scholarly journals Metabolic Pathway Genes Associated with Susceptibility Genes to Coronary Artery Disease

2018 ◽  
Vol 2018 ◽  
pp. 1-12 ◽  
Author(s):  
Heng Lu ◽  
Yi Chen ◽  
Linlin Li
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Metabolic Pathway ◽  
Metabolic Pathways ◽  
Blood Lipids ◽  
Single Gene ◽  
Susceptibility Genes ◽  
Metabolic Factors ◽  
Citrate Cycle ◽  
Artery Disease

Coronary artery disease (CAD) is one of the leading threats to global health. Previous research has proven that metabolic pathway disorders, such as high blood lipids and diabetes, are one of the risk factors that mostly cause CAD. However, the crosstalk between metabolic pathways and CAD was mostly studied on physiology processes by analyzing a single gene function. A canonical correlation analysis was used to identify the metabolic pathways, which were integrated as a unit to coexpress with CAD susceptibility genes, and to resolve additional metabolic factors that are related to CAD. Seven pathways, including citrate cycle, ubiquinone, terpenoid quinone biosynthesis, and N-glycan biosynthesis, were identified as an integrated unit coexpressed with CAD genes. These pathways could not be revealed as a coexpressed pathway through traditional methods as each single gene has weak correlation. Furthermore, sets of genes in these pathways were candidate markers for diagnosis and detection from patients’ serum.

scholarly journals Metabolic Signatures in Coronary Artery Disease: Results from the BioHEART-CT Study

Cells ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 980
Author(s):  
Stephen T. Vernon ◽  
Owen Tang ◽  
Taiyun Kim ◽  
Adam S. Chan ◽  
Katharine A. Kott ◽  
...  
Keyword(s):  
Risk Factors ◽  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Metabolic Pathways ◽  
Plasma Metabolites ◽  
Effective Prevention ◽  
Calcified Plaque ◽  
Novel Biomarkers ◽  
Traditional Risk Factors ◽  
Artery Disease

Despite effective prevention programs targeting cardiovascular risk factors, coronary artery disease (CAD) remains the leading cause of death. Novel biomarkers are needed for improved risk stratification and primary prevention. To assess for independent associations between plasma metabolites and specific CAD plaque phenotypes we performed liquid chromatography mass-spectrometry on plasma from 1002 patients in the BioHEART-CT study. Four metabolites were examined as candidate biomarkers. Dimethylguanidino valerate (DMGV) was associated with presence and amount of CAD (OR) 1.41 (95% Confidence Interval [CI] 1.12–1.79, p = 0.004), calcified plaque, and obstructive CAD (p < 0.05 for both). The association with amount of plaque remained after adjustment for traditional risk factors, ß-coefficient 0.17 (95% CI 0.02–0.32, p = 0.026). Glutamate was associated with the presence of non-calcified plaque, OR 1.48 (95% CI 1.09–2.01, p = 0.011). Phenylalanine was associated with amount of CAD, ß-coefficient 0.33 (95% CI 0.04–0.62, p = 0.025), amount of calcified plaque, (ß-coefficient 0.88, 95% CI 0.23–1.53, p = 0.008), and obstructive CAD, OR 1.84 (95% CI 1.01–3.31, p = 0.046). Trimethylamine N-oxide was negatively associated non-calcified plaque OR 0.72 (95% CI 0.53–0.97, p = 0.029) and the association remained when adjusted for traditional risk factors. In targeted metabolomic analyses including 53 known metabolites and controlling for a 5% false discovery rate, DMGV was strongly associated with the presence of calcified plaque, OR 1.59 (95% CI 1.26–2.01, p = 0.006), obstructive CAD, OR 2.33 (95% CI 1.59–3.43, p = 0.0009), and amount of CAD, ß-coefficient 0.3 (95% CI 0.14–0.45, p = 0.014). In multivariate analyses the lipid and nucleotide metabolic pathways were both associated with the presence of CAD, after adjustment for traditional risk factors. We report novel associations between CAD plaque phenotypes and four metabolites previously associated with CAD. We also identified two metabolic pathways strongly associated with CAD, independent of traditional risk factors. These pathways warrant further investigation at both a biomarker and mechanistic level.

