We created a MI model in 16-week-old male apolipoprotein E-deficient mice (<i>n</i> = 42), which were randomly assigned to exercise group (MI-Ex) and sedentary group (MI-Sed).
In general, our findings reveal a critical role of apolipoprotein E in regulating Ly6G<sup>+</sup> neutrophil activation and NET formation, resulting in limiting myocardial injury after myocardial infarction.
We recently described that apolipoprotein E (ApoE) deficient mice with a mutation in the fibrillin-1 (Fbn1) gene (ApoE<sup>-/-</sup>Fbn1<sup>C1039G+/-</sup>) develop accelerated atherosclerosis, plaque rupture, myocardial infarction, cerebral hypoxia and sudden death.
The effect of the APOE e4-allele on the association between lifestyle factors (smoking, physical activity, being overweight, occupational attainment) and cognitive performance (trail making test [TMT] B, verbal fluency test [VFT]) was analyzed via multivariate generalized linear modeling adjusted for APOE e2-allele, age, gender, education, stroke, and heart attack.
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.
Corresponding HRs for highest versus lowest apoE tertile in ε33 carriers were 1.18 (1.03-1.36) for IHD and 1.21 (0.98-1.49) for MI in men, and 0.91 (0.78-1.06) and 0.93 (0.71-1.21) in women.
Using microarray mRNA expression profiling, we identified genes whose expression in the hearts of dKO mice changed substantially during disease progression [at 21 d of age (no CAD), 31 d of age (small myocardial infarctions), and 43 d of age (extensive myocardial infarctions) vs. CAD-free SR-BI(+/-)/apoE(-/-) controls].
We investigated a possible interaction of apolipoprotein E (APOE) gene with birthplace on the risk of myocardial infarction (MI) and coronary atherosclerosis.
For the CDR-SB, there were 3-way interactions between the APOE ε4, time and either myocardial infarction (LR χ² = 17.83, 2 df, p = 0.0001) or stroke (LR χ² = 11.48, 2 df, p = 0.003.
Our data suggest that LRP8 R952Q variant may have an additive effect to APOE epsilon2/epsilon3/epsilon4 genotype in determining ApoE concentrations and risk of MI in an Italian population.
The aim of this study was to investigate the possibility of interactions between CETP, PPARA, APOE, and APOAI polymorphisms and HDL-C, apolipoprotein (apo) A-I, lipoprotein (Lp) A-I, and Lp A-I:A-II in a sample selected from the Prospective Epidemiological Study of Myocardial Infarction (PRIME) study population who remained free of cardiovascular events over 5 years of follow-up.
In healthy blood donors and in patients with CAD complicated by myocardial infarction (MI) four apolipoprotein gene polymorphisms [APO (a) PNR, APO E, APO CI and APO CII] were determined and plasma levels of total homocysteine, total cholesterol (TC), triglycerides (TG), HDL-cholesterol (HLD-C) and apolipoproteins (apo A-I, Apo B, Apo E) were measured.
Apolipoprotein E polymorphisms influence effect of pravastatin on survival after myocardial infarction in a Mediterranean population: the GISSI-Prevenzione study.
This study supports the hypothesis that the APOE*2 and APOE*4 variants increase susceptibility to MI in the presence of high saturated fat and could explain inconsistent findings on the effects of these variants on MI in various populations.
These results indicated that carriers of APOE-epsilon4 allele have a distinct plasma lipids profile and carrier of this allele with low levels of HDL-C and with high levels of LDL-C may be susceptible to CAD and myocardial infarction specially in diabetic patients.
In patients without hypercholesterolaemia, the APOE allele epsilon4 was highly predictive for the presence of premature MI (epsilon4 55% vs. epsilon3 45% vs. epsilon2 28%; P < 0.0001; hazard ratio 1.75, 95%CI 1.19-2.57).