NO is synthesized from l-arginine through the action of the nitric oxide synthase (NOS) family of enzymes, which includes three isoforms: endothelial NOS (eNOS), neuronal NOS (nNOS) and inducible NOS (iNOS). iNOS-derived NO has been associated with the pathogenesis and progression of several diseases, including liver diseases, insulin resistance, obesity and diseases of the cardiovascular system.
This study suggests that Lp(a)-lowering by 50 mg/dL (105 nmol/L) short-term (ie, 5 years) may reduce CVD by 20% in a secondary prevention setting.High Lp(a) (Lipoprotein[a]) is associated with high risk of incident cardiovascular disease (CVD) in observational studies of individuals without CVD at baseline<sup>1, 2</sup>, that is, in a primary prevention setting.
Patients with metabolic syndrome (MetS) are at high risk of developing cardiovascular disease (CVD) and lipoprotein(a) (Lp(a)) is an independent risk factor for CVD.
Cytochrome P450 2D6 (CYP2D6) and endothelial nitric oxide synthase (eNOS) are important in the cardiovascular disease susceptibility and drug response.
The low frequency of the APOE ∊4 allele may suggest a low genetic risk of Hakka population for cardiovascular disease, Alzheimer's disease, and other diseases.
Fasting Apolipoprotein B48 (ApoB48) is reported to be a well surrogate marker for postprandial lipidemia and have been repeatedly associated with cardiovascular disease.
Lipoprotein (a) and 10-year Cardiovascular Disease Incidence in Apparently Healthy Individuals: A Sex-based Sensitivity Analysis from ATTICA Cohort Study.
Several lipoprotein(a)-lowering therapies are currently being developed with the long-term goal of reducing cardiovascular disease and mortality; however, the relationship between lipoprotein(a) and mortality is unclear.
Intraindividual (or 'visit-to-visit') variability of total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), apolipoprotein B, high-density lipoprotein cholesterol (HDL-C), non-HDL-C, and triglyceride have all been found to associate with CVD outcomes, independent of their mean absolute levels, independent of each other, and independent of other traditional risk factors.
Lowering apolipoprotein B secretion from HepG2 cells and decreasing the level of low-density lipoprotein (LDL)-cholesterol oxidation are mechanisms related to the prevention of cardiovascular diseases (CVD).
To compare the association of triglyceride-lowering variants in the lipoprotein lipase (LPL) gene and LDL-C-lowering variants in the LDL receptor gene (LDLR) with the risk of cardiovascular disease per unit change in ApoB.
Inherited abnormalities in apolipoprotein E (ApoE) or low-density lipoprotein receptor (LDLR) function result in early onset cardiovascular disease and death.
The high prevalence of short sleep duration and its strong association with elevated apoB in adults who are metabolically unhealthy overweight/obese suggest an increased risk of cardiovascular disease in this population.
Those with evidence of CAD were significantly more likely to be male, inactive, diabetic and with a family history of CVD than participants without CAD.About 20% of patients had lipoprotein(a) (Lp(a)) concentrations above 106.9 nmol/L (fifth quintile).
Malondialdehyde, lipoprotein-a, lipoprotein ratios, comprehensive lipid tetrad index and atherogenic index as surrogate markers for cardiovascular disease in patients with psoriasis: a case-control study.
Lipoprotein (a) [Lp(a)] is an established causal risk factor for cardiovascular disease (CVD), independently of low-density lipoproteins (LDL) and other risk factors.