scholarly journals The Synergistic Effect of Plasminogen Activator Inhibitor-1 (PAI-1) Polymorphisms and Metabolic Syndrome on Coronary Artery Disease in the Korean Population

2020 ◽  
Vol 10 (4) ◽  
pp. 257
Author(s):  
Han Sung Park ◽  
Jung-Hoon Sung ◽  
Chang Soo Ryu ◽  
Jeong Yong Lee ◽  
Eun Ju Ko ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Metabolic Syndrome ◽  
Coronary Artery ◽  
Synergistic Effect ◽  
Odds Ratio ◽  
Metabolic Syndrome Component ◽  
The Metabolic Syndrome ◽  
Artery Disease ◽  
Cad Risk ◽  
Pai 1

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.

The relationship between the metabolic syndrome defined by various criteria and the extent of coronary artery disease

2008 ◽  
Vol 197 (2) ◽  
pp. 944-950 ◽  
Author(s):  
Takatoshi Kasai ◽  
Katsumi Miyauchi ◽  
Naozumi Kubota ◽  
Hiroshi Tamura ◽  
Takahiko Kojima ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Metabolic Syndrome ◽  
Coronary Artery ◽  
The Metabolic Syndrome ◽  
Artery Disease ◽  
The Relationship

scholarly journals Which features of the metabolic syndrome predict the presence of angiographic coronary artery disease?

2003 ◽  
Vol 41 (6) ◽  
pp. 344-345
Author(s):  
Sandra P. Reyna ◽  
Joseph B. Muhlestein ◽  
John F. Carlquist ◽  
Dale G. Renlund ◽  
Donald L. Lappé ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Metabolic Syndrome ◽  
Coronary Artery ◽  
The Metabolic Syndrome ◽  
Artery Disease

P6191Proprotein convertase subtilisin/kexin type 9 (PCSK9) plasma levels are associated with the metabolic syndrome in patients with stable coronary artery disease

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
C Caselli ◽  
R Ragusa ◽  
S Del Turco ◽  
G Basta ◽  
A Saraste ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Metabolic Syndrome ◽  
Coronary Artery ◽  
Plasma Levels ◽  
Hdl Cholesterol ◽  
Homa Index ◽  
Cholesterol Levels ◽  
The Metabolic Syndrome ◽  
Artery Disease ◽  
Stable Cad

Abstract Background PCSK9 is a key regulator of serum LDL-cholesterol levels. The relation of PCSK9 with other components of cardiovascular and coronary artery disease (CAD) risk is still debated. Purpose To evaluate the association of PCSK9 plasma levels with cardiovascular and coronary risk profile, in patients with symptoms of suspected stable CAD enrolled in the EVINCI study. Methods PCSK9 was measured in 522 patients (60.4±8.8 years, 318 males) with symptoms of stable CAD Individual risk was characterized by clinical and bio-humoral variables, including lipid/glucose/inflammatory profiles. Obstructive CAD was firstly ruled-in by multimodality non-invasive imaging and, subsequently, assessed by invasive coronary angiography. Results Patients were divided into groups according to PCSK9 quartiles: I (<138 ng/mL), II-III (138–264 ng/mL), and IV (>264 ng/mL) (Table). The prevalence of obstructive CAD at invasive angiography and statin treatment did not differ among groups. Compared with patients in quartile IV, patients in quartile I, had a higher prevalence of metabolic syndrome and higher values of body mass index. Among biomarkers, all cholesterol lipoproteins levels progressively increased from quartile I to IV, while insulin and HOMA index values decreased (Table). At multivariable analyses adjusted for medical treatment, the only clinical or bio-humoral variables independently associated with PCSK9 levels were presence of the metabolic syndrome (Coeff. −0.195, SE 0.05, p<0.0001) and HDL cholesterol levels (Coeff. 0.444, SE 0.06, p<0.0001), respectively. Table 1 Clinical Variables Quartile I Quartile II–III Quartile IV Biomarkers Quartile I Quartile II–III Quartile IV <138 ng/L 138–264 ng/L >264 ng/L <138 ng/L 138–264 ng/L >264 ng/L (n=130) (n=261) (n=131) (n=130) (n=261) (n=131) Age, years 61±9 60±9 61±8 Glucose, mg/dL 110±30 117±41 109±29 Male gender 86 (66) 161 (62) 71 (55) Insulin, mUI/mL 13.3±12.5* 11.3±10.1 10.3±10.1 Family history 38 (29)# 86 (33) 58 (44) HOMA index 3.9±4.5* 3.5±4.1 2.9±3.3 Hypertension 78 (60) 164 (63) 88 (67) Tryglicerides, mg/dL 128±86 128±87 118±68 Hypercholesterolemia 72 (55) 158 (61) 81 (62) Total cholesterol, mg/dL 171±43* 181±45 203±55 Diabetes mellitus 43 (33) 91 (35) 37 (28) LDL, mg/dL 99±36* 104±38 119±45 Metabolic Syndrome 45 (35)# 72 (28) 19 (15) HDL, mg/dL 46±13* 52±15 61±19 BMI, kg/m2 28.02±4.00* 28.03±4.25 26.95±4.56 Total/HDL cholesterol 3.8±1.2* 3.7±1.2 3.5±1.1 Significant CAD at ICA 18 (14) 46 (18) 24 (18) hs-CRP, mg/dL 0.41±0.61 0.39±1.38 0.41±0.83 Statins treatment 68 (52) 143 (55) 58 (44) Interleukin 6, ng/L 1.60±2.75 1.30±2.49 1.30±1.68 Chi square test: #p<0.05. ANOVA: I vs. IV Quartile: *p<0.05. Conclusion In patients with stable CAD, low plasma levels of PCSK9 are associated with the prevalence of metabolic syndrome and its individual components, including, in particular, HDL cholesterol. Acknowledgement/Funding AMGEN grant, EU FP7-CP-FP506 2007 project (grant agreement no. 222915)

