tybjærg-Hansen A, Kamstrup PR, Afzal S. Effect of APOE ε Genotype on Lipoprotein(a) and the Associated Risk of Myocardial Infarction and Aortic Valve Stenosis. Journal of Clinical Endocrinology and Metabolism. 2017 sep. 1;102(9):3390-3399. https://doi.org/10.1210/jc.2017-01049

Author

Kritharides, Leonard ; Nordestgaard, Børge G ; Tybjærg-Hansen, Anne ; Kamstrup, Pia R ; Afzal, Shoaib. / Effect of APOE ε Genotype on Lipoprotein(a) and the Associated Risk of Myocardial Infarction and Aortic Valve Stenosis. I: Journal of Clinical Endocrinology and Metabolism. 2017 ; Bind 102, Nr. 9. s. 3390-3399.

Bibtex

@article{d567d6ffd199436c9bda98e7ca3bf3e6,
title = "Effect of APOE ε Genotype on Lipoprotein(a) and the Associated Risk of Myocardial Infarction and Aortic Valve Stenosis",
abstract = "Context: APOEε2/3/4 genotypes affect plasma lipoprotein(a); however, the effects of APOE genotypes on the prediction of myocardial infarction and aortic valve stenosis by lipoprotein(a) are unknown.Objective: We tested the hypothesis that APOEε2/3/4 genotype affects plasma lipoprotein(a), the contribution of plasma apoE levels to this association as well as the associated risk of myocardial infarction and aortic valve stenosis.Design and Outcome Measures: In 46,615 individuals from the general population, we examined plasma lipoprotein(a), APOE ε2/3/4, and incidence of myocardial infarction (n = 1807) and aortic valve stenosis (n = 345) over 37 years of follow-up (range: 0.3 to 38 years).Results: Compared with ε33, age- and sex-adjusted lipoprotein(a) concentrations were lower by 15% in ε23, by 24% in ε24, and by 36% in ε22; adjusted for plasma apolipoprotein E, corresponding values were 22%, 28%, and 62%. These reductions were independent of LPA genotypes. Compared with ε2 carriers with lipoprotein(a) ≤50 mg/dL, the hazard ratio for myocardial infarction was 1.26 (95% confidence interval: 1.06 to 1.49) for ε2 noncarriers with lipoprotein(a) ≤50 mg/dL, 1.68 (1.21 to 2.32) for ε2 carriers with lipoprotein(a) >50 mg/dL, and 1.92 (1.59 to 2.32) for ε2 noncarriers with lipoprotein(a) >50 mg/dL (interaction, P = 0.57); corresponding values for aortic valve stenosis were 1.05 (0.74 to 1.51), 1.49 (0.72 to 3.08), and 2.04 (1.46 to 2.26) (interaction, P = 0.50). Further adjustment for APOE ε2/3/4 genotype had minimal influence on these risk estimates.Conclusions: APOE ε2 is a strong genetic determinant of low lipoprotein(a) concentrations but does not modify the causal association of lipoprotein(a) with myocardial infarction or aortic valve stenosis.",
keywords = "Adult, Age Factors, Aged, Aortic Valve Stenosis, Apolipoproteins E, Biomarkers, Denmark, Female, Genetic Predisposition to Disease, Genotype, Humans, Incidence, Lipoprotein(a), Male, Middle Aged, Myocardial Infarction, Prognosis, Proportional Hazards Models, Registries, Regression Analysis, Retrospective Studies, Risk Assessment, Sex Factors, Survival Rate, Comparative Study, Journal Article",
author = "Leonard Kritharides and Nordestgaard, {B{\o}rge G} and Anne Tybj{\ae}rg-Hansen and Kamstrup, {Pia R} and Shoaib Afzal",
year = "2017",
month = sep,
day = "1",
doi = "10.1210/jc.2017-01049",
language = "English",
volume = "102",
pages = "3390--3399",
journal = "Journal of Clinical Endocrinology and Metabolism",
issn = "0021-972X",
publisher = "Oxford University Press",
number = "9",

}

RIS

TY - JOUR

T1 - Effect of APOE ε Genotype on Lipoprotein(a) and the Associated Risk of Myocardial Infarction and Aortic Valve Stenosis

