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)

Recent evidence suggests that an inflammatory process has a significant role in the evolution of atherosclerosis. A chronic inflammatory response in the blood vessel's wall causes the formation of a lesion that narrows the artery's lumen and may cause such conditions as stable angina (SA). Destabilization of the atheromatous lesion, blood clot formation and rapid narrowing of the artery lumen may appear as part of an acute process, superimposed on the chronic inflammation. Such an acute process may be the mechanism underlying acute conditions such as unstable angina (UA) or myocardial infarction. Recent studies are trying to shed light on the process which causes destabilization of the atheromatous lesion. These studies implicate T lymphocytes and, especially, T helper 1 (Th1) cells (a sub-population of T lymphocytes) as having an important role in the destabilization of the lesion. Interferon gamma, an important cytokine secreted by Th1 cells, diminishes the production of collagen by smooth muscle cells and activates macrophages which destroy collagen and elastin. Furthermore, interferon gamma encourages clot formation and disrupts production of nitric oxide by endothelial cells. These qualities of interferon gamma support the hypothesis by which Th1 cells play a significant role in the evolution of UA. Unlike Th1 cells, Th2 cells, another sub-population of T lymphocytes, may help protect the atheromatous lesion from destabilization. This hypothesis is supported by the qualities of interleukin 10, one of the important cytokine secreted by Th2 cells. Interleukin 10 diminishes the secretion of interferon-gamma, inhibits the secretion of enzymes which destroy connective tissue in the atheromatous lesion and interferes with clot formation on the unstable lesion.
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PMID:[The role of cytokines secreted by T cells in the pathogenesis of angina pectoris]. 1451 65

The aim of this study was to analyze (i) ratios between pro-inflammatory cytokines interleukin 6 (IL-6), interleukin 1 (IL-1), tumour necrosis factor alpha (TNF-alpha) and anti-inflammatory cytokine interleukin 10 (IL-10) in patients with acute myocardial infarction (AMI) and stable angina pectoris (ii) as well as correlation between IL-6 and IL-10 in AMI and (iii) correlation between IL-6 and lipoproteins in AMI.The total of 71 patients were enrolled in this study, 41 of them with AMI (study group) and 30 with stable angina pectoris (control group). The concentrations of cytokines and lipoproteins were measured from blood samples. Pro-inflammatory to anti-inflammatory cytokine ratios were calculated by dividing concentrations of pro-inflammatory cytokines with IL-10. In statistical analyses we used descriptive statistics, normality tests and analysis of correlation.IL-6: IL-10 ratio is significantly higher in AMI than in stable angina (P < 0,001), TNF-alpha: IL-10 is also higher in study group but the difference is not significant. We found positive linear correlation between IL-6 and IL-10 (r =0,43; p = 0,015) and negative linear correlation between IL-6 and high density lipoprotein HDL (r = -0,47; p= 0,008) in AMI.IL-6: IL-10 ratio is higher in AMI than in stable angina. There is linear correlation between IL-6 and IL-10 and IL-6 and HDL in AMI.
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PMID:Correlation between interleukin 6 and interleukin 10 in acute myocardial infarction. 2000 96

Acute coronary syndrome (ACS) is a clinical syndrome caused by acute myocardial ischemia and a severe stage of coronary atherosclerosis heart disease. The aim of this study was to clarify whether ramipril was a therapeutic agent against monocyte chemoattractant protein 1 (MCP-1), interleukin 18 (IL-18), and interleukin 10 (IL-10) in elderly patients with ACS. A total of 190 subjects including 72 elderly patients with ACS (78.1% male, mean age 67.12 +/- 5.06 years), 60 elderly patients with stable angina pectoris (76.9% male, mean age 68.00 +/- 4.52 years), and 58 healthy volunteers (77.8% male, mean age 65.96 +/- 4.18 years) were recruited into the study. Serum MCP-1, IL-10, and IL-18 were determined in 132 elderly patients by enzyme-linked immunosorbent assay (ELISA) before and after treatment with low doses of ramipril (2.5-5 mg/day), and were determined in 58 healthy volunteers. The levels of serum MCP-1 and IL-18 were much higher in elderly patients with ACS than those in elderly patients with SAP and healthy volunteers. After treating with ramipril, the levels of MCP-1 and IL-18 were decreased in elderly patients with ACS. Moreover, ramipril significantly increased serum IL-10 in elderly patients with ACS. Ramipril plays an important role in elderly patients with ACS. With decreasing MCP-1 and IL-18, it can ameliorate cytokine-associated cardiac damage. This study may provide a new recognition of angiotensin-converting enzyme inhibitor for the treatment of ACS.
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PMID:Effects of ramipril on serum monocyte chemoattractant protein 1, interleukin-18, and interleukin-10 in elderly patients with acute coronary syndrome. 2033 66