Paraoxonase-1 Genotype and Angiogram Positive Coronary Artery Disease.
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SUBMITTER: Mungmunpuntipantip R
PROVIDER: S-EPMC10263450 | biostudies-literature | 2023 Apr
REPOSITORIES: biostudies-literature
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Paraoxonase-1 Genotype and Angiogram Positive Coronary Artery Disease.
Mungmunpuntipantip Rujittika R Wiwanitkit Viroj V
Arquivos brasileiros de cardiologia 20230407 3
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Project description:BackgroundIt has been shown that increased serum PON1 levels are protective against several disorders. Several single nucleotide polymorphisms (SNPs) of the PON1 gene have been reported to be associated with serum enzyme protein levels and activity.ObjectiveTo investigate the association of SNPs of PON1 and serum paraoxonase activity with coronary artery disease (CAD).MethodsA total of 601 unrelated patients who underwent coronary angiography including those who had >50% stenosis (N=266) and those with <30% stenosis (N=335) were studied. The Paraoxonase gene rs662 and rs840560 SNPs were determined using the ARMS-PCR method and the rs705379 SNP was genotyped using PCR-RFLP analysis. Serum paraoxonase activity was measured using paraoxon as a substrate. A p value of p<0.05 was considered as significant.ResultsSerum paraoxonase activity was not significantly different between the study groups. After adjustment for age, sex, hypertension, diabetes mellitus and dyslipidemia, the GG genotype and co-dominant model of rs662 was positively associated with a positive angiogram (respectively, OR=2.424, 95%CI [1.123-5.233], p<0.05, OR=1.663, 95%CI [1.086-2.547]). Serum paraoxonase activity was significantly higher in the G allele and GG variant of rs662, A allele and AA variant of rs854560 and C allele and CC variant of rs705379. The haplotype analysis has shown that the ATC haplotype was significantly more prevalent among the angiogram negative group. The analysis between groups indicated that the A allele of rs662 was significantly associated with lower paraoxonase activity in the positive angiogram group (p=0.019).ConclusionsThe presence of the G allele of the rs662 single nucleotide polymorphism is independently associated to increased risk of CAD.
| S-EPMC9563872 | biostudies-literature
Project description:We wanted to explore the genomic regions 1p13, 1q41, 9p21 and 10q11, which are among the labeled âtop 12 golden lociâ linked to coronary artery disease (CAD) risk, in order to see whether their geographic variation could be explained by demographic effects. To do this, we have genotyped these risk regions in a set of Mediterranean populations. Genomic DNA was extracted from blood cells using a Blood Midi kit (Omega Biotek, USA) according to manufacturer's procedures. DNA samples were genotyped for a combined set of 366 SNPs using an Illumina Custom GoldenGate Panel. SNPs were selected as a representative set of the common variation in the four genomic regions, according to the following criteria: i) average coverage of 1 SNP every 1.5 kb, ii) minor allele frequency (MAF) higher than 0.05 in CEU and TSI HapMap populations, iii) given priority to markers not in linkage disequilibrium (LD) (r2<0.8) in European populations, and iv) prioritizing markers previously associated with CAD. These criteria were applied giving preference to tag SNPs.
2016-11-24 | E-MTAB-5265 | biostudies-arrayexpress
Project description:Spanning three decades in research, Paraoxonases (PON1) carried potential of dealing with neurotoxicity of organophosphates entering the circulation and preventing cholinergic crisis. In the past few years, the Paraoxonase multigene family (PON1, PON2, PON3) has been shown to play an important role in pathogenesis of cardiovascular disorders including coronary artery disease (CAD). The PON genes are clustered in tandem on the long arm of human chromosome 7 (q21, 22). All of them have been shown to act as antioxidants. Of them, PON3 is the least studied member as its exact physiological substrate is still not clear. This has further led to limitation in our understanding of its role in pathogenesis of CAD and development of the potential therapeutic agents which might modulate its activity, expression in circulation and tissues. In the present review, we discuss the structure and activity of human PON3 enzyme and its Single nucleotide variants that could potentially lead to new clinical strategies in prevention and treatment of CAD.
