scholarly journals Comparison of Tumor Necrosis Factor-α Level in Coronary Artery Disease and Coronary Slow Flow of Thrombolysis in Myocardial Infarction

2019 ◽  
Vol 11 (3) ◽  
pp. 299-303
Author(s):  
Muhammad Diah ◽  
Rahmawati Rahmawati ◽  
Aznan Lelo ◽  
Zulfikri Muhktar ◽  
Dharma Lindarto ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Healthy Subjects ◽  
Slow Flow ◽  
Timi Frame Count ◽  
Tnf Α ◽  
Significant Difference ◽  
Coronary Slow Flow ◽  
Artery Disease ◽  
Α Level

BACKGROUND: Tumor necrosis factor (TNF)-α, an important primary pro-inflammatory cytokine, has a crucial role in the pathogenesis of atherosclerosis. Since the pathophysiological mechanism of coronary slow flow (CSF) is not fully understood, we investigated the level of TNF-α in coronary artery disease (CAD), CSF and healthy subjects.METHODS: This study was conducted in cross-sectional design involving 16 CAD, 18 CSF and 18 healthy subjects. Coronary angiography was recorded at the left anterior oblique, cranial, right anterior oblique, caudal, and horizontal positions. The flow in coronary arteries of the subjects were assessed using Thrombolysis in the Myocardial Infarction (TIMI) frame count method. Peripheral blood-derived serum was collected and level of TNF-α was determined by using highly sensitive enzymelinked immunosorbent assay (ELISA).RESULTS: No significant difference in level of TNF-α in CAD, CSF and healthy subjects (2.72±2.64 pg/mL, 1.88±0.8 pg/mL, 1.64±0.35 pg/mL, respectively) (p=0.087). In addition, there was no correlation between the concentration of TNF-α and TIMI frame count (r<0.2, p>0.05).CONCLUSION: There was no significant difference of TNF-α level in CAD, CSF and healthy subjects. In addition, there was no correlation between the TNF-α level with TIMI frame count as well. Nevertheless, further clinical studies with more subjects are needed.KEYWORDS: TNF-alpha, coronary artery disease, coronary slow flow 

scholarly journals IL-32 Serum Levels in Coronary Artery Disease Patient and its Relationship with IL-6 and TNF-α Serum Levels

2021 ◽  
Author(s):  
Mina Mohammad-Rezaei ◽  
Reza Ahmadi ◽  
Ali Rafiei ◽  
Arsalan Khaledifar ◽  
Shohila Fatahi ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Serum Levels ◽  
Arterial Stenosis ◽  
Enzyme Linked Immunosorbent Assay ◽  
Control Subjects ◽  
Tnf Α ◽  
Significant Difference ◽  
Major Vessel ◽  
Artery Disease

Abstract Coronary Artery Disease (CAD) is a chronic inflammatory disease caused by atherosclerosis and arteries become clogged due to plaque formation, fat accumulation, and various sorts of immune cells. IL-32 is a new proinflammatory cytokine, which enhances inflammation through inducing different inflammatory cytokines. The purpose of current research was to assess IL-32 serum levels in coronary artery disease subjects and its relationship with serum levels of IL-6 and TNF-α. Forty-two subjects diagnosed with CAD and thirty-nine control subjects were enrolled in the research. Serum levels of IL-6, TNF-α, and IL-32 were measured using the enzyme-linked immunosorbent assay (ELISA). IL-32, TNF-α, and IL-6 serum levels were significantly higher by 2.7, 3.48, and 3.2-fold in the CAD subjects than in control subjects, respectively. Moreover, no significant difference was found in TNF-α, IL-6 and IL-32 serum levels with the clogged arteries number in the CAD group. TNF-α and IL-32 serum levels in the CAD subjects with cardiac arterial stenosis in one major vessel were significantly increased than CAD subjects with cardiac arterial stenosis in more than one major vessels. ROC curve analysis revealed that serum levels of IL-32, TNF-α, and IL-6 showed good abilities in predicting CAD. Also, Multiple logistic regression analyses suggested that TNF-α, IL-6, and IL-32, serum levels of LDL and ox-LDL were independently related to the presence of CAD, while HDL serum levels were not. TNF-α, IL-32, and IL-6 showed an increase in CAD group and serum levels of these cytokines showed good abilities in predicting CAD. Our data suggested the involvement of TNF-α and IL-32 in the early stage of CAD.

