Effect Of APOE ε Genotype On Lipoprotein(a) And The Associated Risk Of Myocardial Infarction And Aortic Valve Stenosis.

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Effect Of APOE ε Genotype On Lipoprotein(a) And The Associated Risk Of Myocardial Infarction And Aortic Valve Stenosis.

J Clin Endocrinol Metab. 2017 Jun 23;:

Authors: Kritharides L, Nordestgaard BG, Tybjærg-Hansen A, Kamstrup PR, Afzal S

Abstract
Context: Lipoprotein(a) is a genetic risk factor for myocardial infarction and aortic valve stenosis. APOE ε2/3/4 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 APOE ε2/3/4 genotype affects plasma lipoprotein(a), the contribution of plasma apoE levels this effect, and 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 0.3-38 years).
Results: Compared to ε33(frequency:55.6%), age and sex adjusted lipoprotein(a) concentrations were lower by 15% in ε23(12.4%), by 24% in ε24(2.9%), and by 36% in ε22(0.7%); adjusted for plasma apolipoprotein E, corresponding values were 22%, 28%, and 62%. APOE ε4 was also associated with lower lipoprotein(a) than ε3, but this effect attenuated after adjustment. These reductions were independent of LPA genotypes. Compared to ε2 carriers with lipoprotein(a)≤50mg/dL, the hazard ratio for myocardial infarction was 1.26(95%CI:1.06-1.49) for ε2 non-carriers with lipoprotein(a)≤50mg/dL, 1.68(1.21-2.32) for ε2 carriers with lipoprotein(a)>50mg/dL, and 1.92(1.59-2.32) for ε2 non-carriers with lipoprotein(a)>50mg/dL (interaction:P=0.57); corresponding values for aortic valve stenosis were 1.05(0.74-1.51), 1.49(0.72-3.08), and 2.04(1.46-2.26)(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.

PMID: 28651346 [PubMed - as supplied by publisher]

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