Opium may affect coronary artery disease by inducing inflammation but not through the expression of CD9, CD36, and CD68

2021 ◽  
pp. jim-2021-001935
Author(s):  
Mohammad Amin Momeni-Moghaddam ◽  
Gholamreza Asadikaram ◽  
Mohammad Masoumi ◽  
Erfan Sadeghi ◽  
Hamed Akbari ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Messenger Rna ◽  
Molecular Mechanisms ◽  
Control Group ◽  
Mrna Levels ◽  
Tnf Α ◽  
Opium Addiction ◽  
Ifn Γ ◽  
Artery Disease

The molecular mechanisms of opium with regard to coronary artery disease (CAD) have not yet been determined. The aim of the present study was to evaluate the effect of opium on the expression of scavenger receptors including CD36, CD68, and CD9 tetraspanin in monocytes and the plasma levels of tumor necrosis factor alpha (TNF-α), interferon gamma (IFN-γ), malondialdehyde (MDA), and nitric oxide metabolites (NOx) in patients with CAD with and without opium addiction. This case–control study was conducted in three groups: (1) opium-addicted patients with CAD (CAD+OA, n=30); (2) patients with CAD with no opium addiction (CAD, n=30); and (3) individuals without CAD and opium addiction as the control group (Ctrl, n=17). Protein and messenger RNA (mRNA) levels of CD9, CD36, and CD68 were evaluated by flow cytometry and reverse transcription-quantitative PCR methods, respectively. Consumption of atorvastatin, aspirin, and glyceryl trinitrate was found to be higher in the CAD groups compared with the control group. The plasma level of TNF-α was significantly higher in the CAD+OA group than in the CAD and Ctrl groups (p=0.001 and p=0.005, respectively). MDA levels significantly increased in the CAD and CAD+OA groups in comparison with the Ctrl group (p=0.010 and p=0.002, respectively). No significant differences were found in CD9, CD36, CD68, IFN-γ, and NOx between the three groups. The findings demonstrated that opium did not have a significant effect on the expression of CD36, CD68, and CD9 at the gene and protein levels, but it might be involved in the development of CAD by inducing inflammation through other mechanisms.

TUMOR NECROSIS FACTOR ALFA IN VERY ELDERLY PATIENTS WITH CORONARY ARTERY DISEASE

2021 ◽  
pp. 64-70
Author(s):  
С.В. Тополянская ◽  
Т.А. Елисеева ◽  
О.Н. Вакуленко ◽  
Л.И. Дворецкий
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Elderly Patients ◽  
Type I Collagen ◽  
Cholesterol Concentration ◽  
Control Group ◽  
Type I ◽  
Very Elderly ◽  
Tnf Α ◽  
Artery Disease

Представлены результаты исследования концентрации TNF-α, а также взаимосвязи этого цитокина с рядом патологических состояний у больных старческого возраста c ИБС по сравнению с контрольной группой больных без ИБС. Средняя концентрация TNF-α достигала 9,2±4,7 пг/мл (3,9-31,9 пг/мл) при нормальных значениях TNF-α <8,1 пг/мл. Повышение уровня TNF-α обнаружено у 54,6 % больных. У больных ИБС средняя концентрация TNF-α достигала 10±4,9 пг/мл, тогда как в группе пациентов без ИБС - 6,1±1,8 пг/мл (р=0,000001). Содержание TNF-α было выше у пациентов с ХСН (р=0,002) и гиперурикемией (р=0,000006). Была выявлена достоверная позитивная корреляция уровня TNF-α и мочевой кислоты (р<0,000001), мочевины (р=0,00004), креатинина (р=0,002) и β-Cross Laps (продуктов деградации коллагена), р=0,0001, в сыворотке крови. Обнаружена отрицательная корреляция TNF-α и холестерина ЛПВП (р=0,00005), а также лептина (р=0,01). Отмечено снижение концентрации TNF-α с возрастом (р=0,006). The results of a study of the concentration of TNF-α as well as the relationship of this cytokine with a number of pathological conditions in very elderly patients with coronary artery disease compared with the control group of patients without CAD are presented in the article. The average group concentration of TNF-α reached 9,2±4,7 pg/ml (from 3,9 to 31,9 pg/ml) with normal TNF-α values of less than 8,1 pg/ml. An increase in the level of TNF-α was detected in 54,6 % of patients. In patients with coronary artery disease the average concentration of TNF-α reached 10±4,9 pg/ml, while in the group of patients without CAD - 6,1±1,8 pg/ ml (р=0,000001). TNF-α content was higher in patients with chronic heart failure (р=0,002) and with hyperuricemia (р=0,000006). The correlation analysis revealed a significant positive correlation between the level of TNF-α and uric acid (р<0,000001), between the concentration of TNF-α and the content of β-Cross Laps (degradation products of type I collagen) (р=0,0001), as well as serum creatinine (р=0,002) and urea (p=0,00004) levels. In addition, a negative correlation was found between the values of TNF-α and high-density lipoprotein cholesterol concentration (р=0,00005), as well as leptin level (h=0,01). A decrease in the concentration of TNF-а was observed with increasing age of the patients (р=0,006).