Association of high mobility group box 1 protein with coronary artery disease

2019 ◽  
Vol 27 (4) ◽  
pp. 251-255 ◽  
Author(s):  
Necla Benlier ◽  
Mustafa Bilge Erdoğan ◽  
Serdar Keçioğlu ◽  
Nuri Orhan ◽  
Hülya Çiçek
Keyword(s):  
Risk Factors ◽  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Healthy Subjects ◽  
High Mobility ◽  
High Mobility Group ◽  
Control Group ◽  
Protein Levels ◽  
Significant Difference ◽  
Artery Disease

Background Recently, the role of inflammation in coronary artery disease and the association of inflammatory biomarkers with adverse outcomes have been investigated in many studies. We investigated the relationship between high serum mobility group box 1 protein levels and established risk factors for coronary artery disease. Methods Fifty-five patients who presented to our Cardiovascular Surgery Clinic and subsequently underwent coronary artery bypass surgery for coronary artery disease and 50 healthy subjects presenting to the cardiology outpatient clinic without any cardiovascular problem were included in the study. The mean age was 61.47 ± 9.38 years for patients and 58.20 ± 10.15 years for controls. Results There was no statistically significant difference between groups with respect to age or sex. Family history of coronary artery disease, aspirin use, hypertension, and type 2 diabetes were significantly more prevalent in the patient group versus the control group. A significant difference was found between patients and healthy controls with respect to high mobility group box 1 protein levels ( p = 0.001). Conclusions Serum high mobility group box 1 protein was significantly increased in patients with coronary artery disease in comparison to healthy subjects. No associations were found between high mobility group box 1 protein level and certain risk factors for coronary artery disease.

scholarly journals Could neutrophil/lymphocyte ratio be an indicator of coronary artery disease, coronary artery ectasia and coronary slow flow?

2016 ◽  
Vol 44 (6) ◽  
pp. 1443-1453 ◽  
Author(s):  
Mücahid Yılmaz ◽  
Hasan Korkmaz ◽  
Mehmet Nail Bilen ◽  
Ökkeş Uku ◽  
Ertuğrul Kurtoğlu
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Slow Flow ◽  
Coronary Artery Ectasia ◽  
Operating Characteristics ◽  
Coronary Anatomy ◽  
Neutrophil Lymphocyte Ratio ◽  
Lymphocyte Ratio ◽  
Coronary Slow Flow ◽  
Artery Disease

Objective To determine whether neutrophil/lymphocyte ratio (NLR) differed between patients with isolated coronary artery disease (CAD), isolated coronary artery ectasia (CAE), coronary slow flow and normal coronary anatomy. Methods Patients who underwent coronary angiography were consecutively enrolled into one of four groups: CAD, coronary slow flow, CAE and normal coronary anatomy. Results The CAD ( n = 40), coronary slow flow ( n = 40), and CAE ( n = 40) groups had similar NLRs (2.51 ± 0.7, 2.40 ± 0.8, 2.6 ± 0.6, respectively) that were significantly higher than patients with normal coronary anatomy ( n = 40; NLR, 1.73 ± 0.7). Receiver operating characteristics demonstrated that with NLR > 2.12, specificity in predicting isolated CAD was 85% and sensitivity was 75%, with NLR > 2.22 specificity in predicting isolated CAE was 86% and sensitivity was 75%. With NLR > 1.92, specificity in predicting coronary slow flow was 89% and sensitivity was 75%. Multivariate logistic regression analyses identified NLR as an independent predictor of isolated CAE (β = −0.499, 95% CI −0.502, −0.178; P <  0.001), CAD (β = −0.426, 95% CI −1.321, −0.408; P <  0.001), and coronary slow flow (β = −0.430, 95% CI −0.811, −0.240; P = 0.001 Table 2 ). Conclusions NLR was higher in patients with CAD, coronary slow flow and CAE versus normal coronary anatomy. NLR may be an indicator of CAD, CAE and coronary slow flow.