scholarly journals Comparison of the Reduction of LDL-C or nonHDL-C induced by Red Yeast Rice Extract, Xuezhikang, between Fasting and Postprandial States in Patients with Coronary Artery Disease

2020 ◽  
Author(s):  
Li-Yuan Zhu ◽  
Xing-Yu Wen ◽  
Qun-Yan Xiang ◽  
Li-Ling Guo ◽  
Jin Xu ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Blood Lipids ◽  
Density Lipoprotein ◽  
Lipoprotein Cholesterol ◽  
Red Yeast Rice ◽  
Red Yeast ◽  
Significant Difference ◽  
Artery Disease ◽  
Standard Breakfast

Abstract Background: Xuezhikang, an extract of red yeast rice, effectively lowers fasting and postprandial triglyceride (TG) levels. It was unknown that whether Xuezhikang could contribute the lipid management goals, low-density lipoprotein cholesterol (LDL-C) and non-high-density lipoprotein cholesterol (nonHDL-C) at fasting and postprandial states in patients with coronary artery disease (CAD).Methods: Fifty CAD patients were divided into Xuezhikang (XZK, n=25) group and control (CON, n=25) group randomly to receive red yeast rice exact, 1200mg/d Xuezhikang capsules or not for 6 weeks (6w). Blood lipids were detected repeatedly before and after 6w at 0, 2, 4 and 6 hours (h) after a standard breakfast with 800kcal.Result: When taking all patients as a whole (n=50), serum LDL-C level decreased while TG and RC levels increased significantly at 2, 4 and 6 h after breakfast (P＜0.05). Serum nonHDL-C level mildly but significantly increased at 4h and 6h after breakfast (P＜0.05). Short-term Xuezhikang treatment decreased tAUCs of TC, TG, LDL-C, nonHDL-C and RC whereas increased that of HDL-C significantly (P＜0.05). Serum LDL-C level showed a drop of 27.8%, 28.1%, 26.2%, 25.3% at 0, 2, 4 and 6 h, respectively, after breakfast. Serum nonHDL-C level showed a drop of 27.6%, 28.7%, 29.0% and 28.0% at 0, 2, 4 and 6 h, respectively. There was no significant difference in the percentages of reduction in LDL-C or nonHDL-C level among four time-points.Conclusions: Xuezhikang significantly decreased LDL-C or nonHDL-C level with similar percentages of reduction between fasting and postprandial states in patients with CAD, indicating that postprandial blood lipids detected at the same time point after a daily meal could replace fasting blood lipids to evaluate the efficacy of cholesterol-lowering therapy in CAD patients, unwilling or unable to keep a fasting state.

General approach to diagnosis of cardiomyopathies

ESC CardioMed ◽  
2018 ◽  
pp. 1437-1443
Author(s):  
Claudio Rapezzi ◽  
Massimiliano Lorenzini
Keyword(s):  
Coronary Artery Disease ◽  
Congenital Heart Disease ◽  
Heart Disease ◽  
Coronary Artery ◽  
Congenital Heart ◽  
Single Gene ◽  
Valvular Disease ◽  
Phenotype Definition ◽  
Artery Disease ◽  
Diagnostic Work

Cardiomyopathies are defined as myocardial disorders in which the heart muscle is structurally and functionally abnormal in the absence of coronary artery disease, hypertension, valvular disease, and congenital heart disease sufficient to explain the observed myocardial abnormality. They are grouped into specific morphological and functional phenotypes, with each phenotype subclassified into genetic and non-genetic forms (genetic in this context means single gene mutations). Hence, from a clinical perspective, this leads to a diagnostic work-up that consists of three steps: (1) phenotype definition; (2) exclusion of coronary artery disease, hypertension, valvular disease, or congenital heart disease that could explain the observed myocardial abnormalities; and (3) identification of the underlying disease cause, genetic or acquired.

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