Abstract 468: The 3’-utr of Adiponectin Q Gene Harbours Common Susceptibility Variants and Haplotypes for Metabolic Risk Traits

Hypertension ◽  
2012 ◽  
Vol 60 (suppl_1) ◽  
Author(s):  
Nduna Dzimiri ◽  
Mohammed Al-Najai ◽  
Editha Andres ◽  
Samar El-Hawari ◽  
Mary Grace Vigilla ◽  
...  

Adiponectin (ADIPOQ) is a hormone that modules several metabolic processes and is thought to contribute to the suppression of the metabolic derangements that may lead to metabolic syndrome. In the present study, we performed a population-based association study by real-time PCR for 8 SNPs in a total of 4650 Saudi individuals harbouring various metabolic risk traits. Among these SNPs, rs1063537 T allele [Odds ratio(95% Confidence Interval = 1.16(1.04-1.30); p=0.011], rs1063537 CT+TT genotypes [1.16(1.02-1.33); p=0.024], rs2082940 T [1.12(1.01-1.24); p=0.035] and CT+TT [1.37(1.02-1.83); p=0.039] as well as rs1063539 C [1.13(1.01-1.20); p=0.035] conferred risk for myocardial infarction (MI; 3060 cases vs 1590 controls). The rs2241766 T [1.26(1.02-1.54); p=0.028], rs6773957 AG+GG [1.15(1.01-1.31); p=0.030], rs4686804 CT+ TT [1.15(1.01-1.30); p=0.033] were associated with obesity (1757 vs 2576). The rs2241766 T was likewise implicated in low high density lipoprotein levels (lHDL; 1926 vs 2393) [1.29(1.06-1.58); p=0.013] and primary hypertension (HTN; 3533 cases vs 1590) [1.25(1.01-1.55); p=0.039], while rs9842733 T was associated with HTN [1.44(1.03-2.01); p=0.032] and hypercholesterolaemia (hChol; 1681 vs 2739) [1.32(1.01-1.72); p=0.043]. An 8-mer haplotype GTGCCTCA constructed from the 8 SNPs and its derivatives were commonly implicated in MI (Χ 2 =4.12; p=0.042) and HTN (Χ 2 =6.40; p=0.011) and obesity (Χ 2 =5.18; p=0.023). On the other hand, hChol levels were associated with the 5-mer TTATT (Χ 2 = 9.56; p = 0.002) and its 4-mer derivative TTAT (Χ 2 = 7.56; p=0.006) while lHDL was linked with the TCCA (Χ 2 = 5.06; p = 0.025). These results demonstrate that the 3’UTR of the ADIPOQ gene harbours common susceptibility variants and haplotypes for the important determinants of metabolic syndrome and cardiovascular risk traits, possibly pointing to a common underlying pathway to coronary artery disease.

2000 ◽  
Vol 83 (03) ◽  
pp. 404-407 ◽  
Author(s):  
Michael Klein ◽  
Hans Dauben ◽  
Christiane Moser ◽  
Emmeran Gams ◽  
Rüdiger Scharf ◽  
...  

SummaryRecently, we have demonstrated that human platelet antigen 1b (HPA-1b or PlA2) is a hereditary risk factor for platelet thrombogenicity leading to premature myocardial infarction in preexisting coronary artery disease. However, HPA-1b does not represent a risk factor for coronary artery disease itself. The aim of our present study was to evaluate the role of HPA-1b on the outcome in patients after coronaryartery bypass surgery. We prospectively determined the HPA-1 genotype in 261 consecutive patients prior to saphenous-vein coronaryartery bypass grafting. The patients were followed for one year. Among patients with bypass occlusion, myocardial infarction, or death more than 30 days after surgery, the prevalence of HPA-1b was significantly higher than among patients without postoperative complications (60 percent, 6/10, vs. 24 percent, 58/241, p <0.05, odds ratio 4.7). Using a stepwise logistic regression analysis with the variables HPA1b, age, sex, body mass index, smoking (pack-years), hypertension, diabetes, cholesterol and triglyceride concentration, only HPA-1b had a significant association with bypass occlusion, myocardial infarction, or death after bypass surgery (p = 0.019, odds ratio 4.7). This study shows that HPA-1b is a hereditary risk factor for bypass occlusion, myocardial infarction, or death in patients after coronary-artery bypass surgery.