scholarly journals Effect of genistein and daidzein on platelet aggregation and monocyte and endothelial function

2003 ◽  
Vol 89 (5) ◽  
pp. 607-615 ◽  
Author(s):  
Nicole Gottstein ◽  
Benjamin A. Ewins ◽  
Clair Eccleston ◽  
Gary P. Hubbard ◽  
Ian C. Kavanagh ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Endothelial Cells ◽  
Coronary Artery ◽  
Platelet Aggregation ◽  
No Production ◽  
Mrna Levels ◽  
Dependent Manner ◽  
Tnf Α ◽  
Artery Disease

There has been much recent interest in the cardiovascular benefits of dietary isoflavones. The aim of the presentin vitrostudies was to investigate potential anti-thrombogenic and anti-atherogenic effects of the isoflavones genistein and daidzein in platelets, macrophages and endothelial cells. Pre-treatment with either isoflavone inhibited collagen-induced platelet aggregation in a dose-dependent manner. In a macrophage cell line (RAW 264·7) activated with interferon γ plus lipopolysaccharide, both isoflavones were found to inhibit NO production and tumour necrosis factor α (TNF-α) secretion dose-dependently, but they did not affect mRNA levels for inducible nitric oxide synthase and cyclo-oxygenase-2. Both isoflavones also dose-dependently decreased monocyte chemoattractant protein-1 secretion induced by TNF-α in human umbilical vein endothelial cells. Compared with daidzein, genistein exerted greater inhibitory effects for all parameters studied. The present data contributes to our knowledge on the molecular mechanisms by which isoflavones may protect against coronary artery disease. Further studies are required to determine whether the effects of isoflavones observed in the currentin vitrostudies are relevant to the aetiology of coronary artery diseasein vivo.

Elevated level of circulatory sTLT1 induces inflammation through SYK/MEK/ERK signalling in coronary artery disease

2019 ◽  
Vol 133 (22) ◽  
pp. 2283-2299
Author(s):  
Apabrita Ayan Das ◽  
Devasmita Chakravarty ◽  
Debmalya Bhunia ◽  
Surajit Ghosh ◽  
Prakash C. Mandal ◽  
...  
Keyword(s):  
Risk Factors ◽  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Chronic Inflammation ◽  
Ex Vivo ◽  
Human Subjects ◽  
Critical Role ◽  
Atherosclerotic Cardiovascular Disease ◽  
Tnf Α ◽  
Artery Disease

