Lack of Association of Lipoprotein Lipase Gene Polymorphisms With Coronary Artery Disease in the Saudi Arab Population

2003 ◽  
Vol 127 (5) ◽  
pp. 597-600 ◽  
Author(s):  
Khaled K. Abu-Amero ◽  
Carol A. Wyngaard ◽  
Olyan M. Al-Boudari ◽  
Marios Kambouris ◽  
Nduna Dzimiri

Abstract Context.—Previous studies reported an association of certain polymorphisms in the lipoprotein lipase (LPL) gene with the risk of coronary artery disease (CAD); however, these studies were small and inconsistent. In addition, none of these studies attempted to establish such an association in the Arab population. Objective.—To determine whether 2 LPL polymorphisms (LPL-HindIII and LPL-PvuII located on introns 8 and 6, respectively, of the LPL gene) can be considered as independent risk factors or as predictors for CAD in Arabs. Design.—We used polymerase chain reaction and restriction enzyme digestion to determine the distribution of the LPL-HindIII and LPL-PvuII polymorphisms among healthy blood donors of Arabic origin (BD group) and angiographically confirmed CAD patients (CAD group) with identical ethnic backgrounds. Results.—For the HindIII genotypes, within the BD group (n = 410), the +/+ genotype was found in 206 individuals (50.2%), 173 (42.2%) carried the +/− genotype, and 31 (7.6%) carried the −/− genotype. Within the CAD group (n = 352), the +/+ genotype was found in 189 individuals (53.7%), 138 (39.2%) carried the +/− genotype, and 25 (7.1%) carried the −/− genotype. P values of .38, .45, and .92 were obtained for the +/+, +/−, and −/− genotypes, respectively. For the PvuII genotypes, within the BD group (n = 511), the +/+ genotype was found in 182 individuals (35.6%), 248 (48.5%) carried the +/− genotype, and 81 (15.9%) carried the −/− genotype. Within the CAD group (n = 431), the +/+ genotype was found in 138 individuals (32%), 225 (52.2%) carried the +/− genotype, and 68 (15.8%) carried the −/− genotype. P values of .28, .29, and .98 were obtained for the +/+, +/−, and −/− genotypes, respectively. The distribution and the allele frequency of these 2 LPL variants were similar in CAD and BD study groups and followed the Hardy-Weinberg equilibrium. Conclusion.—There was no difference in the distribution of both LPL polymorphisms between the healthy group and the CAD group. Therefore, these 2 LPL polymorphisms cannot be considered as independent risk factors or as predictors for CAD in this population.

2020 ◽  
Author(s):  
Yueqiao Si ◽  
Wenjun Fan ◽  
Chao Han ◽  
Jingyi Liu ◽  
Lixian Sun

Abstract Background: The atherogenic index of plasma (AIP), triglyceride-glucose (TyG) index, and monocyte-to-lymphocyte ratio (MLR) are strongly associated with atherogenesis of the coronary artery. This study aimed to investigate the association of the AIP, TyG index, and MLR with subclinical coronary artery disease (CAD) and evaluate their ability to predict subclinical CAD.Methods: A total of 697 asymptomatic patients were enrolled in this study and assigned to the subclinical CAD group (n=332) and control group (n=365). The clinical data, coronary artery calcification score, and calculated AIP, TyG index, and MLR were collected by graduate students in the cardiology division. Multivariate logistic regression models were set up to assess the risk factors for subclinical CAD.Results: The AIP, TyG index and MLR values were higher in the subclinical CAD group than in the control group (all P<0.05). In addition to the classic independent clinical risk factors, increased AIP, TyG index and MLR values were all independent risk factors for subclinical CAD (all P<0.05). The AUCs were higher after combining clinical risk factors than the AIP, TyG index, or MLR alone (all P<0.05).Conclusions: The AIP, TyG index and MLR are independent risk factors for subclinical CAD, which can be useful for improving the diagnosis and prevention of CAD.