Author(s):  
Sifat Jubaira ◽  
Forhadul Haque Mollah ◽  
Tahrim Mehdi ◽  
M Iqbal Arslan

The study was designed to explore serum copper as a risk factor for coronary artery disease (CAD). In this case-control study 30 healthy controls and 60 diagnosed cases of acute myocardial infarction (AMI) were enrolled. Serum copper concentration and serum lipid profile were measured in all study subjects. Serum copper level was significantly higher in AMI as compared to controls. The concentrations of serum TC, TG, LDL-C level were found to be significantly higher in cases as compared to controls. The concentration serum HDL-C was found to be significantly lower in cases as compared to controls. CAD leads to raised serum copper level and it has positive correlation with TC, TG and LDL-C but negative correlation with HDL-C in males.Keywords: Coronary artery disease; serum copper; acute myocardial infarction; total cholesterol; triglyceride; low density lipoprotein cholesterol. DOI: 10.3329/bjpp.v24i1.5730Bangladesh J Physiol Pharmacol 2008; 24(1&2) : 7-9


2007 ◽  
Vol 41 (9) ◽  
pp. 1345-1351 ◽  
Author(s):  
John S Sampalis ◽  
Stéphane Bissonnette ◽  
Rafik Habib ◽  
Stella Boukas

Background: The aim of lipid-lowering treatment is to reduce the risk for cardiovascular events. Patients not at target lipid levels while on hydroxymethylglutaryl coenzyme A reductase inhibitors (statin) monotherapy are at increased cardiovascular risk. Objective: To describe the impact of coadministration of ezetimibe with a statin on the estimated 10 year risk for coronary artery disease (E-RCAD) in patients with hypercholesterolemia and above-target low-density lipoprotein cholesterol (LDL-C) levels after statin monotherapy. Methods: Post hoc analysis was conducted of a prospective, open-label, single-cohort, multicenter Canadian study of 953 patients who were treated for 6 weeks with ezetimibe 10 mg/day coadministered with their current statin at an unaltered dose. For each patient, E-RCAD at baseline and at 6 weeks was calculated using the Framingham model. The primary outcome measure of the analysis was the change in E-RCAD. Results: A total of 825 patients with data at baseline and 6 weeks were included in the analysis. There were 423 (51.3%) patients with hypertension, 107 (13.0%) with diabetes mellitus but not metabolic syndrome, 160 (19.4%) with metabolic syndrome but not diabetes mellitus, and 235 (28.5%) with both diabetes mellitus and metabolic syndrome. After 6 weeks of ezetimibe coadministration with statin therapy, mean E-RCAD was reduced by 4.1% from 15.6% to 11.5%, which is equivalent to a 25.3% risk reduction (p < 0.001). Of the 225 (27.3%) patients with high E-RCAD (≥20.1%) at baseline, 144 (64.0%) converted to a lower E-RCAD category (p < 0.001). Patients with both diabetes mellitus and metabolic syndrome experienced the highest mean percent reduction in E-RCAD of –29.4% (p < 0.001). Conclusions: For patients with above-target LDL-C levels while on statin monotherapy, coadministration of ezetimibe with the statin is effective in significantly reducing the E-RCAD.


