Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002962 (angina)
 21,142 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aim was to investigate circulating E-selectin and Intercellular Adhesion Molecule-1 (ICAM-1) in acute myocardial infarction. Our study was carried out in 80 patients, 40 hospitalized for acute myocardial infarction (AMI), 20 suffering from chronic stable angina and 20 healthy control subjects. Samples of venous blood were taken from all patients at the moment of hospitalization and after 2, 4, 6, 8, 10, 12 and 24 hours from the thrombolytic treatment (AMI + urokinase) or conventional therapy (AMI + nitroglycerin), for the dosage of creatinine kinase (CK) and adhesion molecules. The CK was determined by means of a Hitachi 901 automatic analyser using an enzymatic method (reagents Boheringer-Biochemia, Germany). Soluble E-selectin (sE-selectin) and soluble ICAM-1 (sICAM-1) were measured in the serum using a specific immunoassay (British Biotechnology Products). The serum levels of Tumor Necrosis Factor (TNF-alpha) were evaluated using an immunoenzymatic assay to quantitate the serum levels of the cytokine (British Biotechnology Products). Patients with acute myocardial infarction (AMI) had increased serum levels of soluble E-selectin (sE-selectin; AMI + urokinase = 312 +/- 20 ng/ml; AMI + nitroglycerin = 334 +/- 15 ng/ml) and soluble ICAM-1 (sICAM-1; AMI + urokinase = 629 +/- 30 ng/ml; AMI + nitroglycerin = 655 +/- 25 ng/ml) compared to both patients with chronic angina (sE-selectin = 67 +/- 10 ng/ml; sICAM-1 = 230 +/- 20 ng/ml) and healthy control subjects (sE-selectin = 53 +/- 15 ng/ml; sICAM-1 200 +/- 16 ng/ml). Furthermore patients with acute myocardial infarction also had increased serum levels of Tumor Necrosis Factor (TNF-alpha = 309 +/- 10 pg/ml; control subjects = 13 +/- 5 pg/ml). Thrombolytic therapy with urokinase (1,000,000 IU as an intravenous bolus for 5 minutes, followed by an infusion of an additional 1,000,000 IU for the following two hours) succeeded in producing reperfusion and reduced the serum levels of sE-selectin (52 +/- 13 ng/ml) and sICAM-1 (202 +/- 31 ng/ml). In contrast patients not eligible for thrombolytic therapy and therefore treated with conventional therapy (a continuous i.v. infusion of nitroglycerin at the dose of 50 mg/die) did not show any significant reduction in both sE-selectin and sICAM-1 throughout the study. Our results confirm previous experimental data and indicate that adhesion mechanisms supporting leukocyte-endothelium interaction may also be operative in human acute myocardial infarction.
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PMID:Thrombolytic therapy with urokinase reduces increased circulating endothelial adhesion molecules in acute myocardial infarction. 882 73

In 14 patients with stable angina pectoris we examined the effect of pentoxifyline (PTX) on oxidative metabolism of TNF-alpha-priming neutrophils. The control group consisted of 21 patients with stable angina pectoris without pentoxifylline administration. Blood samples for examination were taken from basilic vein (peripheral blood) and coronary sinus immediately before PTCA procedure. In PTX-group was found the significant decrease in spontaneous CL of TNF-alpha-priming neutrophils from coronary sinus blood (1231.0 +/- 119.4 mV x min), in comparison to the control group (1374 +/- 124.4 mV x min). In PTX-group was found the significant decrease in fMLP stimulated CL of TNF-alpha-priming neutrophils from peripheral blood (4219.0 +/- 707.2 mV x min) and coronary sinus blood (4322.0 +/- 664.4 mV x min), in comparison to the control group (5248.0 +/- 595.8 mV x min and 4973.0 +/- 536.5 mV x min; respectively). There were no differences between both groups in PMA stimulated CL of TNF-alpha-priming neutrophils.
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PMID:[The effect of pentoxifylline on oxidative metabolism in neutrophils primed with tumor necrosis factor alpha in patients with stable angina pectoris]. 976 Aug 17