Abstract The role of inflammation in all phases of atherosclerotic process is well established and soluble TREM-like transcript 1 (sTLT1) is reported to be associated with chronic inflammation. Yet, no information is available about the involvement of sTLT1 in atherosclerotic cardiovascular disease. Present study was undertaken to determine the pathophysiological significance of sTLT1 in atherosclerosis by employing an observational study on human subjects (n=117) followed by experiments in human macrophages and atherosclerotic apolipoprotein E (apoE)−/− mice. Plasma level of sTLT1 was found to be significantly (P<0.05) higher in clinical (2342 ± 184 pg/ml) and subclinical cases (1773 ± 118 pg/ml) than healthy controls (461 ± 57 pg/ml). Moreover, statistical analyses further indicated that sTLT1 was not only associated with common risk factors for Coronary Artery Disease (CAD) in both clinical and subclinical groups but also strongly correlated with disease severity. Ex vivo studies on macrophages showed that sTLT1 interacts with Fcɣ receptor I (FcɣRI) to activate spleen tyrosine kinase (SYK)-mediated downstream MAP kinase signalling cascade to activate nuclear factor-κ B (NF-kB). Activation of NF-kB induces secretion of tumour necrosis factor-α (TNF-α) from macrophage cells that plays pivotal role in governing the persistence of chronic inflammation. Atherosclerotic apoE−/− mice also showed high levels of sTLT1 and TNF-α in nearly occluded aortic stage indicating the contribution of sTLT1 in inflammation. Our results clearly demonstrate that sTLT1 is clinically related to the risk factors of CAD. We also showed that binding of sTLT1 with macrophage membrane receptor, FcɣR1 initiates inflammatory signals in macrophages suggesting its critical role in thrombus development and atherosclerosis.

scholarly journals Optimizing diagnosis of obstructive coronary artery disease by CT angiography: RCT's final results and 12-months follow-up

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
J.P Dias Ferreira Reis ◽  
R Ramos ◽  
P Modas Daniel ◽  
S Aguiar Rosa ◽  
L Almeida Morais ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Functional Test ◽  
Control Group ◽  
Diagnostic Strategy ◽  
Coronary Syndrome ◽  
Tertiary Center ◽  
Safety Endpoint ◽  
Artery Disease ◽  
Primary Safety Endpoint

Abstract Aim In patients (pts) with suspected coronary artery disease (CAD), computed tomographic angiography (CTA) may improve pt selection for invasive coronary angiography (ICA) as alternative to functional testing. However. the role of CTA in symptomatic pts after abnormal functional test (FT) is incompletely defined. Methods and results This randomized clinical trial conducted in single academic tertiary center selected 218 symptomatic pts with mild to moderately abnormal FT referred to ICA to receive either the originally intended ICA (n=103) or CTA (n=115). CTA interpretation and subsequent care decisions were made by the clinical team. Pts with high risk features on FT, previous acute coronary syndrome, previously documented CAD, chronic kidney disease (GFR&lt;60ml/min/1.73m2) or persistent atrial fibrillation were excluded. The primary endpoint was the percentage of ICA with no significant obstructive CAD (no stenosis ≥50%) in each group. Diagnostic (DY) and revascularization (RY) yields of ICA in either group were also assessed. Pts were followed up for at least 1 year for the primary safety endpoint of all cause death/ nonfatal myocardial infarction/ stroke. Unplanned revascularization (UP) and symptomatic status (SS) were also evaluated. Pts averaged 68±9 years of age, 60% were male, 29% were diabetic. Nuclear perfusion stress test was used in 33.9% in CTA group and 31.1% in control group (p=0.655). Mean post (functional) test probability of obstructive CAD was 34%. Overall prevalence of obstructive CAD was 32.1%. In the CTA group, ICA was cancelled by referring physicians in 83 of the pts (72.2%) after receiving CTA results. For those undergoing ICA, non-obstructive CAD was found in 5 pts (15.6%) in the CTA-guided arm and 60 (58.3%) in the usual care arm (p&lt;0.001 Mean cumulative radiation exposure related to diagnostic work up was similar in both groups (6±14 vs 5±14mSv, p=0.152). Both DY (84.4% vs 41.7, p&lt;0.001) and RY (71.9% vs 38.8%, p=0.001) yields were significantly higher for CTA-guided ICA as compared to standard FT-guided ICA. The rate of the primary safety endpoint was similar between both groups (1.9% vs 0%, p=0.244), as well as the rates of UP (0.9% vs 0.9%, p=1.000) and SS (persistent angina: 29.6% vs 24.8%, p=0.425). Conclusions In pts with suspected CAD and mild to moderately abnormal ischemia test, a diagnostic strategy including CTA as gatekeeper is safe, effective and significantly improves diagnostic and revascularization yields of ICA. Funding Acknowledgement Type of funding source: None

scholarly journals Association of TNF-α (-308G/A) Gene Polymorphism with Circulating TNF-α Levels and Excessive Daytime Sleepiness in Adults with Coronary Artery Disease and Concomitant Obstructive Sleep Apnea

