scholarly journals Local inflammation, endothelial dysfunction and fibrinolysis in coronary heart disease

2006 ◽  
Vol 110 (3) ◽  
pp. 327-328 ◽  
Author(s):  
Gordon D. O. Lowe
Keyword(s):  
Coronary Heart Disease ◽  
Heart Disease ◽  
Epidemiological Studies ◽  
Risk Scores ◽  
Tumour Necrosis Factor Α ◽  
Tnf Α ◽  
Arterial Inflammation ◽  
Factor Α ◽  
Circulating Inflammatory Markers ◽  
Necrosis Factor

Prospective epidemiological studies have shown associations of circulating inflammatory markers with risk of CHD (coronary heart disease); however, these associations are modest after adjustment for confounding by established risk factors, and do not add significantly to the predictive value of current clinical risk scores. In contrast, experimental human studies of local arterial inflammation, such as the brachial artery infusion of TNF-α (tumour necrosis factor-α) model reported in this issue of Clinical Science by Robinson and co-workers, are of value in elucidating the pathophysiology of atherothrombosis.

Vascular and fibrinolytic effects of intra-arterial tumour necrosis factor-α in patients with coronary heart disease

2006 ◽  
Vol 110 (3) ◽  
pp. 353-360 ◽  
Author(s):  
Simon D. Robinson ◽  
Pamela Dawson ◽  
Christopher A. Ludlam ◽  
Nicholas A. Boon ◽  
David E. Newby
Keyword(s):  
Coronary Heart Disease ◽  
Heart Disease ◽  
Vascular Inflammation ◽  
Tumour Necrosis Factor Α ◽  
Stable Coronary Heart Disease ◽  
Tnf Α ◽  
Factor Α ◽  
Serum Crp ◽  
Necrosis Factor ◽  
Pai 1

Elevated plasma t-PA (tissue plasminogen activator) and serum CRP (C-reactive protein) concentrations are associated with an adverse cardiovascular risk. In the present study, we investigated whether acute local inflammation causes vascular dysfunction and influences t-PA release in patients with stable coronary heart disease. Serum CRP, plasma t-PA and PAI-1 (plasminogen activator inhibitor type 1) concentrations were determined in 95 patients with stable coronary heart disease. A representative subpopulation of 12 male patients received an intra-brachial infusion of TNF-α (tumour necrosis factor-α) and saline placebo using a randomized double-blind cross-over study design. Forearm blood flow and plasma fibrinolytic and inflammatory variables were measured. Serum CRP concentrations correlated with plasma t-PA concentrations (r=0.37, P<0.001) and t-PA/PAI-1 ratio (r=−0.21, P<0.05). Intra-arterial TNF-α caused a rise in t-PA concentrations (P<0.001) without affecting blood flow or PAI-1 concentrations. TNF-α pretreatment impaired acetylcholine- and sodium nitroprusside-induced vasodilatation (P<0.001 for both) whilst doubling bradykinin-induced t-PA release (P=0.006). In patients with stable coronary heart disease, plasma fibrinolytic factors correlate with a systemic inflammatory marker and local vascular inflammation directly impairs vasomotor function whilst enhancing endothelial t-PA release. We suggest that the adverse prognosis associated with elevated plasma t-PA concentrations relates to the underlying causative association with vascular inflammation and injury.

Differential effect of selective block of α2-adrenoreceptors on plasma levels of tumour necrosis factor-α, interleukin-6 and corticosterone induced by bacterial lipopolysaccharide in mice

1995 ◽  
Vol 144 (3) ◽  
pp. 457-462 ◽  
Author(s):  
G Haskó ◽  
I J Elenkov ◽  
V Kvetan ◽  
E S Vizi
Keyword(s):  
Tumour Necrosis Factor ◽  
Interleukin 6 ◽  
Plasma Levels ◽  
Tumour Necrosis ◽  
Endotoxin Shock ◽  
Bacterial Lipopolysaccharide ◽  
Tumour Necrosis Factor Α ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