TNF-alpha (so-called cachectin), IL-1 and 6 are important regulating agents in the homeostasis of energy in the organism, as among others they control processes of apoptosis and thus also the volume of adipose and muscular tissues. They are produced not only in immunocompetent cells but also in adipocytes and muscle cells. The cytokine system is then activated not only in tumours and infections but elevated values were found also in obesity, NIDDM, in myocardial infarction and in advanced decompensated cardiac patients. By acting on phosphorylation of IRS-1 and PI-3 kinase TNF-alpha promotes significantly insulin resistance, causes deterioration of diabetes, as well as elevated body temperature, sleepiness and anorexia. In a group of 65 patients, mostly with android obesity, in hyperleptinaemic and insulin resistant probands with coronarographically confirmed microvascular angina pectoris (n = 22) or IHD, mostly after a myocardial infarction (n = 43) with one or more significant stenoses on the epicardial coronary arteries in half the patients positive or elevated TNF-alpha was found and in 28% also IL-6. This increase did not correlate however with BMI, the percentage of body fat, IRI and C peptide levels nor with cortisol and leptin levels. Insulin resistant subjects had more frequently elevated homocysteine and Lp(a) values which are further two independent risk factors of atherothrombogenesis. Hyperhomocysteinaemia can be favourably influenced by vitamin fortification of the diet or by administration of folate and pyridoxine (1 tablet per day) involving negligible financial costs.
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PMID:[Relation between cytokines (TNF-alpha, IL-1 and 6) and homocysteine in android obesity and the phenomenon of insulin resistance syndromes]. 1042 20

The changes in serum concentrations of cytokines such as interleukin-1 (IL-1) beta, interleukin-6 (IL-6), tumor necrosis factor (TNF) alpha and a soluble-intercellular adhesion molecule (sICAM-1) has been investigated in patients with stable angina and acute myocardial infarction. Thirty-four patients with stable angina (SA), 15 with acute myocardial infarction (AMI), and 20 subjects in the control (C) group were included in the study. The mean serum concentrations of sICAM-1, IL-1-beta, IL-6, and TNF-alpha differed significantly among the three groups. Serum concentrations of IL-1 beta, sICAM-1, and TNF-alpha were comparable in the AMI and SA groups and higher than those found in the C group (p < 0.001). The serum concentration of IL-6 was more than twice as high in the AMI group as compared to the other two groups (p < 0.001). The mean serum concentrations of IL-1 beta, TNF-alpha, and IL-6 were comparable in the AMI and SA groups and higher than in the C group.
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PMID:Circulating interleukin-1 beta, interleukin-6, tumor necrosis factor-alpha, and soluble ICAM-1 in patients with chronic stable angina and myocardial infarction. 1122 83

TNF-alpha as a pleiotropic, proinflammatory cytokine seems to play a role in the pathogenesis of atherosclerosis and coronary artery disease (CAD). TNF-alpha is binding to two cell surface receptors and its serum activity is modified by soluble forms of these receptors: sTNF-R I and sTNF-R II. The aim of this study was to assess serum concentrations of TNF-alpha, sTNF-R I and sTNF-R II in patients (pts) with CAD. We examined serum concentrations of TNF-alpha, sTNF-R I and sTNF-R II by ELISA in: 45 pts with stable exertional angina (group I); 32 pts with unstable angina (group II) within 6, 24, and 48 h after the chest pain; and 23 pts before and 6, 24, and 48 h after PTCA (group III). The control group (group C) consisted of 20 healthy subjects. We evaluated: clinical state of patients and results of some diagnostic examinations (lipids, ECG, echocardiography, coronary angiography). Mean serum concentrations of TNF-alpha were significantly higher in pts ith CAD (group I: 18.25 +/- 5.5 pg/ml; group II: 17.24 +/- 4.0 pg/ml; group III: 18.70 +/- 0.6 pg/ml; p < 0.001) than in healthy pts (8.31 +/- 1.4 pg/ml). In turn mean serum concentrations of sTNF-R I were significantly higher both in group I (1399.6 +/- 536.3 pg/ml; p < 0.05) and III (1544.0 +/- 391.4 pg/ml; p < 0.01) than in control group (1093.9 +/- 456.9 pg/ml). There were not differences in mean serum concentrations of sTNF-R II. We found no differences between mean serum concentrations of TNF-alpha, sTNF-R I and sTNF-R II either after the chest pain (group II); or before and after PTCA (group III). In group I mean TNF-alpha correlated with serum triglycerides and HDL-cholesterol (r = 0.412 and r = -0.424; p < 0.01); sTNF-R I correlated with LDL-cholesterol (r = -0.309; p < 0.05); and sTNF-R II correlated with total cholesterol and LDL-cholesterol (r = 0.311 and r = 0.316; p < 0.05). The serum concentrations of TNF-alpha are increased in patients with CAD, but this does not reflect the clinical state of patients. In pts with stable angina these increased levels of TNF-alpha may be accompanied with higher concentrations of sTNF-R I--it seems to be the compensatory mechanism in long-term atherosclerosis. Lipid disturbances may influence the cytokines metabolism in pts with CAD.
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PMID:[Tumor necrosis factor alpha and its soluble receptors in serum of patients with coronary artery disease]. 1157 24