scholarly journals The effect of effort test on the levels of ischemia modified albumin, 7-ketocholesterol and cholestan-3β , 5α , 6β -triol and their role in the diagnosis of coronary artery disease

2019 ◽  
Vol 38 (3) ◽  
pp. 249-255 ◽  
Author(s):  
Muhammed Emin Keles ◽  
Afshin Samadi ◽  
Selen Yilmaz Isikhan ◽  
Yusuf Ziya Sener ◽  
Ali Sezgin ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Healthy Subjects ◽  
Test Group ◽  
Study Groups ◽  
Ischemia Modified Albumin ◽  
Significant Difference ◽  
Post Test ◽  
Group 2 ◽  
Artery Disease

Summary Background Oxysterols have been shown to play a role in plaque formation while ischemia modified albumin (IMA) is widely accepted as an acute marker for ischemia. The effort test is one of the methods used to identify the presence of coronary artery disease. Thus, there may be a relationship between effort test result and the levels of IMA, 7-ketocholesterol (7-KC) and cholestane-3β,5α,6β-triol (C-triol). Methods Thirty patients who underwent effort test and 30 healthy subjects were included in the study. IMA levels were determined with the albumin-cobalt binding test, 7-KC and C-triol levels were determined with LC-MS/MS. Among the patients, two subgroups were identified according to the results of the effort test, group 1 consisted of patients with a positive effort test (n = 12), and group 2 consisted of patients who had a negative effort test (n = 18). Results 7-KC levels of patients were significantly higher compared to healthy subjects (39.87 ± 2.13 ng/mL, 20.26 ± 1.35 ng/mL; p=0.001). In patients, post-test 7-KC levels were significantly lower than pre-test levels (post-test vs. pre-test: 37.73 ± 2.44 ng/mL vs. 41.07 ± 2.18 ng/mL; p<0.001). There was a significant difference in post-test 7-KC levels among all study groups (negative, positive and healthy: 37.73 ± 2.44 ng/mL, 39.87 ± 2.13 ng/mL, 20.26 ± 1.35 ng/mL, respectively). There was no significant difference in IMA levels. Conclusions Patients with positive effort test had significantly higher levels of 7-KC. Additionally, after the effort test, the 7-KC value was reduced. 7-KC is a biomarker of oxidative damage and its value or changes before and after the effort test may be used as a biomarker in the diagnosis and follow-up of coronary artery disease.

scholarly journals CXCL9: a biomarker for the coronary slow flow phenomenon in patients with coronary artery disease

2019 ◽  
Author(s):  
youfeng Liang ◽  
xianhe Lin ◽  
yuanyuan Xu ◽  
chunmiao Wang ◽  
Qi Zhou
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Multivariate Logistic Regression Analysis ◽  
Serum Levels ◽  
Slow Flow ◽  
Flow Phenomenon ◽  
Coronary Slow Flow ◽  
Ifn Γ ◽  
Artery Disease ◽  
Coronary Slow Flow Phenomenon