2002 ◽  
Vol 126 (9) ◽  
pp. 1087-1090
Author(s):  
Khaled K. Abu-Amero ◽  
Carol A. Wyngaard ◽  
Marios Kambouris ◽  
Nduna Dzimiri

Abstract Background.—No reports are available on the distribution of the 20210 G→A prothrombin variant among Middle Eastern Arabs. Additionally, to date, studies that attempt to establish this polymorphism as an independent risk factor or as a predictor for coronary artery disease (CAD) have yielded conflicting results. Objective.—To determine the prevalence of the 20210 G→A prothrombin variant among Middle Eastern Arabs and to evaluate the potential relevance of this variant to Arab patients with angiographically documented CAD. Methods and Results.—We used the polymerase chain reaction and restriction enzyme digestion to determine the prevalence of this polymorphism in 613 individuals from Arabic ethnic origin with CAD and from 593 healthy blood donors (BDs) from an identical ethnic background. Within the BD group (n = 593), 10 individuals (1.7%) were heterozygous, 583 individuals (98.3%) were normal, and none were homozygous for the 20210 G→A prothrombin variant. Within the CAD group (n = 613), 13 individuals (2.1%) were heterozygous, 600 individuals (97.9%) were normal, and none were homozygous for the 20210 G→A prothrombin variant. A χ2 analysis was used to evaluate any significance in the distribution of genotypes. A value of 1.23 was obtained. Values less than 3.84 indicate no statistically significant difference between the heterozygous carriers of the 20210A allele in both study groups. Conclusion.—In our population of Middle Eastern Arabs, the presence of the 20210 G→A prothrombin variant is not associated with patients with angiographically documented CAD. Therefore, this variant cannot be considered as an independent risk factor or as a predictor for CAD in this population.


1999 ◽  
Vol 123 (12) ◽  
pp. 1241-1245
Author(s):  
Nduna Dzimiri ◽  
Brian F. Meyer ◽  
Syed S. Hussain ◽  
Chona Basco ◽  
Barima Afrane ◽  
...  

Abstract Background.—The apolipoprotein E alleles ε2 and ε4 have been reported as independent risk factors for coronary artery disease (CAD) and as predictors for the development of atherosclerosis. Methods and Results.—We determined by polymerase chain reaction the distribution of apolipoprotein E polymorphism in 320 Saudi blood donors (BD), 96 CAD patients, and 40 control subjects who had undergone angiography. Compared to controls, only ε4 was elevated in CAD patients. More than 61% (P &lt; .0001) of the patients had angina, and 52.1% (P &lt; .05) were diabetic; both of these factors were strongly associated with the presence of allele ε2. The ε2 allele was also associated with hypertension, elevated serum triglycerides, and total cholesterol. On the other hand, the allele ε4 appeared to be associated with increased risk of CAD and was also associated with hypertension, 3-vessel disease, and restenosis. Conclusions.—Accordingly, ε4 may be associated with increased risk of CAD, whereas ε2 appears to be a predictor of several risk factors for atherosclerosis.


1990 ◽  
Vol 85 (1) ◽  
pp. 96
Author(s):  
J.C. Chamberlain ◽  
J.A. Thorn ◽  
R. Morgan ◽  
A. Bishop ◽  
A. Rees ◽  
...  

2021 ◽  
Author(s):  
Yong Li ◽  
Lei Chen ◽  
Min Zhang ◽  
Wensu Chen

Abstract Background This study is the first to explore the influence of the apolipoprotein E gene (APOE) and blood lipid metabolism on coronary artery disease (CAD) with atrial fibrillation.Methods In this study, there were a total of 2048 participants, including 400 patients in the control group (CAD- AF-), 126 AF patients without CAD (CAD- AF+), 1294 CAD patients without AF (CAD+ AF-) and 228 CAD patients with AF (CAD+ AF+). Blood lipid levels and APOE genotypes were determined by collecting blood samples from the patients.Results Compared with CAD patients without AF, the age and Lp (a) levels of CAD patients with AF were significantly higher. Among CAD patients, the frequencies of E3/E3 and ε3 genotypes in patients with AF were significantly lower than those in patients without AF, and the frequencies of E4/E4 and ε4 genotypes were significantly increased. Spearman correlation analysis showed that in CAD patients, Lp(a) levels in the ε4 group were significantly higher than those in the group of patients without ε4, and there was a significant correlation between ε4 and Lp (a) levels (p<0.001, r=0.106). Multivariate logistic regression analysis found that the increase in Lp (a) levels (p=0.023) and age (p=0.01) were independent risk factors for CAD patients who develop AF.Conclusion Patients with AF had increased age, ε4 frequencies and Lp (a) levels among CAD patients, age and Lp (a) levels may be independent risk factors for CAD patients to develop AF.


