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1.
J Cell Mol Med ; 28(12): e18474, 2024 Jun.
Article in English | MEDLINE | ID: mdl-38896027

ABSTRACT

Our previous study reckons that the impact of the rs1801133 variant of 5,10-methylenetetrahydrofolate reductase (MTHFR) on coronary artery disease (CAD) is possibly mediated by cardiometabolic disorder. This study is performed to verify this hypothesis. Four hundred and thirty CAD patients and 216 CAD-free individuals were enrolled in this case-control study. The rs1801133 variant was genotyped by PCR-RFLP. Severity of coronary lesions was evaluated by number of stenotic coronary vessels and extent of coronary stenosis. The rs1801133 T allele significantly increased homocysteine levels in patients with CAD and CAD-free individuals. Individuals with the T allele of rs1801133 had an increased risk of developing CAD. In contrast, individuals with the TT genotype of rs1801133 were at high risk of multiple vessel lesions. The carriers of CT genotype had higher levels of systolic blood pressure (SBP), low-density lipoprotein cholesterol (LDL-C), and high-sensitivity C-reactive protein (hs-CRP), and lower levels of apolipoprotein A1 (APOA1) than those with CC genotype in male patients with CAD. The receiver operating characteristic (ROC) curve and precision-recall (PR) curve indicated that hyperhomocysteinemia was sensitive to predict the severity of CAD. Multivariate logistic regression revealed that homocysteine, rs1801133, age, smoking, weight, body mass index (BMI), lipoprotein(a) [Lp(a)], and hs-CRP were independent risk factors for CAD. The increased risk of CAD and severity of coronary lesions associated with rs1801133 in the Chinese Han population were attributed, at least partly, to high homocysteine levels. Hyperhomocysteinemia had a high predictive value for severe CAD or multiple vessel lesions.


Subject(s)
Coronary Artery Disease , Homocysteine , Methylenetetrahydrofolate Reductase (NADPH2) , Polymorphism, Single Nucleotide , Humans , Homocysteine/blood , Male , Coronary Artery Disease/genetics , Coronary Artery Disease/blood , Coronary Artery Disease/pathology , Middle Aged , Female , Case-Control Studies , Methylenetetrahydrofolate Reductase (NADPH2)/genetics , Severity of Illness Index , Aged , Risk Factors , Genetic Predisposition to Disease , ROC Curve , Genotype , C-Reactive Protein/metabolism , C-Reactive Protein/genetics , Alleles , Apolipoprotein A-I/genetics , Apolipoprotein A-I/blood
2.
Sci Rep ; 14(1): 13171, 2024 06 07.
Article in English | MEDLINE | ID: mdl-38849492

ABSTRACT

Angiotensin-converting enzyme (ACE) is closely related to cardiometabolic risk factors and atherosclerosis. This study aims to investigate whether the insertion/deletion (I/D) variant of ACE gene impacts cardiometabolic risk factors, premature coronary artery disease (PCAD), and severity of coronary lesions. PubMed, Cochrane Library, Central, CINAHL, and ClinicalTrials.gov were searched until December 22, 2023. 94,270 individuals were included for the analysis. Carriers of DD genotype had higher levels of triglycerides (TG), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), systolic blood pressure (SBP), diastolic blood pressure (DBP), body mass index (BMI), and waist circumference (WC) than carriers of II or ID genotypes. In addition, carriers of DD genotype were at high risk of PCAD and multiple vessel lesions. The impacts of ACE I/D variant on lipid levels were significant in American individuals but stronger in male individuals. In contrast, the impacts of ACE I/D variant on PCAD and severity of coronary lesions were primarily significant in Caucasian individuals. This study indicates that the ACE I/D variant has a slight but significant impact on cardiometabolic risk factors, PCAD, and severity of coronary lesions. Angiotensin-converting enzyme inhibitors (ACEI) may benefit high-risk populations with ACE DD genotype to prevent PCAD and multiple vessel lesions.PROSPERO registration number: CRD42023426732.


Subject(s)
Cardiometabolic Risk Factors , Coronary Artery Disease , INDEL Mutation , Peptidyl-Dipeptidase A , Humans , Peptidyl-Dipeptidase A/genetics , Coronary Artery Disease/genetics , Male , Female , Blood Pressure , Genetic Predisposition to Disease , Severity of Illness Index , Middle Aged , Genotype , Body Mass Index , Risk Factors , Triglycerides/blood , Adult
3.
Article in Chinese | WPRIM (Western Pacific) | ID: wpr-421482

ABSTRACT

ObjectiveTo investigate the relationship between nonalcoholic fatty liver disease(NAFLD)and the severity of coronary artery disease (CAD).MethodsRetrospective cross-sectional studies were conducted to examine the relationship between NAFLD and the severity of CAD. CAD was diagnosed by coronary angiography and NAFLD by type-B ultrasound.ResultsThe logistic regression analysis showed that hypertension, NAFLD, diabetes, smoking, and high level of γ-glutamyltransferase were risk factors of multiplevessel lesions and occlusion of CAD( P<0.05 or P<0.01 ) , and high levels of total cholesterol and alanine aminotransferase were risk factors of multiple-vessel lesions ( P<0. 05 or P<0.01 ) , family history was a risk factor of occlusion of CAD, whereas, high level of high-density lipoprotein cholesterol was an important protective factor of multiple-vessel lesions and occlusion of CAD ( P<0. 01 ). NAFLD was a dependent risk factor of multiple-vessel lesions and occlusion of CAD( P<0.05 or P<0. 01 ). ConclusionsNAFLD could be regarded as a main risk factor of the severity of CAD. Clinicians should pay more attention to the prevention and treatment of NAFLD in order to improve the outcome of CAD.

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