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 designation of atherosclerosis as a chronic inflammatory process represents an interesting paradigmatic shift for cardiologists. The plasma concentrations of interleukin-6 and its hepatic byproduct, C-reactive protein, may reflect the intensity of occult plaque inflammation and the vulnerability to rupture. Monocyte chemoattractant protein-1 and interleukin-8 play a crucial role in initiating atherosclerosis by recruiting monocytes/macrophages to the vessel wall, which promotes atherosclerotic lesions and plaque vulnerability. In addition, circulating levels of these proinflammatory cytokines increase in patients with acute myocardial infarction and unstable angina, but not in those with stable angina. Also, the plasma concentrations of these cytokines increase after percutaneous coronary intervention, causing late restenosis after the procedure. Angiotensin II and other atherogenic factors induce these cytokines in the cardiovascular tissues through the activation of transcription factors, such as nuclear factor-kappaB or peroxisome proliferator-activated receptors. Conversely, HMG-CoA reductase inhibitors (statins) can potently inhibit these proinflammatory factors in the vessels. A small GTP-binding protein, Rho, may be a key molecule to explain the anti-inflammatory effects of statins. Interleukin-10 also exerts anti-inflammatory effects on the cardiovascular tissues, possibly by deactivating proinflammatory cytokines and inducible nitric oxide synthase. Gene therapy using interleukin-10 may be a promising means for untreatable or complicated cases of cardiovascular diseases. Thus, therapeutic modulations of these inflammatory cytokines may be useful in the prevention of atherosclerosis and future cardiovascular events.
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PMID:Inflammatory cytokines and cardiovascular disease. 1456 Nov 60

The aim of this study was to assess the plasma levels of VEGF and interleukin-10 in patients with acute myocardial infarction (AMI) and stable chronic angina (SA) and correlate the values with traditional CHD risk factors, left ventricular ejection fraction (LVEF) and established inflammatory marker hsCRP. Fifty patients with AMI and 30 with SA were enrolled. IL-10 levels in AMI patients were lower than in SA patients (9.81 +/- 5.0 versus 22.63 +/- 8.38 pg/ml, p < 0.00001). IL-10 levels were lower in AMI and SA patients with multiple CHD risk factors than in patients < or = 2 risk factors (SA: 19.48 +/- 2.94 versus 23.77 +/- 2.94 pg/ml; p < 0.005; AMI: 8.64 +/- 4.43 versus 11.85 +/- 4.09 pg/ml; p < 0.05) and patients with AMI and single-vessel than with multi-vessel disease (8.45 +/- 3.86 versus 10.72 +/- 3.95 pg/ml; p < 0.05). VEGF levels in AMI patients were higher than in SA patients (312.0 +/- 67.0 versus 221.0 + /- 50 pg/ml; p < 0.005). VEGF levels were higher in AMI patients with multi-vessel disease than in patients with single-vessel disease (348.74 +/- 45.23 versus 252.05 +/- 21.12 pg/ml; p < 0.005), with LVEF <40% and Killip class III-IV than in patients with LVEF >40% and Killip class I-II (338.8 +/- 51.59 versus 271.8 +/- 50.51 pg/ml; p < 0.005 and 340.71 +/- 52.94 versus 275.45 +/- 49.48 pg/ml; p < 0.05, respectively) and with chest pain > 6 h versus < 6 h (330.03 +/- 58.58 versus 292 +/- 57.53 pg/ml; p < 0.05). HsCRP concentrations in AMI patients were higher than in SA (1.24 +/- 0.47 versus 0.42 +/- 0.14; p < 0.0001). HsCRP was correlated with IL-10 (r = -0.413; p < 0.05) and VEGF (r = 0.319; p < 0.05). Acute myocardial infarction is associated with elevated VEGF levels and decreased concentration of IL-10. There is a significant correlation between levels of inflamatory markers and CHD risk factors and the function of the left ventricle on admission.
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PMID:The pro- and anti-inflammatory markers in patients with acute myocardial infarction and chronic stable angina. 1525 85