Abstract Background: Atherosclerosis is a chronic inflammatory disease. The pathology underlying the disease consists of accumulation of the extracellular matrix, lipid and inflammatory cells. Coronary Slow Flow Phenomenon (CSFP) is closely related to inflammatory responses, while chemokines play an important role in the progression of atherosclerosis. However, the relationship between chemokines and CSFP is unclear. In this study, our aims were to evaluate the association between CXC Chemokines 9 (CXCL9) levels and CSFP in patients with coronary artery disease. Methods: We studied 46 patients diagnosed with CSFP and classed them as the CSFP group. 50 patients with normal coronary angiography (CAG) were randomly selected as the no-CSFP group in our study. The mean TIMI frame count was used to measure coronary blood flow velocity. The clinical and biochemical index, including serum levels of IL1, IL-6, IL-10, CXCL9, CD40L and interferon-γ (IFN-γ), were analyzed in all subjects. Results: The serum levels of IL-1, IL-6, IL-10, CXCL9, CD40L, IFN-γ and CXCL9 in the CSFP group were significantly higher than those in the no-CSFP group, with the differences being statistically significant (p<0.001). Furthermore, Pearson's correlation analysis reflected a significant positive correlation (r=0.171, p=0.01) in CXCL9 levels. Multivariate logistic regression analysis showed that CXCL9 are important risk factors for CSFP (β=1.795, P=0.000). Subsequent ROC curve analyses indicated that the serum CXCL9 levels demonstrated a high diagnostic value in differentiating patients with CSFP from that of normal controls (Area Under the Curve = 0.758) and the serum CXCL9 level of 131.915 mg/L was a predictor of CSFP, with a sensitivity of 54.3% and a specificity of 96.0%. Conclusions: Our findings are indicative of the potential clinical implications of CXCL9 in the occurrence and development of CSFP.

Evaluation of blood rheology in patients with coronary slow flow or non-obstructive coronary artery disease

2013 ◽  
Vol 53 (4) ◽  
pp. 317-326 ◽  
Author(s):  
Muhammet Bilgi ◽  
Hakan Güllü ◽  
İlknur Kozanoğlu ◽  
Hakan Özdoğu ◽  
Nurzen Sezgin ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Obstructive Coronary Artery Disease ◽  
Blood Rheology ◽  
Slow Flow ◽  
Coronary Slow Flow ◽  
Artery Disease

Biological and clinical implications of TNF-α promoter and CYP1B1 gene variations in Coronary Artery Disease susceptibility

2021 ◽  
Vol 22 ◽  
Author(s):  
Rashid Mir ◽  
Imadeldin Elfaki ◽  
Chandan K. Jha ◽  
Jamsheed Javid ◽  
Abdullatif Taha Babakr ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Gene Polymorphism ◽  
P Value ◽  
Inflammatory Disorder ◽  
Genotype Distribution ◽  
Direct Dna Sequencing ◽  
Tnf Α ◽  
Significant Difference ◽  
Artery Disease