scholarly journals Polygenic Hyperlipidemias and Coronary Artery Disease Risk

2020 ◽  
Vol 13 (2) ◽  
Author(s):  
Pietari Ripatti ◽  
Joel T. Rämö ◽  
Nina J. Mars ◽  
Yu Fu ◽  
Jake Lin ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Odds Ratio ◽  
Genome Wide Association Study ◽  
Disease Risk ◽  
Risk Scores ◽  
Lipid Levels ◽  
Artery Disease ◽  
The Impact ◽  
Cad Risk

Background: Hyperlipidemia is a highly heritable risk factor for coronary artery disease (CAD). While monogenic familial hypercholesterolemia associates with severely increased CAD risk, it remains less clear to what extent a high polygenic load of a large number of LDL (low-density lipoprotein) cholesterol (LDL-C) or triglyceride (TG)-increasing variants associates with increased CAD risk. Methods: We derived polygenic risk scores (PRSs) with ≈6M variants separately for LDL-C and TG with weights from a UK Biobank–based genome-wide association study with ≈324K samples. We evaluated the impact of polygenic hypercholesterolemia and hypertriglyceridemia to lipid levels in 27 039 individuals from the National FINRISK Study (FINRISK) cohort and to CAD risk in 135 638 individuals (13 753 CAD cases) from the FinnGen project (FinnGen). Results: In FINRISK, median LDL-C was 3.39 (95% CI, 3.38–3.40) mmol/L, and it ranged from 2.87 (95% CI, 2.82–2.94) to 3.78 (95% CI, 3.71–3.83) mmol/L between the lowest and highest 5% of the LDL-C PRS distribution. Median TG was 1.19 (95% CI, 1.18–1.20) mmol/L, ranging from 0.97 (95% CI, 0.94–1.00) to 1.55 (95% CI, 1.48–1.61) mmol/L with the TG PRS. In FinnGen, comparing the highest 5% of the PRS to the lowest 95%, CAD odds ratio was 1.36 (95% CI, 1.24–1.49) for the LDL-C PRS and 1.31 (95% CI, 1.19–1.43) for the TG PRS. These estimates were only slightly attenuated when adjusting for a CAD PRS (odds ratio, 1.26 [95% CI, 1.16–1.38] for LDL-C and 1.24 [95% CI, 1.13–1.36] for TG PRS). Conclusions: The CAD risk associated with a high polygenic load for lipid-increasing variants was proportional to their impact on lipid levels and partially overlapping with a CAD PRS. In contrast with a PRS for CAD, the lipid PRSs point to known and directly modifiable risk factors providing additional guidance for clinical translation.

scholarly journals Small, Dense Lipoprotein Particles and Reduced Paraoxonase-1 in Patients with the Metabolic Syndrome

2005 ◽  
Vol 90 (4) ◽  
pp. 2264-2269 ◽  
Author(s):  
Marie-Claude Blatter Garin ◽  
Barbara Kalix ◽  
Alfredo Morabia ◽  
Richard W. James
Keyword(s):  
Coronary Artery Disease ◽  
Metabolic Syndrome ◽  
Coronary Artery ◽  
Coronary Disease ◽  
Density Lipoprotein ◽  
Lipoprotein Cholesterol ◽  
Paraoxonase 1 ◽  
Lipoprotein Particles ◽  
The Metabolic Syndrome ◽  
Artery Disease

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.

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