Several lines of evidence indicate that increased inflammatory activity in peripheral blood is associated with the acute coronary syndrome. Systemic inflammation in clinically stable conditions of coronary artery disease has been less studied. We examined cytokine profiles in 20 patients who had acute coronary syndrome, 45 who had angiographically verified coronary artery disease and stable angina pectoris, and 45 healthy controls. Circulating levels of C-reactive protein, interleukin-1 receptor antagonist, interleukin-2 receptor, interleukin-6, interleukin-10, and interleukin-18 were determined. Subpopulations of peripheral immune cells, including neutrophil-platelet aggregates, were analyzed by 3-color flow cytometry using a panel of monoclonal antibodies. Patients who had acute coronary syndrome and stable angina pectoris had significantly higher levels of C-reactive protein, interleukin-6, and interleukin-1 receptor antagonist than did controls, whereas levels of interleukin-2 receptor, interleukin-10, and interleukin-18 were similar across groups. Patients had significantly more neutrophils, and the numbers of neutrophil-platelet aggregates were particularly large in patients who had stable angina pectoris. High levels of C-reactive protein, interleukin-6, and interleukin-1 receptor antagonist in patients were significantly related to numbers of neutrophils and neutrophil-platelet aggregates but not to other immune cell subpopulations. The data suggest that the interaction between neutrophils and platelets is an important component of proinflammatory activity seen in peripheral blood of stable and unstable forms of coronary artery disease.
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PMID:Circulating levels of proinflammatory cytokines and neutrophil-platelet aggregates in patients with coronary artery disease. 1569 27

To assess the value of serial C-reactive protein (CRP), serum amyloid A (SAA), tumor necrosis factor-alpha (TNF-alpha) and interleukin-10 (IL-10) evaluation in the risk stratification in patients undergoing percutaneous coronary intervention. The study was designed as a prospective cohort trial with a 1-year follow-up. Eighty patients (70 with stable angina, 10 with unstable angina) were enrolled. Blood samples were collected before the procedure and after 6 and 24 h, and 1 month. Clinical follow-up visits were performed (*with exercise test) 7 days* and 1*, 3, 6* and 12 months after the procedure. Any symptoms of restenosis were verified angiographically. Multivariate logistic regression analysis identified increased preprocedural TNF-alpha and CRP levels and elevated CRP concentrations evaluated 24 h after the procedure as significant predictors of both clinical restenosis and major adverse cardiac events (MACE), while high SAA values at 24 h accurately predicted clinical restenosis. Patients, who were in the highest tertile of, either, baseline TNF-alpha and/or baseline CRP/CRP at 24 h, were more prone to develop restenosis and MACE than stratified only on the basis of a single marker. Our data indicate that combined analysis of CRP and TNF-alpha might be an effective approach to the clinical restenosis and MACE prediction. Additionally, long-term outcome is markedly influenced by the periprocedural activation of inflammation.
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PMID:Combined periprocedural evaluation of CRP and TNF-alpha enhances the prediction of clinical restenosis and major adverse cardiac events in patients undergoing percutaneous coronary interventions. 1594 95

The plasma levels of inflammatory cytokine interleukin-6 (IL-6) and anti-inflammatory cytokine interleukin-10 (IL-10) in the patients with unstable angina or stable angina were determined and compared. In 30 patients with unstable angina and 22 patients with stable angina, plasma levels of IL-10 and IL-6 were detected by ELISA and plasma lipid parameters by lipid research clinical methods respectively. The results showed plasma levels of IL-10 were significantly lower in unstable angina group than in stable angina group (P = 0.005), while those of IL-6 were significantly increased in unstable angina group as compared with those in stable angina group (P = 0.039). There was a significantly negative correlation between IL-10 and IL-6 in patients with unstable angina (r = -0.41, P = 0.003). In the unstable angina group, IL-6 levels were obviously positively correlated with TC (r = 0.314, P = 0.023), but not with TG and HDL. There were no significant correlations between IL-10 and plasma lipid parameters. It was suggested that the decreased IL-10 and increased IL-6 might be associated with the atheromatous plaque stability and progression of coronary heart diseases. IL-10 may play an important role in preventing coronary vascular lesions.
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PMID:Plasma levels of the anti-inflammatory cytokine IL-10 and inflammatory cytokine IL-6 in patients with unstable angina. 1669 12