The aim of the study was the assessment of selected inflammatory markers in patients with stable and unstable angina pectoris, in comparison to patients with dyslipidemia without coronary artery disease. The study group included 61 patients (37-79 years old), divided into three subgroups: group I. 26 (43%) with unstable angina, group 2. 19 (26%) with stable angina, group III. 16 (26%) dyslipidemia without coronary artery disease. We measured serum levels of cytokines (IL-1B, IL-1Ra, IL-2, IL-6, TNF-alpha), immunoglobulins (IgG, IgE, IgM), fibrinogen. C-reactive protein and subclass of lymphocytes T CD4 and T CD8. In stable and unstable angina pectoris group we found lower percentage of T CD4, T CD8 and higher level of TNF-alpha. In unstable angina group the level of IL-1 beta was lower and the concentration of C-reactive protein, IgE was higher in comparison to group without coronary artery disease. Observed immunoregulatory disorders confirm immune mechanism in the origin of unstable angina pectoris.
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PMID:[Selected inflammatory markers in patients with acute coronary syndrome]. 1236 2

This study investigated whether the myocardium is involved in the acute inflammatory reaction associated with bursts of unstable angina (UA). We looked for the presence of activated DR+ inflammatory cells and the expression patterns, localization, and immunostaining identification of genes for cytokines (IL-1beta, TNF-alpha, IL-6, and IFN-gamma), MCP-1, and iNOS in the left ventricle biopsies from 2-vessel disease anginal patients, 24 with UA and 12 with stable angina (SA), who underwent coronary bypass surgery. Biopsy specimens from 6 patients with mitral stenosis who underwent valve replacement were examined as control hearts (CHs). Plasma levels of IL-2 soluble receptor (sIL-2R) were measured as a marker of systemic immune reaction. In CHs, DR+ cells were undetectable, and cytokine and iNOS mRNA expression were negligible. UA patients had higher sIL-2R levels than SA patients (P<0.01), and their biopsy specimens showed both numerous DR+ cells identified as lymphocytes, macrophages, endothelial cells, and elevated expression levels of cytokine and iNOS genes (from 2.4- to 6.1-fold vs SA; P<0.01). Cytokine and iNOS genes and proteins were localized in endothelial cells without involvement of myocytes. IL-1beta and MCP-1 mRNAs were nearly undetectable. No significant differences were found in the number of DR+ cells, levels of cytokine, and iNOS genes between potentially ischemic and nonischemic left ventricle areas. In SA specimens, DR+ cells were very rare and only mRNAs for TNF-alpha and iNOS genes were overexpressed versus CHs. These results indicated that an acute immunomediated inflammatory reaction, essentially involving coronary microvessels, is demonstrable in UA patients.
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PMID:Immunomediated and ischemia-independent inflammation of coronary microvessels in unstable angina. 1277 81

Interleukin-1 plays a role in normal homeostasis and in the inflammatory response which is deemed to be responsible for the development of major chronic diseases that are highly prevalent in the elderly. Aim of this study is to evaluate the factors influencing the serum levels of Interleukin-1 beta, in a large and representative population. Data were from the InCHIANTI project, a study of factors contributing to the decline of mobility in late life, which sampled people living in two sites in the surroundings of Florence. Blood samples were obtained from 1,292 participants and frozen aliquots were stored at -80 degrees C. The serum levels of several cytokines were measured by enzyme linked immunosorbent assay using an ultrasensitive commercial kit. Interleukin-1 beta serum levels were associated with congestive heart failure (p > 0.001) and angina (p = 0.02), with Ca2+ serum levels (p = 0.02), and with a history of dyslipidemia (p = 0.05). We found no association between serum IL-1beta level and age, sex, consumption of cardioactive drugs and serum levels of IL-1Ra, IL-6, sIL-6R, IL-10 and TNF-alpha. Our data could lend support to the hypothesis that IL-1beta is mainly involved in the functional alterations of cardiomyocytes under conditions marked by mononuclear cell infiltration and by downregulation of calcium.
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PMID:Serum IL-1beta levels in health and disease: a population-based study. 'The InCHIANTI study'. 1289 Apr 53