2021 ◽  
Vol 8 ◽  
Author(s):  
Bo Wang ◽  
Zhaodong Guo ◽  
Jin Liu ◽  
Huanqiang Li ◽  
Ziling Mai ◽  
...  

Background: Previous studies reported that patients with coronary artery disease (CAD) and well-controlled baseline LDL-C (&lt;1.8 mmol/L) still had higher long-term all-cause mortality. However, no study has been conducted to explore the independent risk factors for long-term mortality. In addition, there also was no study evaluating the population attributable risk (PAR) of independent risk factors in combination with their prevalence and relative risk. Therefore, we aimed to identify the independent risk factors and estimate their PAR in patients with CAD and well-controlled baseline LDL-C (&lt;1.8 mmol/L).Methods: We analyzed 4,863 consecutive CAD patients with well-controlled baseline LDL-C admitted to Guangdong Provincial People's Hospital in China from January 2007 to December 2018. Independent risk factors for long-term all-cause death were evaluated through stepwise approach and multivariable Cox regression analysis. PAR of independent risk factors was calculated with their hazard ratio and prevalence among our cohort.Results: The overall mortality was 16.00% (n = 778) over a median follow-up period of 5.93 years. Independent risk factors for all-cause death included malnutrition, age ≥75 years, congestive heart failure (CHF), chronic kidney disease (CKD) and atrial fibrillation. Among these risk factors of interest, the hazard ratio (HR) of severe malnutrition was the highest (HR 2.82, 95% CI: 1.86–4.26), and the PAR of mild malnutrition was the highest (19.49%, 95% CI: 0.65–36.01%).Conclusion: Malnutrition, age ≥75 years, CHF, CKD and atrial fibrillation were independent predictors for long-term all-cause mortality in CAD patients with well-controlled LDL-C levels. Considering prevalence of these risk factors, more attention should be paid to the occurrence of mild malnutrition for these patients.Clinical Trial Registration:ClinicalTrials.gov, identifier: NCT04407936.


2019 ◽  
Vol 133 (22) ◽  
pp. 2283-2299
Author(s):  
Apabrita Ayan Das ◽  
Devasmita Chakravarty ◽  
Debmalya Bhunia ◽  
Surajit Ghosh ◽  
Prakash C. Mandal ◽  
...  

Abstract The role of inflammation in all phases of atherosclerotic process is well established and soluble TREM-like transcript 1 (sTLT1) is reported to be associated with chronic inflammation. Yet, no information is available about the involvement of sTLT1 in atherosclerotic cardiovascular disease. Present study was undertaken to determine the pathophysiological significance of sTLT1 in atherosclerosis by employing an observational study on human subjects (n=117) followed by experiments in human macrophages and atherosclerotic apolipoprotein E (apoE)−/− mice. Plasma level of sTLT1 was found to be significantly (P<0.05) higher in clinical (2342 ± 184 pg/ml) and subclinical cases (1773 ± 118 pg/ml) than healthy controls (461 ± 57 pg/ml). Moreover, statistical analyses further indicated that sTLT1 was not only associated with common risk factors for Coronary Artery Disease (CAD) in both clinical and subclinical groups but also strongly correlated with disease severity. Ex vivo studies on macrophages showed that sTLT1 interacts with Fcɣ receptor I (FcɣRI) to activate spleen tyrosine kinase (SYK)-mediated downstream MAP kinase signalling cascade to activate nuclear factor-κ B (NF-kB). Activation of NF-kB induces secretion of tumour necrosis factor-α (TNF-α) from macrophage cells that plays pivotal role in governing the persistence of chronic inflammation. Atherosclerotic apoE−/− mice also showed high levels of sTLT1 and TNF-α in nearly occluded aortic stage indicating the contribution of sTLT1 in inflammation. Our results clearly demonstrate that sTLT1 is clinically related to the risk factors of CAD. We also showed that binding of sTLT1 with macrophage membrane receptor, FcɣR1 initiates inflammatory signals in macrophages suggesting its critical role in thrombus development and atherosclerosis.


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