2021 ◽  
Vol 10 (15) ◽  
pp. 3413
Author(s):  
Afrouz Behboudi ◽  
Tilia Thelander ◽  
Duygu Yazici ◽  
Yeliz Celik ◽  
Tülay Yucel-Lindberg ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Obstructive Sleep Apnea ◽  
Coronary Artery ◽  
Sleep Apnea ◽  
Gene Polymorphism ◽  
Excessive Daytime Sleepiness ◽  
Daytime Sleepiness ◽  
Obstructive Sleep ◽  
Tnf Α ◽  
Artery Disease

Obstructive sleep apnea (OSA) is common in patients with coronary artery disease (CAD), in which inflammatory activity has a crucial role. The manifestation of OSA varies significantly between individuals in clinical cohorts; not all adults with OSA demonstrate the same set of symptoms; i.e., excessive daytime sleepiness (EDS) and/or increased levels of inflammatory biomarkers. The further exploration of the molecular basis of these differences is therefore essential for a better understanding of the OSA phenotypes in cardiac patients. In this current secondary analysis of the Randomized Intervention with Continuous Positive Airway Pressure in CAD and OSA (RICCADSA) trial (Trial Registry: ClinicalTrials.gov; No: NCT 00519597), we aimed to address the association of tumor necrosis factor alpha (TNF-α)-308G/A gene polymorphism with circulating TNF-α levels and EDS among 326 participants. CAD patients with OSA (apnea–hypopnea-index (AHI) ≥ 15 events/h; n = 256) were categorized as having EDS (n = 100) or no-EDS (n = 156) based on the Epworth Sleepiness Scale score with a cut-off of 10. CAD patients with no-OSA (AHI < 5 events/h; n = 70) were included as a control group. The results demonstrated no significant differences regarding the distribution of the TNF-α alleles and genotypes between CAD patients with vs. without OSA. In a multivariate analysis, the oxygen desaturation index and TNF-α genotypes from GG to GA and GA to AA as well as the TNF-α-308A allele carriage were significantly associated with the circulating TNF-α levels. Moreover, the TNF-α-308A allele was associated with a decreased risk for EDS (odds ratio 0.64, 95% confidence interval 0.41–0.99; p = 0.043) independent of age, sex, obesity, OSA severity and the circulating TNF-α levels. We conclude that the TNF-α-308A allele appears to modulate circulatory TNF-α levels and mitigate EDS in adults with CAD and concomitant OSA.

CD14+CD16+ monocytes in coronary artery disease and their relationship to serum TNF-α levels

2004 ◽  
Vol 92 (08) ◽  
pp. 419-424 ◽  
Author(s):  
Stefan Blankenberg ◽  
Christine Espinola-Klein ◽  
Joern Dopheide ◽  
Christoph Bickel ◽  
Karl Lackner ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Animal Studies ◽  
Inflammatory Diseases ◽  
Serum Concentrations ◽  
Tnf Α ◽  
Hs Crp ◽  
Artery Disease ◽  
Fourth Quartile

SummaryMonocytes play a central role in the inflammatory disease atherosclerosis. CD14+CD16+ monocytes are considered proinflammatory monocytes, as they have an increased capacity to produce proinflammatory cytokines, such as TNF-α, and are elevated in various inflammatory diseases. We hypothesized that patients with coronary artery disease (CAD) have increased levels of CD14+CD16+ monocytes, and that CD14+CD16+ monocytes are associated with inflammation markers. We investigated CD14+CD16+ monocytes in 247 patients with CAD and 61 control subjects using flow cytometry. In addition serum concentrations of TNF-α, IL-6, and Hs-CRP were assessed. Patients with CAD had higher levels of CD14+CD16+ monocytes than controls (13.6% versus 11.4%; p<0.001). Logistic regression analysis including quartiles of CD14+CD16+ monocytes showed that CD14+CD16+ monocytes were associated with prevalence of CAD (OR 4.9, 95% CI 2.5–19.1, for subjects in the fourth quartile in comparison to subjects in the first quartile). The association between CD14+CD16+ monocytes and CAD remained independently significant after adjustment for most potential confounders (OR 5.0, 95% CI 1.2-20.0). Serum concentrations of TNF-α were elevated in subjects within the highest quartiles of CD14+CD16+ monocytes (p=0.018). Our study showed that increased numbers of CD14+CD16+ monocytes are associated with coronary atherosclerosis and TNF-α. In accordance, recent animal studies suggest a possibly important role of these monocytes in the development of atherosclerosis.

