CYTOKINE RESISTIN IN METABOLIC AND CARDIOVASCULAR DISEASE.

2021 ◽  
pp. 49-50
Author(s):  
Prajakta Kadu

The rise in metabolic syndromes is known to be the root cause of major cardiovascular diseases mainly Coronary Artery Disease (CAD) in India. A biological marker will thus help to determine the disease before its onset and help cure it at early stages, reducing the chances of development of further complications. There are various pro-inammatory markers (cytokines) which can be used to determine the onset of disease one such marker known is resistin. Resistin is known to be a pro-inammatory adipokine secreted mainly from Peripheral mononuclear cell (PMNC), bone marrow cells and macrophages in humans [1]. Inammatory response is generated due to rise in metabolic syndromes which in turn leads to the secretion of various cytokines. The levels of these cytokines released help in determining the severity of disease.

2018 ◽  
Vol 17 (4) ◽  
pp. 171-179
Author(s):  
A. M. Chernyavskiy ◽  
A. V. Fomichev ◽  
N. A. Nikitin ◽  
O. V. Poveshchenko ◽  
J. E. Kareva ◽  
...  

Purpose.To evaluate the changes of myocardial perfusion using 99mТс-MIBI single-photon emission computed tomography (SPECT) after the intramyocardial implantation of erythropoietin preconditioned autologous bone marrow cells (ABMC) in laser channels during coronary artery disease (CAD) surgery.Materials and methods.Randomized study of 40 patients (mean age 58.0 ± 6.9, 9 females) with diffuse and (or) distal right coronary artery disease (RCA). Patients of the study group (n= 23) underwent coronary artery bypass grafting (CABG) of the left coronary artery (LCA) system and intramyocardial implantation of erythropoietin preconditioned ABMC in the left ventricular (LV) inferior wall. Patients of the control group (n= 17) underwent CABG of the LCA system only. 99mТс-MIBI SPECT performed 1–2 days before and 12 months after surgery.Results.In study group after 12-month follow-up the summed stress score in a typical RCA supply area (SSSRCA) improved from 7.0 [5.5; 10.5] to 4.0 [1.0; 5.5] (p<0.01), summed rest score (SRSRCA) improved from 3.0 [0.0; 7.0] to 1.0 [0.0; 3.5] (p<0.01), and summed different score (SDSRCA) improved from 3.0 [1.0; 4.0] to 1.0 [0.0; 2.0] (p= 0.03). Control group patients after 12-month follow-up showed significant improvement of SSS RCA only – from 8.0 [6.0; 12.0] to 5.0 [4.0; 7.0] (p<0.01).Conclusion.After 12-month follow-up in patients with diffuse and (or) distal RCA disease, the procedure of intramyocardial implantation of the erythropoietin preconditioned ABMC in laser channels is demonstrated to be safe and induces the improvement of myocardial perfusion.  


Author(s):  
Rutao Wang ◽  
Scot Garg ◽  
Chao Gao ◽  
Hideyuki Kawashima ◽  
Masafumi Ono ◽  
...  

Abstract Aims To investigate the impact of established cardiovascular disease (CVD) on 10-year all-cause death following coronary revascularization in patients with complex coronary artery disease (CAD). Methods The SYNTAXES study assessed vital status out to 10 years of patients with complex CAD enrolled in the SYNTAX trial. The relative efficacy of PCI versus CABG in terms of 10-year all-cause death was assessed according to co-existing CVD. Results Established CVD status was recorded in 1771 (98.3%) patients, of whom 827 (46.7%) had established CVD. Compared to those without CVD, patients with CVD had a significantly higher risk of 10-year all-cause death (31.4% vs. 21.7%; adjusted HR: 1.40; 95% CI 1.08–1.80, p = 0.010). In patients with CVD, PCI had a non-significant numerically higher risk of 10-year all-cause death compared with CABG (35.9% vs. 27.2%; adjusted HR: 1.14; 95% CI 0.83–1.58, p = 0.412). The relative treatment effects of PCI versus CABG on 10-year all-cause death in patients with complex CAD were similar irrespective of the presence of CVD (p-interaction = 0.986). Only those patients with CVD in ≥ 2 territories had a higher risk of 10-year all-cause death (adjusted HR: 2.99, 95% CI 2.11–4.23, p < 0.001) compared to those without CVD. Conclusions The presence of CVD involving more than one territory was associated with a significantly increased risk of 10-year all-cause death, which was non-significantly higher in complex CAD patients treated with PCI compared with CABG. Acceptable long-term outcomes were observed, suggesting that patients with established CVD should not be precluded from undergoing invasive angiography or revascularization. Trial registration SYNTAX: ClinicalTrials.gov reference: NCT00114972. SYNTAX Extended Survival: ClinicalTrials.gov reference: NCT03417050. Graphic abstract