Management of acute coronary syndromes, particularly unstable angina, acute myocardial infarction and non-Q-wave myocardial infarction, is one of the most common and costly problems facing modern medicine. Furthermore, the increasing availability of new research and clinical information relevant to the treatment of these conditions means that continuing reappraisal of management strategies is necessary. Accordingly, the Ushuaia conference, Tierra Del Fuego, Argentina, was convened to discuss current approaches and future treatment prospects for patients with these conditions. The conference was comprised of leading Argentinian cardiologists whose primary aim was to formulate consensus recommendations regarding the management of patients with acute coronary syndromes. The first of the major recommendations for the pharmacological management of acute coronary syndromes arising from the Ushuaia Consensus Conference was that aspirin (200 to 500mg initially, then 100 to 325 mg/day) should be administered to all patients except those for whom aspirin is absolutely (or relatively, depending on the clinician's discretion) contraindicated. In such cases, ticlopidine is a suitable alternative. Intravenous nitrates are indicated for patients with angina pain (24 to 48 hours' duration), ECG changes, recurrence of angina, or signs of heart failure; in other cases, oral, transdermal or sublingual nitrates may be administered. Use of beta-blockers is recommended except when absolutely contraindicated or when there is a strong suspicion of vasospasm as a dominant mechanism in angina. Intravenous administration of these agents is preferred in patients with tachycardia, arterial hypertension or angina. Calcium antagonists are generally not recommended as first choice therapy, but can be indicated (preferably using agents that decrease heart rate) when beta-blockers are contraindicated or when there is a strong suspicion of vasospasm as a dominant mechanism in angina. Calcium antagonists are also useful in combination with other drugs in patients with high blood pressure or treatment-refractory recurrent angina. Subcutaneous low molecular weight heparins and intravenous unfractionated heparin provide similar results and are indicated in a number of clinical situations. Emergency videocoronary angiography (VCA) is indicated in patients with persistent clinical and haemodynamic instability, recurrent ischaemia with heart failure, and refractory angina. Patients should also be referred for VCA if they have signs of left ventricular dysfunction, post-acute myocardial infarction angina with ECG changes, or ischaemia during functional studies. Post-VCA treatment will be determined by anatomical findings during VCA. Future prospects in the management of acute coronary syndromes include the development of more accurate prognostic markers and means of stratifying risk, such as sophisticated ECG criteria, serum markers of necrosis (e.g. troponin T and I), markers of thrombosis (e.g. D-dimer and fibrinopeptide A levels), markers of inflammation (e.g. reactive protein C, cell adhesion receptor expression, neopterine), and markers of 'good' prognosis (e.g. interleukin-10). Other pharmacological approaches under investigation include platelet IIb/IIIa receptor antagonists, clopidogrel and hirudin. Novel agents, such as anti-Xa, pentasaccharide, anti-tissue factor compounds, Ib receptor-blocking agents, agents that influence vascular endothelium and control cellular acidosis (e.g. HOE 642), macrolide antibiotics, HLA-DR system blockers and fusion compounds, are also in various stages of investigation or development.
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PMID:Current treatment and future prospects for the management of acute coronary syndromes: consensus recommendations of the 1997 ushuaia conference, tierra del fuego, Argentina. 1837 Apr 92

Cytokines are responsible for the modulation of immunological and inflammatory processes and play a significant role in the pathogenesis of coronary artery disease. We estimated the levels of pro-/anti-inflammatory cytokines in South Indian patients with coronary artery disease. The study population comprised of groups 1-3: 100 patients each with acute myocardial infarction, unstable angina, and stable angina, respectively, and group 4 (100 healthy controls). Cytokine levels (interleukin-6, interleukin-8, interleukin-10, and tumor necrosis factor-alpha) were estimated by enzyme-linked immunosorbent assay (ELISA). Interleukin-6, interleukin-8, and tumor necrosis factor-alpha levels were significantly higher in patients from groups 1 and 2, than in group 3 and controls. Acute myocardial infarction patients exhibited higher serum levels of interleukin-10 compared with other groups and control subjects. Patients with unstable angina had significantly lower interleukin-10 concentrations than those with stable angina. The ratios of pro-/anti-inflammatory cytokines in all the study groups increased significantly when patients with unstable angina were compared to other groups. In patients with acute myocardial infarction, interleukin-10 and tumor necrosis factor-alpha levels showed significant correlation with established risk factors such as body mass index, blood pressure, and lipid levels. Acute myocardial infarction patients show elevation in proinflammatory and anti-inflammatory cytokines, while unstable angina is associated with low levels of serum interleukin-10. Higher levels of anti-inflammatory cytokine interleukin-10 may be needed to provide protection in unstable angina. These cytokines are markers of coronary artery disease and may be used for the identification of high-risk patients with unstable angina/acute myocardial infarction.
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PMID:Role of pro-/anti-inflammatory cytokines and their correlation with established risk factors in South Indians with coronary artery disease. 1879 48