| S-EPMC6995636 | biostudies-literature
Project description:BackgroundParaoxonase-1 (PON1) is an antioxidant enzyme, that resides on high-density lipoprotein (HDL). PON1-activity, is heavily influenced by the PON1-Q192R polymorphism. PON1 is considered to protect against atherosclerosis, but it is unclear whether this relation is independent of its carrier, HDL. In order to evaluate the atheroprotective potential of PON1, we assessed the relationships among PON1-genotype, PON1-activity and risk of future coronary artery disease (CAD), in a large prospective case-control study.Methodology/principal findingsCases (n = 1138) were apparently healthy men and women aged 45-79 years who developed fatal or nonfatal CAD during a mean follow-up of 6 years. Controls (n = 2237) were matched by age, sex and enrollment time. PON1-activity was similar in cases and controls (60.7+/-45.3 versus 62.6+/-45.8 U/L, p = 0.3) and correlated with HDL-cholesterol levels (r = 0.16, p<0.0001). The PON1-Q192R polymorphism had a profound impact on PON1-activity, but did not predict CAD risk (Odds Ratio [OR] per R allele 0.98[0.84-1.15], p = 0.8). Using conditional logistic regression, quartiles of PON1-activity showed a modest inverse relation with CAD risk (OR for the highest versus the lowest quartile 0.77[0.63-0.95], p = 0.01; p-trend = 0.06). PON1-activity adjusted for Q192R polymorphism correlated better with HDL-cholesterol (r = 0.26, p<0.0001) and more linearly predicted CAD risk (0.79[0.64-0.98], p = 0.03; p-trend = 0.008). However, these relationships were abolished after adjustment for HDL (particles-cholesterol-size) and apolipoproteinA-I (0.94[0.74-1.18], p-trend = 0.3).Conclusions/significanceThis study, shows that PON1-activity inversely relates to CAD risk, but not independent of HDL, due to its close association with the HDL-particle. These data strongly suggest that a low PON1-activity is not a causal factor in atherogenesis.
| S-EPMC2728540 | biostudies-literature
Project description:BackgroundFamilial hypercholesterolaemia (FH) patients have elevated levels of low-density lipoprotein cholesterol, rendering them at high risk of premature coronary artery disease (PCAD). However, the FH prevalence among angiogram-proven PCAD (AP-PCAD) patients and their status of coronary risk factors (CRFs) have not been reported in the Asian population.ObjectivesThis study aimed to (1) determine the prevalence of clinically diagnosed FH among AP-PCAD patients, (2) compare CRFs between AP-PCAD patients with control groups, and (3) identify the independent predictors of PCAD.MethodsAP-PCAD patients and FH patients without PCAD were recruited from Cardiology and Specialist Lipid Clinics. Subjects were divided into AP-PCAD with FH (G1), AP-PCAD without FH (G2), FH without PCAD (G3) and normal controls (G4). Medical records were collected from the clinic database and standardised questionnaires. FH was clinically diagnosed using Dutch Lipid Clinic Network Criteria.ResultsA total of 572 subjects were recruited (males:86.4%; mean±SD age: 55.6±8.5years). The prevalence of Definite, Potential and All FH among AP-PCAD patients were 6%(19/319), 16% (51/319) and 45.5% (145/319) respectively. G1 had higher central obesity, family history of PCAD and family history of hypercholesterolaemia compared to other groups. Among all subjects, diabetes [OR(95% CI): 4.7(2.9,7.7)], hypertension [OR(95% CI): 14.1(7.8,25.6)], FH [OR(95% CI): 2.9(1.5,5.5)] and Potential (Definite and Probable) FH [OR(95% CI): 4.5(2.1,9.6)] were independent predictors for PCAD. Among FH patients, family history of PCAD [OR(95% CI): 3.0(1.4,6.3)] and Definite FH [OR(95% CI): 7.1(1.9,27.4)] were independent predictors for PCAD.ConclusionPotential FH is common among AP-PCAD patients and contributes greatly to the AP-PCAD. FH-PCAD subjects have greater proportions of various risk factors compared to other groups. Presence of FH, diabetes, hypertension, obesity and family history of PCAD are independent predictors of PCAD. FH with PCAD is in very-high-risk category, hence, early management of modifiable CRFs in these patients are warranted.
| S-EPMC9439256 | biostudies-literature
Project description:BackgroundParaoxonase-1 (PON1), a glycoprotein associated with serum high-density lipoprotein (HDL), has a central role in metabolizing lipid peroxides, exhibiting antiatherogenic properties. The polymorphism p.Q192R has been previously associated with coronary artery disease (CAD) susceptibility and clopidogrel response.PurposeWe aimed at investigating the association of PON1 p.Q192R with CAD and clopidogrel response in Colombian population.Patients and methodsThe study was conducted among 163 patients diagnosed with CAD and treated with clopidogrel. The allele frequencies for the PON1 192Q and 192R alleles were determined in cases and Latin-American controls obtained from the public database gnomAD (n = 17,711). Response to clopidogrel was determined by assessing the platelet function using the INNOVANCE PFA-200 System. We determined the association between PON1 p.Q192R polymorphism, increased susceptibility to CAD and high on-treatment platelet reactivity (HPR) by using odds ratio (OR) and 95% confidence interval (CI) on four genetic models.ResultsThe allele frequencies for the PON1 192Q and 192R alleles were 0.60 and 0.40, respectively. The allele distribution was found to be statistically different from the control group and other ethnic groups. The allele 192R was positively associated with decreased susceptibility to CAD under a dominant model (OR, 0.58; 95% CI, 0.42-0.8; P < 0.01). We found no association between the polymorphism and HPR.ConclusionWe propose that PON1 p.Q192R is a potentially useful marker for CAD susceptibility in the Colombian population and lacks association with HPR under clopidogrel treatment.