AU - Kritharides, Leonard

AU - Nordestgaard, Børge G

AU - Tybjærg-Hansen, Anne

AU - Kamstrup, Pia R

AU - Afzal, Shoaib

PY - 2017/9/1

Y1 - 2017/9/1

N2 - Context: APOEε2/3/4 genotypes affect plasma lipoprotein(a); however, the effects of APOE genotypes on the prediction of myocardial infarction and aortic valve stenosis by lipoprotein(a) are unknown.Objective: We tested the hypothesis that APOEε2/3/4 genotype affects plasma lipoprotein(a), the contribution of plasma apoE levels to this association as well as the associated risk of myocardial infarction and aortic valve stenosis.Design and Outcome Measures: In 46,615 individuals from the general population, we examined plasma lipoprotein(a), APOE ε2/3/4, and incidence of myocardial infarction (n = 1807) and aortic valve stenosis (n = 345) over 37 years of follow-up (range: 0.3 to 38 years).Results: Compared with ε33, age- and sex-adjusted lipoprotein(a) concentrations were lower by 15% in ε23, by 24% in ε24, and by 36% in ε22; adjusted for plasma apolipoprotein E, corresponding values were 22%, 28%, and 62%. These reductions were independent of LPA genotypes. Compared with ε2 carriers with lipoprotein(a) ≤50 mg/dL, the hazard ratio for myocardial infarction was 1.26 (95% confidence interval: 1.06 to 1.49) for ε2 noncarriers with lipoprotein(a) ≤50 mg/dL, 1.68 (1.21 to 2.32) for ε2 carriers with lipoprotein(a) >50 mg/dL, and 1.92 (1.59 to 2.32) for ε2 noncarriers with lipoprotein(a) >50 mg/dL (interaction, P = 0.57); corresponding values for aortic valve stenosis were 1.05 (0.74 to 1.51), 1.49 (0.72 to 3.08), and 2.04 (1.46 to 2.26) (interaction, P = 0.50). Further adjustment for APOE ε2/3/4 genotype had minimal influence on these risk estimates.Conclusions: APOE ε2 is a strong genetic determinant of low lipoprotein(a) concentrations but does not modify the causal association of lipoprotein(a) with myocardial infarction or aortic valve stenosis.

AB - Context: APOEε2/3/4 genotypes affect plasma lipoprotein(a); however, the effects of APOE genotypes on the prediction of myocardial infarction and aortic valve stenosis by lipoprotein(a) are unknown.Objective: We tested the hypothesis that APOEε2/3/4 genotype affects plasma lipoprotein(a), the contribution of plasma apoE levels to this association as well as the associated risk of myocardial infarction and aortic valve stenosis.Design and Outcome Measures: In 46,615 individuals from the general population, we examined plasma lipoprotein(a), APOE ε2/3/4, and incidence of myocardial infarction (n = 1807) and aortic valve stenosis (n = 345) over 37 years of follow-up (range: 0.3 to 38 years).Results: Compared with ε33, age- and sex-adjusted lipoprotein(a) concentrations were lower by 15% in ε23, by 24% in ε24, and by 36% in ε22; adjusted for plasma apolipoprotein E, corresponding values were 22%, 28%, and 62%. These reductions were independent of LPA genotypes. Compared with ε2 carriers with lipoprotein(a) ≤50 mg/dL, the hazard ratio for myocardial infarction was 1.26 (95% confidence interval: 1.06 to 1.49) for ε2 noncarriers with lipoprotein(a) ≤50 mg/dL, 1.68 (1.21 to 2.32) for ε2 carriers with lipoprotein(a) >50 mg/dL, and 1.92 (1.59 to 2.32) for ε2 noncarriers with lipoprotein(a) >50 mg/dL (interaction, P = 0.57); corresponding values for aortic valve stenosis were 1.05 (0.74 to 1.51), 1.49 (0.72 to 3.08), and 2.04 (1.46 to 2.26) (interaction, P = 0.50). Further adjustment for APOE ε2/3/4 genotype had minimal influence on these risk estimates.Conclusions: APOE ε2 is a strong genetic determinant of low lipoprotein(a) concentrations but does not modify the causal association of lipoprotein(a) with myocardial infarction or aortic valve stenosis.

KW - Adult

KW - Age Factors

KW - Aged

KW - Aortic Valve Stenosis

KW - Apolipoproteins E

KW - Biomarkers

KW - Denmark

KW - Female

KW - Genetic Predisposition to Disease

KW - Genotype

KW - Humans

KW - Incidence

KW - Lipoprotein(a)

KW - Male

KW - Middle Aged

KW - Myocardial Infarction

KW - Prognosis

KW - Proportional Hazards Models

KW - Registries

KW - Regression Analysis

KW - Retrospective Studies

KW - Risk Assessment

KW - Sex Factors

KW - Survival Rate

KW - Comparative Study

KW - Journal Article

U2 - 10.1210/jc.2017-01049

DO - 10.1210/jc.2017-01049

M3 - Journal article

C2 - 28651346

VL - 102

SP - 3390

EP - 3399

JO - Journal of Clinical Endocrinology and Metabolism

JF - Journal of Clinical Endocrinology and Metabolism

SN - 0021-972X

IS - 9

ER -

ID: 184876195