Author(s):  
Elifcan Gezer ◽  
Mehtap Cevik ◽  
Cansu Selcan Akdeniz ◽  
Ismail Polat Canbolat ◽  
Selen Yurdakul ◽  
...  

Objective: Coronary artery disease (CAD) is the one of the leading cause of morbidity and mortality worldwide and statins are frequently prescribed in the treatment of CAD to help lower blood cholesterol levels. Since the main enzyme involved in the metabolism of statins is CYP3A4, we aimed to investigate the effect of CYP3A4 * 1B genotypes on plasma lipid profile in Turkish cardiovascular disease subject with and without obesity taking statin. Materials and Methods: The study group consisted of 85 cardiovascular disease patients who were prescribed statins and had routine biochemical analysis data. Polymerase chain reaction followed by restriction fragment length polymorphism (PCR-RFLP) assay were performed for genotyping of CYP3A4 *1B (rs2740574) polymorphism. Results: Genotype distribution of CYP3A4 *1B polymorphism was found for homozygous wild (AA) and homozygous polymorphic (GG) genotypes as 94.1% and 5.9% respectively. We did not detect patients with heterozygous genotype in our study group. We found that the mean LDL-c, TG and TC levels were higher in patients with CYP3A4 *1B GG compared to AA genotype. The frequency of CYP3A4 *1B GG genotype frequency (9.5%) was detected higher in the obese patients compared to the non-obese patients (7.7%) (χ2=0.037, p=0.85). Conclusions: Our results demonstrate that CYP3A4 *1B homozygous polymorphic genotype distribution tend to be higher in obese patients compared to non- obese patients with cardiovascular disease which may point *1B allele to have a slight effect on serum lipids during statin therapy. Additional studies with higher samples are needed for evaluating the role of CYP3A4 *1B on lipids in patients under statin therapy.


2014 ◽  
Vol 7 (1) ◽  
pp. 17-23
Author(s):  
JN Saha ◽  
AAS Majumder ◽  
NA Chowdhury ◽  
M Ullah ◽  
MG Azam ◽  
...  

Background: Cardiovascular disease is the leading cause of morbidity and mortality in renal impaired patients. Many of the patients of chronic kidney disease die of cardiovascular disease before requiring dialysis. Cardiovascular disease in renal impaired patient is potentially preventable and treatable. The aim of this study was to evaluate the association between renal impairment and coronary artery disease severity in chronic stable angina patients. Methods: 110 patients with chronic stable angina who got admitted for coronary angiography were included in the study. They were divided into impaired renal function group (with estimated glomerular filtration rate [eGFR] <90 ml/min/1.73m2) and normal renal function group (eGFR e” 90 ml/min/1.73m2) on the basis of eGFR. The severity of the CAD was assessed by angiographic Vessel score and Gensini score. Results: Mean Gensini score was significantly high in impaired renal function group (42.30±24.9 vs 25.65±17.9, p <0.05). There was significant negative correlation between eGFR and vessel score (r=-0.30, p <0.05) and between eGFR and Gensini score (r =-0.65, P <0.05). In multivariate logistic regression analysis, after adjustment of factors eGFR remain independent predictors of severe CAD (P=0.002, OR -5.73). Conclusion: Impaired renal function, assessed by eGFR is associated with angiographic severe coronary artery disease in chronic stable angina patients and this association is independent of conventional cardiovascular risk factors. DOI: http://dx.doi.org/10.3329/cardio.v7i1.20796 Cardiovasc. j. 2014; 7(1): 17-23


2009 ◽  
Vol 94 (1) ◽  
pp. 261-267 ◽  
Author(s):  
A. R. Baker ◽  
A. L. Harte ◽  
N. Howell ◽  
D. C. Pritlove ◽  
A. M. Ranasinghe ◽  
...  

