Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P80098 (monocyte chemoattractant protein)
1,800 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nontraditional atherosclerotic risk factors have become the focus of attention in recent years. In addition, metabolic syndrome is gaining recognition as another multiplex cardiovascular risk factor. However, to date, no studies have investigated the effect of metabolic syndrome on circulating soluble CD40 ligand (sCD40L), monocyte chemoattractant protein 1, cellular adhesion molecules, and disease severity in patients with symptomatic coronary artery diseases. This study was conducted to address this issue. Patients with stable angina who received percutaneous coronary interventions for significant (> or = 70% diameter stenosis) de novo lesions between January 1999 and January 2004 and had preprocedural serum samples were enrolled. Metabolic syndrome was defined by the National Cholesterol Education Program criteria with waist criterion modified into body mass index of more than 25 kg/m2. The serum samples were thawed and analyzed for circulating sCD40L, monocyte chemoattractant protein 1, adhesion molecules, and high sensitivity C-reactive protein (hs-CRP). Coronary severity was assessed by a modified version of Gensini scoring system. A total of 313 patients, 248 males and 65 females, were studied. Among them, 222 (70.9%, 170 males and 52 females) had metabolic syndrome. Patients with metabolic syndrome had higher serum creatinine level and lower low-density lipoprotein cholesterol despite higher triglyceride concentration. In multivariate analysis, patients with metabolic syndrome had higher sCD40L (6057 +/- 275 vs. 5051 +/- 423 pg/mL, P = .037) and more hs-CRP in higher tertiles (P = .005) than patients without, but similar levels of intercellular adhesion molecule 1, vascular cell adhesion molecule 1, and P selectin. Metabolic syndrome was also significantly associated with multiple coronary vessel involvements with 70% or higher diameter stenosis (36.5% double-vessel and 14% triple-vessel diseases vs 30.8% double-vessel and 5.5% triple-vessel diseases, P = .026) and multiple coronary segment involvements with 50% or higher diameter stenosis (P = .014) in multivariate analysis. In conclusion, the presence of metabolic syndrome is independently associated with elevated sCD40L, hs-CRP, and coronary disease severity in patients with coronary artery disease requiring interventional treatment of stable angina.
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PMID:The presence of metabolic syndrome is independently associated with elevated serum CD40 ligand and disease severity in patients with symptomatic coronary artery disease. 1683 37

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

Percutaneous coronary intervention (PCI) can be regarded as a model for mechanical induced plaque rupture. The objective of this study was to evaluate the inflammatory response to PCI in stable coronary artery disease (CAD) by analysing plasma levels of a wide range of inflammatory mediators. Consecutively, we included 36 patients with stable angina pectoris after successful revascularization by PCI with implantation of a bare metal stent (BMS) or a drug eluting stent (DES). Patients were followed for 7 days with serial measurements of inflammatory mediators in plasma. C-reactive protein (CRP) and Pentraxin 3 showed a statistical significant early increase after PCI peaking at 3 days and 3 h, respectively. Vascular cell adhesion molecule-1 (VCAM-1) increased significantly with a peak at 3 days, while E-selectin showed a statistical significant gradual decrease. Markers of platelet mediated inflammation showed increasing (CD40 ligand) and decreasing (P-selectin) levels after PCI. While monocyte chemoattractant protein, CCL21 and CXCL16 increased rapidly in response to PCI, Interleukin-8, CCL19 and RANTES decreased. Patients with DES had significantly lower levels of VCAM-1 and RANTES compared to those with BMS. A femoral access site was associated with higher CRP levels than a radial access site. The use of glycoprotein-IIb/IIIa-inhibitors was associated with significantly higher CD40L and RANTES levels. Our findings underscore the complex nature of the inflammatory responses during PCI in stable CAD, and suggest that simultaneous measurements of several markers may be needed to characterize these PCI-related responses. The responses were only in a minor degree influenced by stent type, access site and the use of glycoprotein-IIb/IIIa-inhibitors.
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PMID:Inflammatory response to percutaneous coronary intervention in stable coronary artery disease. 2037 28