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.
This investigation profiled circulating serum concentrations of microRNAs (miRNAs) in premature cardiovascular disease (CVD) patients screened for the 677C > T polymorphism in methylenetetrahydrofolate reductase (MTHFR), a risk factor for hypertension.
The author summarizes a brief analysis of associated cardiovascular disease and nutritional consequences, exploring the controversial cause-effect on mortality and technique failure.Therapeutic modalities aiming to reduce PPL (angiotensin-converting enzyme inhibitors [ACEI]s and vitamin D therapies) were explored, although it is unclear whether PPL represents a valid therapeutic target or, on the other hand, is solely a manifestation of endothelial dysfunction.
BMI >45 kg/m<sup>2</sup> was associated with higher prevalence of hypertension, systolic and diastolic blood pressure, C-reactive protein, waist circumference, body fat % and family history of heart diseases, enhancing the risk for the occurrence of cardiovascular diseases.
We previously reported that the patients with cholesteryl ester transfer protein (CETP) deficiency (CETP-D) show marked changes in the size and lipid compositions of high-density lipoprotein (HDL) and that they are not protected from atherosclerotic cardiovascular diseases, despite increased serum HDL-cholesterol (HDL-C) levels.
Therefore, there appears to be a need for effective TG-lowering agents.<b>Areas covered</b>: This review presents the most recent advances in hypertriglyceridemia treatment; specifically, it discusses the results of clinical trials and critically comments on apolipoprotein C-III inhibitors, angiopoietin-like 3 inhibitors, alipogene tiparvovec, pradigastat, pemafibrate and novel formulations of omega-3 fatty acids.<b>Expert opinion</b>: In the era of extreme lowering of LDL-C levels with several agents, there seems to be space for novel therapeutic options to combat parameters responsible for residual CVD risk, among which are elevated TGs.
Furthermore, apoC-III and ANGPTL3, both of which are now known to associate with increased atherosclerotic cardiovascular diseases, were enriched in patients with CETP-D compared with normolipidemic subjects (35.9 ± 5.3 vs 27.1 ± 3.7, 2.3 ± 1.1 vs 0.4 ± 1.1, respectively; P < .01).
Cardiovascular disease risk markers included blood lipid profile (total cholesterol, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, and triglyceride levels), high-sensitivity C-reactive protein levels, and homocysteine levels, along with diagnosis of obesity, diabetes mellitus, hypertension, dyslipidemia, and ankle-brachial index measurement.
Elucidating the mechanisms by which elevated MPO leads to poor prognosis and conversely, investigating the beneficial effects of therapeutic MPO inhibition on alleviating disease phenotype, will facilitate future MPO-targeted clinical trials for improving CVD-related outcomes.
In this study, we evaluated the relationships between ET1, cardiac morphology, and incident heart failure or cardiovascular death in participants with no evidence of clinical cardiovascular disease at the time ET1 was measured.