Abstract Context: Visceral adipose tissue (AT) is known to confer a significantly higher risk of type 2 diabetes and cardiovascular disease. Epicardial AT has been shown to be related to cardiovascular disease and myocardial function through unidentified mechanisms. Epicardial AT expresses an inflammatory profile of proteins; however, the mechanisms responsible are yet to be elucidated. Objectives: The objectives of the study were to: 1) examine key mediators of the nuclear factor-κB (NFκB) and c-Jun N-terminal kinase (JNK) pathways in paired epicardial and gluteofemoral (thigh) AT from coronary artery disease (CAD) and control patients and 2) investigate circulating endotoxin levels in CAD and control subjects. Design: Serums and AT biopsies (epicardial and thigh) were obtained from CAD (n = 16) and non-CAD (n = 18) patients. Inflammation was assessed in tissue and serum samples through Western blot, real-time PCR, ELISAs, and activity studies. Results: Western blotting showed epicardial AT had significantly higher NFκB, inhibitory-κB kinase (IKK)-γ, IKKβ, and JNK-1 and -2 compared with thigh AT. Epicardial mRNA data showed strong correlations between CD-68 and toll-like receptor-2, toll-like receptor-4, and TNF-α. Circulating endotoxin was elevated in patients with CAD compared with matched controls [CAD: 6.80 ± 0.28 endotoxin unit(EU)/ml vs. controls: 5.52 ± 0.57 EU/ml; P&lt;0.05]. Conclusion: Epicardial AT from patients with CAD shows increased NFκB, IKKβ, and JNK expression compared with both CAD thigh AT and non-CAD epicardial AT, suggesting a depot-specific as well as a disease-linked response to inflammation. These studies implicate both NFκB and JNK pathways in the inflammatory profile of epicardial AT and highlight the role of the macrophage in the inflammation within this tissue.


Genes ◽  
2021 ◽  
Vol 12 (10) ◽  
pp. 1644
Author(s):  
Bowen Liu ◽  
Amy M. Mason ◽  
Luanluan Sun ◽  
Emanuele Di Angelantonio ◽  
Dipender Gill ◽  
...  

(1) Aim: To investigate the causal effects of T2DM liability and glycated haemoglobin (HbA1c) levels on various cardiovascular disease outcomes, both in the general population and in non-diabetic individuals specifically. (2) Methods: We selected 243 variants as genetic instruments for T2DM liability and 536 variants for HbA1c. Linear Mendelian randomization analyses were performed to estimate the associations of genetically-predicted T2DM liability and HbA1c with 12 cardiovascular disease outcomes in 367,703 unrelated UK Biobank participants of European ancestries. We performed secondary analyses in participants without diabetes (HbA1c < 6.5% with no diagnosed diabetes), and in participants without diabetes or pre-diabetes (HbA1c < 5.7% with no diagnosed diabetes). (3) Results: Genetically-predicted T2DM liability was positively associated (p < 0.004, 0.05/12) with peripheral vascular disease, aortic valve stenosis, coronary artery disease, heart failure, ischaemic stroke, and any stroke. Genetically-predicted HbA1c was positively associated with coronary artery disease and any stroke. Mendelian randomization estimates generally shifted towards the null when excluding diabetic and pre-diabetic participants from analyses. (4) Conclusions: This genetic evidence supports causal effects of T2DM liability and HbA1c on a range of cardiovascular diseases, suggesting that improving glycaemic control could reduce cardiovascular risk in a general population, with greatest benefit in individuals with diabetes.


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