A total of 538 proteins are quantified, with pregnancy zone protein (PZP), leucine-rich α-2-glycoprotein (LRG) and Apolipoprotein C-I (Apo C-I) being upregulated and Apolipoprotein A-I (Apo A-I) and Apolipoprotein A-IV (Apo A-IV) downregulated in early-onset MI patients.
CSL112, a reconstituted, infusible, plasma-derived apolipoprotein A-I: safety and tolerability profiles and implications for management in patients with myocardial infarction.
We aimed to determine whether autoantibodies against apoA-1 (apolipoprotein A-1; anti-apoA-1 IgG) predict incident coronary artery disease (CAD), defined as adjudicated incident myocardial infarction, angina, percutaneous coronary revascularization, or bypass grafting, in the general population.
There were two serious adverse events (myocardial infarctions) in the IONIS-APO(a)<sub>Rx</sub> phase 2 trial, one in the IONIS-APO(a)<sub>Rx</sub> and one in the placebo group, but neither were thought to be treatment related.
In this study we have performed biophysical and biochemical analyses of the structure and functional properties of the A164S variant of apoA-I (1:500 in the Danish general population), which is the first known mutation of apoA-I that leads to an increased risk of ischaemic heart disease (IHD), myocardial infarction and mortality without associated low HDL cholesterol levels.
Bioinformatic analysis of this differential gene-set for associated pathways revealed 1) increasing disease severity in AMI patients is associated with a decreased expression of genes involved in the developmental epithelial-to-mesenchymal transition pathway, and 2) modulation of cholesterol transport genes that include ABCA1, CETP, APOA1, and LDLR is associated with clinical outcome.
Influence of cholesteryl ester transfer protein, peroxisome proliferator-activated receptor alpha, apolipoprotein E, and apolipoprotein A-I polymorphisms on high-density lipoprotein cholesterol, apolipoprotein A-I, lipoprotein A-I, and lipoprotein A-I:A-II concentrations: the Prospective Epidemiological Study of Myocardial Infarction study.
We report a novel apolipoprotein A-I (apoA-I) mutation identified in a 64-year-old patient with marked plasma high density lipoprotein (HDL) cholesterol (4 mg/dl) and apoA-I (5mg/dl) deficiency, prior myocardial infarction, and moderate corneal opacities.
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.
Our results show that levels of ApoB, LDL-C and ApoB/ApoA-1 might be better predictors in children from families of very early MI as compared with ApoA-1, HDL-C and LDL/ApoB.
Our results show that levels of ApoB, LDL-C and ApoB/ApoA-1 might be better predictors in children from families of very early MI as compared with ApoA-1, HDL-C and LDL/ApoB.
The B2 allele of the cholesteryl ester transfer protein TaqIb polymorphism was associated with a significantly lower plasma apoB/apoA(1) ratio, but with no significant difference in the risk of MI.
The APO A-1 to B ratio was inversely associated with both myocardial infarction and stroke and may be an important protective clinical marker for atherosclerosis.
Comparative analysis of apo(a) gene alleles: distribution of pentanucleotide repeats in position -1373 and C/T transition in position +93 among patients with myocardial infarction and a control group in St. Petersburg, Russia.
In addition, in a subgroup of individuals with a higher risk of MI by either high apoB and/or low apoA1 plasma levels the portion of MI patients was clearly smaller within H2H2 homozygotes than within H1H2 or H1H1 genotypes, although-also in these high risk groups-mean age at first MI of H2H2 individuals were higher than of the other two genotypes.
Thus genetic variation in the promoter region of the apo AI gene is associated with differences in apo AI and HDL levels in healthy individuals throughout Europe, but the effect is modulated by gender, environmental factors such as smoking, and a family history of MI.
High density lipoprotein cholesterol and apolipoprotein A-I were higher in children with family history of stable angina than in children with family history of myocardial infarction and control subjects (69 +/- 18 vs. 61 +/- 13 and 60 +/- 13 mg%, p < 0.01; 143 +/- 23 vs. 130 +/- 18 and 129 +/- 18 mg%, p < 0.01, respectively).