Abstract The effect of selective block of α2-adrenoreceptors on plasma levels of tumour necrosis factor-α (TNF-α), interleukin-6 (IL-6) and corticosterone induced by bacterial lipopolysaccharide (LPS) was investigated in mice using ELISA and RIA. It was found that the LPS-induced TNF-α response was significantly blunted in mice pretreated with CH-38083, a novel and highly selective α2-adrenoreceptor antagonist (the α2/α1 ratio is >2000). In contrast, LPS-induced increases in both corticosterone and IL-6 plasma levels were further increased by CH-38083. Since it has recently been shown that the selective block of α2-adrenoreceptors located on noradrenergic axon terminals resulted in an increase in the release of noradrenaline (NA), both in the central and peripheral nervous systems, and, in our experiments, that propranolol prevented the effect of α2-adrenoreceptor blockade on TNF-α plasma levels induced by LPS, it seems likely that the excessive stimulation by NA of β-adrenoreceptors located on cytokine-secreting immune cells is responsible for this action. Since it is generally accepted that increased production of TNF-α is involved in the pathogenesis of inflammation and endotoxin shock on the one hand, and corticosterone and even IL-6 are known to possess anti-inflammatory properties on the other hand, it is suggested that the selective block of α2-adrenoreceptors might be beneficial in the treatment of inflammation and/or endotoxin shock. Journal of Endocrinology (1995) 144, 457–462

scholarly journals Analysis on the Expression and Prognostic Value of LncRNA FAF in Patients with Coronary Heart Disease

2020 ◽  
Vol 2020 ◽  
pp. 1-8
Author(s):  
Hai Xu ◽  
Xiwen Zhang ◽  
Kun Yu ◽  
Gang Zhang ◽  
Yafei Shi ◽  
...  
Keyword(s):  
Risk Factors ◽  
Coronary Heart Disease ◽  
Heart Disease ◽  
Poor Prognosis ◽  
Prognostic Value ◽  
High Sensitivity ◽  
Control Group ◽  
Coronary Lesion ◽  
Tnf Α ◽  
Factor Α

Objective. To investigate the expression and prognostic value of LncRNA FAF in patients with coronary heart disease. Patients and Methods. 97 patients with coronary heart disease who came to our hospital were selected as the research group (RG), and 97 healthy people who came to our hospital for physical examination during the same period were selected as the control group (CG). The serum LncRNA FAF, plasma homocysteine (HCY), lipoprotein A (Lp-a), serum tumor necrosis factor α (TNF-α), and high-sensitivity C-reactive protein (hsCRP) in the two groups of patients were detected, and their correlations were analyzed. Then, the predictive value and risk factors of FAF for poor prognosis of patients with coronary heart disease were analyzed. Results. The expression of LncRNA FAF in the serum of patients in the RG was significantly lower than that in the CG, and the expressions of HCY, Lp-a, TNF-α, and hsCRP were significantly higher than those in the CG (p <0.05). The AUC of FAF in the diagnosis of coronary heart disease was more than 0.9. FAF was negatively correlated with the coronary lesion vessels, HCY, Lp-a, TNF-α, and hsCRP expressions in patients with coronary heart disease ( p < 0.05 ). The ROC of FAF for predicting poor prognosis in patients with coronary heart disease was greater than 0.9. Low expression of FAF; high expressions of HCY, Lp-a, and hsCRP; and increase of coronary lesion vessels were independent risk factors for poor prognosis in patients with coronary heart disease. Conclusions. LncRNA FAF was lowly expressed in the serum of patients with coronary heart disease, and it was of high value in the diagnosis and prediction of poor prognosis of coronary heart disease. It was also an independent risk factor for poor prognosis of patients with coronary heart disease and may be a potential target for diagnosis and treatment of coronary heart disease.

scholarly journals Intracellular NAD+ levels are associated with LPS-induced TNF-α release in pro-inflammatory macrophages

2016 ◽  
Vol 36 (1) ◽  
Author(s):  
Abbas Jawad Al-Shabany ◽  
Alan John Moody ◽  
Andrew David Foey ◽  
Richard Andrew Billington
Keyword(s):  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
Inflammatory Cytokine ◽  
Bacterial Lipopolysaccharide ◽  
Tumour Necrosis Factor Α ◽  
Tnf Α ◽  
Factor Α ◽  
Inflammatory Macrophages ◽  
Inflammatory Macrophage ◽  
Necrosis Factor

Bacterial lipopolysaccharide induces changes in intracellular NAD+ levels in a pro-inflammatory, but not an anti-inflammatory, macrophage model that are correlated with the release of the pro-inflammatory cytokine tumour necrosis factor-α (TNF-α).

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