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.

scholarly journals Assessment of structural and functional myocardial characteristics in patients with chronic coronary artery disease and various glycemic status

2021 ◽  
Vol 20 (7) ◽  
pp. 3077
Author(s):  
M. A. Kokozheva ◽  
B. U. Mardanov ◽  
E. A. Poddubskaya ◽  
V. A. Kutsenko ◽  
M. A. Umetov ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Exercise Tolerance ◽  
Ventricular Hypertrophy ◽  
Left Ventricular ◽  
Control Group ◽  
Glycemic Status ◽  
Artery Disease

Aim. To study the structural and functional myocardial characteristics in patients with exertional angina and type 2 diabetes in comparison with those without diabetes to identify combined hemodynamic changes.Material and methods. Patients were divided into two groups depen - ding on the glycemic status. The first group consisted of 49 patients (mean age, 57,9±1,04 years; male/female, 35/14) with coronary artery disease (CAD) and type 2 diabetes, while the second one (control)  — 51 patients (60,2±0,9 years, 34/17) with CAD and without diabetes. Patients were surveyed using a standard questionnaire that included socio-demographic parameters, behavioral risk factors, clinical status, medications received, and comorbidities. Diagnostic investigations were carried out, including resting electrocardiography, transthoracic echocardiography and cycle ergometry.Results. Among patients with CAD and type 2 diabetes, hypertension occurred 20% more often compared with the control group  — 98 vs 78% (p<0,004). According to the electrocardiography, the combination of diabetes and CAD was characterized by various arrhythmias, which were recorded 2,8 times more often than in the group without diabetes. According to echocardiography, signs of left ventricular hypertrophy, systolic and diastolic dysfunction prevailed in people with diabetes. Mean pulmonary artery pressure in patients with diabetes were higher than in patients without carbohydrate metabolism disorders (p<0,004). According to the stress test, exercise tolerance in experimental group patients was lower than in patients in the control group.Conclusion. The combination of chronic CAD and type 2 diabetes is cha - racterized by a more common combination with hypertension, impaired central and intracardiac hemodynamics, as well as left ventricular hypertrophy. In people with diabetes, impaired systolic and diastolic myocardial function is combined with reduced exercise tolerance.

scholarly journals Patients with New-Onset Tumor of Severe Coronary Artery Disease May be at a Higher Risk of Arrhythmia

2021 ◽  
Vol 2021 ◽  
pp. 1-4
Author(s):  
Palisha Alimu ◽  
Dezhi Yang ◽  
Huatao Zhou ◽  
Yan Wu ◽  
Huiping Guo
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Disease Patient ◽  
Control Group ◽  
Severe Coronary Artery Disease ◽  
Tumor Treatment ◽  
Severe Coronary Artery ◽  
The Difference ◽  
Artery Disease ◽  
New Onset

Background. Arrhythmia is one of the causes of death in severe coronary artery disease patients who also suffered from cancer. Our research aims to compare the incidence of arrhythmia between severe coronary artery disease patient with and without new-onset tumor. Methodology. We enrolled 79 patients (December 2019–December 2020) with severe coronary artery disease in this study, and 40 of them were complicated with new-onset tumor. The details of all subjects were thoroughly obtained; the laboratory tests were implemented including creatinine before coronary angiography. The appraisal of the severity of coronary artery disease was applied by Gensini score. The cardiac inspection includes UCG, 12-lead ECG, and Holter monitor. Results. Among them, there were 40 patients in the experimental group and 39 patients in the control group. The difference at the baseline between the two sets of figures was not statistically significant ( P > 0.05 ). The incidence of arrhythmia between the two groups was statistically significant ( P < 0.05 ). Conclusions. The incidence of arrhythmia in severe coronary artery disease patients who were complicated with new-onset tumor was higher than that in patients with severe coronary artery disease alone, and attention should be paid to arrhythmia before tumor treatment.

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