Background: Background: Cardiovascular diseases (CVD) are important causes of death worldwide. Atherosclerosis is a chronic inflammatory disorder. It is the major cause of CVD and is manifested by ischemic heart disease or coronary artery disease (CAD). TNF-α is a pro-inflammatory cytokine that regulates immune response and promotes the development of atherosclerosis. Cytochrome p450 1B1 (CYP1B1) is an enzyme involved in the metabolism of endogenous and exogenous substrates. Objectives: This study aimed at examining the association of TNF-α rs1800629 G >A and CYP1B1 rs1056827 G>T gene polymorphisms with CAD susceptibility in an Indian cohort. Methods: AS-PCR and direct DNA sequencing were used to examine the association of TNF-α rs1800629 G >A and CYP1B1 rs1056827 G>T gene polymorphism with CAD in an Indian cohort. A total of 100 clinically confirmed cases of CAD and 110 matched apparently healthy controls were genotyped. Results: Allelic and genotypic frequencies did not deviate from Hardy-Weinberg equilibrium in the controls (p>0.05) for TNF-α G-308A and CYP1B1 rs1056827G>A. There was no significant difference between the TNF-α rs1800629 A>G genotype distribution between cases and controls (P-value >0.05). A significant difference was observed between the CYP1B1 rs1056827 G>T genotype distribution between CAD cases and controls (P<0.0003). Our result indicated that in the codominant model, the GA genotype of the CYP1B1 rs1056827 G>T was associated with CAD with OR= 2.21(1.17 to 4.15), RR=1.38(1.07 to 1.78), and P<0.013. In the dominant model, the (GA+AA) genotype was associated with CAD with OR=2.79(1.54 to 5.05) and P<0.007. The CYP1B1 rs1056827 ‘A’ allele was associated with CAD with OR = 2.30 (1.55 to 3.42) and P< 0.0001. Our results indicated that TNF-α 1800629 gene polymorphism was strongly associated with hypercholesteremia (P<0.0009), HDL (P<0.0001), TGL (P<0.039), hypertension (P<0.0001), and smoking (P<0.0001) in patients with Coronary Artery Disease. Similar correlations of CYP1B1 rs1056827 genotypes were reported with cholesterol (P<0.020), HDL (P<0.002), LDL (P<0.006), hypertension (P<0.03), and smoking (P<0.005). Conclusion: It was reported that the GA genotype of the CYP1B1 rs1056827 G>T was strongly associated with susceptibility to Coronary Artery Disease with OR= 2.21(1.17 to 4.15)) and P<0.013, and similarly, its A allele was associated with predisposition to CAD with OR = 2.30(1.55 to 3.42) and P< 0.0001. Our results indicated that TNF-α 1800629 gene polymorphism is not associated with predisposition to Coronary Artery Disease. Nevertheless, these results should be taken with caution and further validated with larger-scale studies before being introduced in the clinical setting.

scholarly journals Polymorphisms of endothelial nitric oxide synthase and hypoxia-inducible factor 1 alpha genes play a role in susceptibility to coronary artery disease

2018 ◽  
Vol 5 (9) ◽  
pp. 2688-2696 ◽  
Author(s):  
Ali Asghar Kiani ◽  
Vahide Heydari Nazarabad ◽  
Kolsoum Ahmadi ◽  
Khatereh Anbari ◽  
Babak Baharvand Ahmadi
Keyword(s):  
Nitric Oxide ◽  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Healthy Subjects ◽  
Significant Difference ◽  
The Difference ◽  
Artery Disease ◽  
Oxide Synthase ◽  
And Control ◽  
Endothelial Nitric Oxide

Objective: Genetics is a known factor in the susceptibility to cardiovascular disease. In this study, polymorphisms of endothelial nitric oxide synthase (eNOS) (T876C and G894T) and hypoxiainducible factor 1 (HIF1) (rs10873142 and rs41508050) in coronary artery disease were compared with healthy subjects, and the relationship between these mutations and risk of coronary artery disease (CAD) was assessed. Methods: Blood samples were collected from 138 patients with obstructive CAD and 115 healthy subjects. Polymerase chain reaction- restriction fragment length polymorphism (PCR-RFLP), Griess test, and enzyme-linked immunosorbent assay (ELISA) were used to measure serum nitric oxide (NO) and paraoxonase antioxidant. Independent t-test was used to examine the relationship between variables. Results: There was no significant difference between genotype frequency in healthy subjects and patients for eNOS and HIF1 alpha polymorphisms. There was no significant difference between these polymorphisms and age, sex, hypertension and lipidemia. Furthermore, the difference in mean serum levels of NO in different genotypes of the G894T gene was not significant between the patient and control groups. However, the difference in mean serum NO levels in different genotypes of the T786C gene was significant between the patient and control groups such that minimum and maximum serum NO levels were observed in individuals bearing TT and TC genotypes, respectively. The difference in mean serum NO levels was higher in patients than in controls, and was statistically significant. Conclusions: The results suggest that the T876C polymorphism could be associated with low serum NO level and implicated as a risk factor for developing CAD. Furthermore, our findings indicate that genetics may not be involved in susceptibility to CAD; however, further comprehensive studies are required.

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