2005 ◽  
Vol 90 (4) ◽  
pp. 2264-2269 ◽  
Author(s):  
Marie-Claude Blatter Garin ◽  
Barbara Kalix ◽  
Alfredo Morabia ◽  
Richard W. James

Abstract The presence of the metabolic syndrome (World Health Organization definition) and its association with lipoprotein abnormalities suggestive of greater susceptibility to oxidative stress have been analyzed in patients with angiographically defined coronary artery disease. The odds ratio for the presence of the metabolic syndrome was significantly higher in coronary artery disease-positive patients (P &lt; 0.001). The metabolic syndrome was also associated with more severe coronary disease (P &lt; 0.01). Patients with the metabolic syndrome had significantly decreased low-density lipoprotein-cholesterol/apolipoprotein B and high-density lipoprotein-cholesterol/apolipoprotein AI ratios, indicative of the presence of small, dense lipoprotein particles. The syndrome was also associated with reduced concentrations and activities of the antioxidant enzyme, paraoxonase-1. The metabolic syndrome is characterized by smaller, denser lipoprotein particles that increase their susceptibility to oxidative modifications and diminished serum paraoxonase-1, which is a major determinant of the antioxidant capacity of high-density lipoproteins. These may be contributory factors to the increased presence and severity of coronary disease in such patients.


2020 ◽  
Vol 10 (4) ◽  
pp. 257
Author(s):  
Han Sung Park ◽  
Jung-Hoon Sung ◽  
Chang Soo Ryu ◽  
Jeong Yong Lee ◽  
Eun Ju Ko ◽  
...  

The most common type of cardiovascular disease is coronary artery disease (CAD), in which a plaque builds up inside the coronary arteries that can lead to a complete blockage of blood flow to the heart, resulting in a heart attack. The CAD may be affected by various factors including age, gender, and lipoprotein disposition as well as genetic factors and metabolic syndrome. In this study, we investigated whether three PAI-1 polymorphisms (−844 G > A, −675 4G > 5G, and +43 G > A) and CAD-related clinical parameters are associated with CAD susceptibility. Genotyping of 463 CAD patients and 401 controls was performed using polymerase chain reaction restriction fragment length polymorphism analysis. We report that the 4G5G genotype (crude odds ratio(COR), 1.392; 95% confidence interval (CI), 1.036–1.871; p = 0.028) and dominant model (4G4G vs. 4G5G + 5G5G; COR, 1.401; 95% CI, 1.060–1.850; p = 0.018; adjust odds ratio, 1.371; 95% CI, 1.027–1.831; p = 0.032) of PAI-1 −675 polymorphisms were associated with increased CAD risk. Haplotype and genotype combinations of PAI-1 −675 and +43 polymorphisms show an increased risk of CAD according to alterations of the −675 polymorphism allele or genotype. Moreover, the PAI-1 -675 polymorphisms show a synergistic effect with the metabolic syndrome component of CAD risk. This study suggests that polymorphisms in the PAI-1 genes along with the metabolic syndrome component of CAD can be useful biomarkers for CAD diagnosis and treatment.


2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Kristian Dimovski ◽  
Marju Orho-Melander ◽  
Isabel Drake

Abstract Background A healthy lifestyle has been shown to reduce the risk of coronary artery disease (CAD). The extent to which lifestyle influences the risk of CAD for people with pre-existing non-modifiable risk factors is less studied. We therefore examined the associations between a favorable lifestyle and incidence of CAD in population subgroups based on gender, age, educational level, and parental history of myocardial infarction. Methods A total of 26,323 men and women from the Malmö Diet and Cancer study were prospectively followed-up for 18 years. A favorable lifestyle was determined using a four-component lifestyle score based on data collected at baseline: no smoking, no obesity, regular physical activity, and a healthy diet. Cox proportional hazards regression models were used to estimate the relative risk of CAD during follow-up and cumulative risk during a 10-year interval. Results A favorable lifestyle was associated with a 44% (95% confidence interval, 38–48%) lower risk of CAD compared to an unfavorable lifestyle. The relative risk was similarly reduced among subjects subdivided by gender, age group, educational level, and parental history of myocardial infarction. These findings corresponded with a reduced standardized 10-year incidence of CAD of around 40% in each subgroup. Conclusion In this population-based cohort, a favorable lifestyle was associated with a significant reduction of CAD across strata of non-modifiable risk factors. These findings provide support for lifestyle modification as a means for risk reduction in a range of subgroups within a general healthy population.


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