scholarly journals Coronary Artery Disease: Association Study of 5 Loci with Angiographic Indices of Disease Severity

2021 ◽  
Vol 2021 ◽  
pp. 1-8
Author(s):  
Neda M. Bogari ◽  
Reem M. Allam ◽  
Abdellatif Bouazzaoui ◽  
Osama Elkhateeb ◽  
Massimo Porqueddu ◽  
...  

Background. Different common gene variants were related to coronary artery disease (CAD) in many studies. Yet, the relation of these loci to the severity of CAD is not completely elucidated. Methods. We enrolled 520 subjects (315 CAD cases and 205 controls). CAD presence and extension were assessed by coronary angiography (CAG). Genotyping of five SNPs (namely, rs2230806 (1051G > A) in ABCA1 on chromosome 9, rs2075291 (553G > T) in ApoA5 on chromosome 11, rs320 in LPL on chromosome 8 intron (T → G at position 481), rs10757278 (c.22114477A > G), and rs2383206 (c.22115026 A > G) on chromosome 9p21 locus) was performed by allele-specific PCR. The degree and site of arterial lesions were used to classify patients, tested for association with CAD severity, and related to allele dosage. Results. The polymorphisms rs2383206 and rs10757278 showed significant associations with 2- and 3-vessel coronary disease (p =0.003 and 0.006, respectively). The homozygous GG genotypes of rs10757278 was associated with higher frequency of left anterior descending (LAD), right coronary artery (RCA) and left circumflex (LCX) diseases (p =0.002, 0.016 and 0.002, respectively). The GG genotypes of rs2383206 were found in higher percentage in patients with left main (LM) trunk and left circumflex (LCX) diseases ( p = 0.013 and 0.002, respectively). Conclusion. SNPs rs10757278 and rs2383206 allele dosage could predict CAD severity in the Saudi Arab population.

2013 ◽  
Vol 61 (9) ◽  
pp. 957-970 ◽  
Author(s):  
Kenneth Chan ◽  
Riyaz S. Patel ◽  
Paul Newcombe ◽  
Christopher P. Nelson ◽  
Atif Qasim ◽  
...  

2019 ◽  
Vol 7 (7) ◽  
pp. 80 ◽  
Author(s):  
Chandan K. Jha ◽  
Rashid Mir ◽  
Imadeldin Elfaki ◽  
Shaheena Banu ◽  
S. M. S. Chahal

Cardiovascular diseases (CVD) are a major cause of death in India and worldwide. Atherosclerosis is caused by the interaction of environmental and genetic factors. Hypercholesterolemia is an example of a classical risk factor for CVD. The low-density lipoprotein receptor (LDLR) is one of the regulating mechanisms the liver uses for cholesterol homeostasis. Gene variations in the LDLR have been reported to cause hypercholesterolemia and consequently CVD. We investigated the association of polymorphisms in the LDLR (rs5925 and rs1529729) with coronary artery disease (CAD) in 200 coronary artery disease patients and 200 matched healthy controls using allele-specific PCR (AS-PCR). The results indicated that the CT genotype of the rs1529729 polymorphism was associated a decreased susceptibility to CAD with an odds ratio (OR) = 0.42 (95% confidence interval (CI), 0.23–0.77), risk ratio (RR) = 0.59 (0.39–0.89), P = 0.0047. The TT genotype of the rs1529729 polymorphism was also associated with decreased susceptibility to CAD with an OR = 0.19 (95% CI, 0.076–0.47), RR = 0.57 (0.47–0.69), P = 0.0003. The GA genotype of the rs5925 polymorphism was associated with decreased susceptibility to CAD with an OR = 0.45 (95% CI, 0.27–0.75), RR = 0.65 (0.47–0.88), P = 0.002. We concluded that the CT and TT genotypes of the rs1529729 polymorphism and the GA genotype of the rs5925 polymorphism are probably associated with decreased susceptibility to CAD. The simplicity of AS-PCR makes it particularly suitable for the rapid, large-scale screening of gene variabilities in the LDLR. AS-PCR could provide significant benefits in clinical applications with its ability to amplify a lower quantity of samples in a cost-saving manner. Nevertheless, these findings need to be validated in well-designed studies with larger sample sizes and in different populations.


Heart ◽  
2013 ◽  
Vol 99 (suppl 2) ◽  
pp. A75.1-A75
Author(s):  
K Chan ◽  
R S Patel ◽  
P Newcombe ◽  
C P Nelson ◽  
A Qasim ◽  
...  

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.


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.


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