| S-EPMC8573264 | biostudies-literature
Project description:OBJECTIVE:HIV-positive (HIV+) individuals experience an increased burden of coronary artery disease (CAD) not adequately accounted for by traditional CAD risk factors. Coronary endothelial function (CEF), a barometer of vascular health, is depressed early in atherosclerosis and predict future events but has not been studied in HIV+ individuals. We tested whether CEF is impaired in HIV+ patients without CAD as compared with an HIV-negative (HIV-) population matched for cardiac risk factors. DESIGN/METHODS:In this observational study, CEF was measured noninvasively by quantifying isometric handgrip exercise-induced changes in coronary vasoreactivity with MRI in 18 participants with HIV but no CAD (HIV+CAD-, based on prior imaging), 36 age-matched and cardiac risk factor-matched healthy participants with neither HIV nor CAD (HIV-CAD-), 41 patients with no HIV but with known CAD (HIV-CAD+), and 17 patients with both HIV and CAD (HIV+CAD+). RESULTS:CEF was significantly depressed in HIV+CAD- patients as compared with that of risk-factor-matched HIV-CAD- patients (P?<?0.0001) and was depressed to the level of that in HIV- participants with established CAD. Mean IL-6 levels were higher in HIV+ participants (P?<?0.0001) and inversely related to CEF in the HIV+ patients (P?=?0.007). CONCLUSION:Marked coronary endothelial dysfunction is present in HIV+ patients without significant CAD and is as severe as that in clinical CAD patients. Furthermore, endothelial dysfunction appears inversely related to the degree of inflammation in HIV+ patients as measured by IL-6. CEF testing in HIV+ patients may be useful for assessing cardiovascular risk and testing new CAD treatment strategies, including those targeting inflammation.
| S-EPMC5626458 | biostudies-literature
Project description:AimTo review and compare the PON-1 arylesterase activity between coronary artery disease (CAD) and non-CAD patients.MethodsData were obtained by searching MEDLINE and Scopus for all investigations published between January 1, 2000 and March 1, 2021 comparing PON-1 arylesterase activity between CAD and controls.ResultsTwenty studies, based on 5417 patients, met the inclusion criteria and were included in the analysis. A random effect model revealed that PON-1 arylesterase activity was significantly lower in the CAD group compared to controls (SMD = -0.587, 95%CI = -0.776 to -0.339, p < 0.0001, I 2 = 92.3%). In CAD patients, the PON-1 arylesterase activity was significantly higher among CAD patients without diabetes mellitus (DM) compared to those with diabetes (SMD: 0.235, 95% CI: 0.014 to 0.456, p = 0.03, I 2 = 0%).ConclusionsPON-1 activity is significantly lower in CAD patients, and those without DM presented a significantly higher PON-1 arylesterase activity.
| S-EPMC8930235 | biostudies-literature
Project description:BackgroundClinical workup for chest pain varies among institutions. Acute coronary syndrome (ACS) is the primary diagnosis to rule out in the differential diagnosis, due to its associated mortality and morbidity. Although studies have demonstrated efficacy of coronary computed tomographic angiography (CCTA) in diagnosis obstructive coronary artery disease (CAD), there is limited evidence in the clinical value of performing cardiac nuclear stress perfusion imaging [myocardial perfusion imaging (MPI)] exam in patients with chest pain after undergoing CCTA. We aim to evaluate clinical value of follow-up nuclear cardiac MPI in patients with chest pain who have undergone recent CCTA.MethodsA total of 1,000 patients were evaluated in this IRB approved retrospective study who presented with symptoms of ACS. Patients who had elevated troponin or abnormal electrocardiogram (ECG) findings at initial presentation or prior to cardiac nuclear MPI were excluded from the study. All patients who underwent 64- or 320-detector row ECG-gated CCTA as well as a follow-up nuclear MPI. Patients who had diagnostics studies limited by artifact [e.g., suboptimal intravenous (IV) contrast bolus in CCTA, motion artifact on CCTA or MPI, etc.] were excluded.ResultsOne hundred patients met the inclusion criteria. Patient demographics include average age 64.3 [32-89] years, 59 male, 41 females. Ninety-five/100 patients had at least one vessel with 50-70% coronary artery diameter stenosis measured on CCTA. There were no focal perfusion abnormalities identified on cardiac nuclear MPI in patients with less than 70% stenosis diagnosed on CCTA. Five percent of patients were identified with coronary arterial narrowing greater than 70% on CCTA and all 5 of these patients have evidence of abnormal cardiac nuclear stress test (perfusion abnormalities, chest pain, abnormal ECG).ConclusionsIn low-to-intermediate risk patients with chest pain and evidence of non-critical coronary artery stenosis (i.e., less than 70% stenosis) diagnosed on CCTA, a follow-up cardiac nuclear perfusion imaging is of limited value.
| S-EPMC7578483 | biostudies-literature
Project description:We aimed to clarify the possible functional role of hsa_circ_0000563 in coronary artery disease. Therefore, the ChIRP-MS was conducted to explore the interaction between BTBD7_hsa_circ_0000563 and proteins on a genomic scale in human peripheral blood mononuclear cell (PBMC). This project is the raw files of the proteins bound to hsa_circ_0000563 found by ChIRP-MS in PBMC.
2023-03-11 | PXD033196 | Pride