This study investigates the association of several inflammatory markers with subclinical and clinical cardiovascular disease in older men and women. Data are from the baseline assessment of 3,045 well-functioning persons aged 70 to 79 years, participating in the Health, Aging and Body Composition study. The study sample was divided into 3 groups: "cardiovascular disease" (diagnosis of congestive heart failure, coronary artery disease, peripheral artery disease, or stroke), "subclinical cardiovascular disease" (positive findings on the Rose questionnaire for angina or claudication, ankle-brachial index <0.9, or electrocardiographic abnormalities), and "no cardiovascular disease." Serum levels of interleukin (IL)-6, C-reactive protein (CRP), tumor necrosis factor (TNF)-alpha, and the soluble receptors IL-6 soluble receptor, IL-2 soluble receptor, TNF soluble receptor I, and TNF soluble receptor II were assessed. Of those with IL-6 levels in the highest compared with the lowest tertile, the odds ratio (OR) for subclinical cardiovascular disease was 1.58 (95% confidence interval [CI] 1.26 to 1.97) and for clinical cardiovascular disease was 2.35 (95% CI 1.79 to 3.09). A similar association was found for TNF-alpha (OR 1.48, 95% CI 1.16 to 1.88 and OR 2.05, 95% CI 1.55 to 2.72, respectively). In adjusted analyses, CRP was not significantly associated with overall subclinical or clinical cardiovascular disease, although additional analyses did find a strong specific association between CRP and congestive heart failure (OR 1.64, 95% CI 1.11 to 2.41). Of the soluble cytokine receptors, only TNF soluble receptor I showed a significant association with clinical cardiovascular disease. Thus, our findings suggest an important role for IL-6 and TNF-alpha in clinical as well as subclinical cardiovascular disease. In this study, CRP had a weaker association with cardiovascular disease than the cytokines.
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PMID:Inflammatory markers and cardiovascular disease (The Health, Aging and Body Composition [Health ABC] Study). 1294 70

Angiotensin (Ang) II is now recognized to be a mediator of a wide variety of inflammatory processes. This study investigated renin-angiotensin system (RAS) components and a number of inflammatory mediators in left ventricular biopsies from 2-vessel disease unstable angina (UA) (n=43) and stable angina (SA) (n=15) patients undergoing coronary bypass surgery. Biopsy samples from 6 patients undergoing valve replacement for mitral stenosis served as controls. UA patients were randomly assigned to angiotensin-converting enzyme (ACE)-inhibitor (ramipril), AT1 antagonist (valsartan), or placebo and treated during the 5 days preceding coronary bypass surgery, performed from 6 to 9 days after coronary angiography. During coronary angiography coronary blood flow was measured and samples were obtained from aorta and coronary sinus for determination of Ang I and Ang II gradients. The hearts of UA patients produced Ang II in a greater amount than in SA patients (P<0.01). UA biopsy samples showed numerous DR+ cells, identified as lymphocytes, macrophages, and endothelial cells. Reverse-transcriptase polymerase chain reaction showed overexpression of AGTN, ACE, and AT1-R genes, as well as upregulation of TNF-alpha, IL-6, IFN-gamma, and iNOS genes (P<0.01), with no differences between nonischemic and potentially ischemic areas. AGTN, ACE, and cytokine genes were mainly localized on endothelial cells. Ramipril and valsartan markedly decreased the expression levels of TNF-alpha, IL-6, and iNOS, and, to a lesser extent, of IFN-gamma genes, but did not affect the number of DR+ cells, with no significant difference between the 2 treatments. These results show that locally generated Ang II amplifies the immunomediated inflammatory process of coronary microvessels occurring in unstable angina.
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PMID:Cardiac angiotensin II participates in coronary microvessel inflammation of unstable angina and strengthens the immunomediated component. 1521 17


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