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)

C-reactive protein (CRP) is a reliable biochemical marker for tissue destruction, necrosis and inflammation. CRP is an essential human acute phase reactant produced in the liver as response to systemic stimuli. The biological half-life of CRP is not influenced by age, liver- or kidney function or pharmacotherapy. CRP values in acute bacterial infections have been appreciated for 70 years. The new standardized CRP analyses yield the possibilities of longitudinal monitoring of chronic inflammatory diseases and help identify complications. The more sensitive measures of the area of reference also supplies new information: As a prognostic marker for microvasculitis, CRP is at present re-writing the agenda for today's research in inflammation, angina pectoris, vascular insults and atherosclerosis.
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PMID:[C-reactive protein]. 1083 77

Inflammation and chronic infections may be important features in the pathogenesis of acute coronary syndromes. We describe 6 systemic markers of inflammation in patients with unstable angina or non-Q-wave myocardial infarction and the relations between these markers, seropositivity to chronic infections, and prognosis. C-reactive protein (CRP), serum amyloid A protein (SAA), fibrinogen, interleukin-6 (IL-6), neopterin, procalcitonin, and serum antibody levels to Chlamydia pneumoniae, Helicobacter pylori, and cytomegalovirus were measured on admission and 48 hours later. One-year clinical follow-up was performed. Plasma levels of acute phase reactants were all elevated on admission and increased further at 48 hours: CRP from 10.1 +/- 2.1 mg/L at baseline to 26.6 +/- 5.1 mg/L at 48 hours (p <0.001); SAA from 27.3 +/- 8.5 to 93.1 +/- 23.2 mg/dl (p <0.005); fibrinogen from 3.2 +/- 0.1 to 3.8 +/- 0.1 g/L (p <0.0001); whereas initial high levels of IL-6 tended also to increase from 9.8 +/- 2 to 15.3 +/- 3.1 pg/ml (p = NS). In contrast, neopterin and procalcitonin remained unchanged. We found no association between levels of each inflammatory marker and the serologic status. Furthermore, levels of inflammatory proteins in patients seronegative to all 3 agents were comparable to those of patients seropositive to 2 or 3 infectious agents. The composite end points of death, myocardial infarction, recurrent angina, or revascularization at 1-year follow-up did not differ according to the serologic status. Thus, in patients with acute coronary syndromes, the acute phase proteins increased over the first 2 days of hospitalization. This initial inflammatory reaction as well as the 1-year clinical outcome did not differ according to the initial serologic status of Chlamydia pneumoniae, Helicobacter pylori, or cytomegalovirus.
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PMID:Effect of prior exposure to Chlamydia pneumoniae, Helicobacter pylori, or cytomegalovirus on the degree of inflammation and one-year prognosis of patients with unstable angina pectoris or non-Q-wave acute myocardial infarction. 1094 28

The time course of vascular endothelial growth factor (VEGF) and hepatocyte growth factor (HGF) release in patients with acute myocardial infarction (AMI) is unknown. Blood samples were obtained at the time of admission and 3, 7, 14 and 21 days later in 32 patients with AMI and 30 control patients. Serum VEGF and HGF, as well as C-reactive protein (CRP) and amyloid A protein (SAA), were determined. Both serum VEGF and HGF levels on admission in patients with AMI were higher than control values and peaked on day 7. VEGF levels in patients with preinfarction angina were higher than in patients with no preinfarction angina, whereas the HGF level did not differ. Both CRP and SAA levels peaked on day 3, and the CRP level on day 3 correlate with both VEGF and HGF levels on day 7. We hypothesized that the serum VEGF level is associated with preinfarction ischemia and the increase in VEGF and HGF on day 7 of AMI may represent a response to acute inflammation.
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PMID:Serial changes in serum VEGF and HGF in patients with acute myocardial infarction. 1096 88

Plasma levels of secretory nonpancreatic type II phospholipase A2 (sPLA2) are increased in various chronic inflammatory diseases; this increase is correlated with disease severity. sPLA2 plays a possible role in atherogenesis and is highly expressed in atheromatous plaques. Thus, this study prospectively examined whether plasma levels of sPLA2 may have a prognostic value in patients with unstable angina, which is known to have inflammatory features. Plasma levels of sPLA2 were measured in 52 patients with unstable angina, in 107 patients with stable angina, and in 96 control subjects by radioimmunoassay. sPLA2 levels were significantly higher in patients with unstable angina than in those with stable angina and in control subjects. sPLA2 remained elevated after stabilization of disease. The levels were not increased in the blood in the coronary sinus. Kaplan-Meier analysis demonstrated that patients with unstable angina and with the higher sPLA2 levels had a significantly higher probability of developing clinical coronary events during a follow-up period of 2 years compared with those with the lower levels. In multivariate Cox hazard analysis, the higher levels of sPLA2 were a significant predictor of developing coronary events in patients with unstable angina, independent of other risk factors, including C-reactive protein levels, an established inflammatory predictor. In conclusion, the increase in circulating levels of sPLA2 predicts clinical coronary events independently of other risk factors in patients with unstable angina. sPLA2 levels were persistently elevated but the elevated levels may not be derived from coronary circulation.
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PMID:Prognostic value of plasma levels of secretory type II phospholipase A2 in patients with unstable angina pectoris. 1101 89

Procarboxypeptidase U (proCPU) is the plasma precursor of carboxypeptidase U (CPU, carboxypeptidase R. plasma carboxypeptidase B or activated thrombin-activatable fibrinolysis inhibitor, TAFIa). CPU removes C-terminal lysine residues that act as plasminogen binding sites from partially degraded fibrin, thereby down-regulating plasminogen activation and fibrinolysis. The present study was carried out as a pilot study to examine whether the plasma proCPU concentration is related to the presence of coronary artery disease (CAD) and/or to levels of established risk indicators for CAD, in a case-control study of 110 men requiring coronary artery bypass grafting (CABG) because of stable angina pectoris. The preoperative plasma proCPU level in the CABG patients was significantly higher than in population-based controls (1029 +/- 154 vs. 974 +/- 140 U/L, p <0.05). In addition, in a subset of the patients (n = 31 ) the proCPU concentration, which was significantly lower on the third postoperative day (-17 +/- 10%), had increased significantly on the sixth day (+14 +/- 12%) after surgery, compared with the preoperative level. In both patients and controls, proCPU concentration was strongly and positively associated with factor VII amidolytic activity and protein C activity, suggesting a common mechanism modulating the plasma levels of these proteins. Otherwise, statistically significant correlations with proCPU were group-specific. In the patients, proCPU correlated significantly with plasma fibrinogen and protein S. In the controls, proCPU correlated significantly with concentrations of cholesterol in plasma. VLDL and LDL. In addition, proCPU correlated significantly with C-reactive protein and haptoglobin levels in the controls only, indicating that also inflammatory mechanisms are involved in the regulation of plasma proCPU. These results suggest that a mechanism exists by which fibrinolytic function is impaired in a manner that is likely to result in more stable fibrin deposits and increase the risk of precocious CAD as well as early occlusion of venous bypass grafts.
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PMID:Plasma procarboxypeptidase U in men with symptomatic coronary artery disease. 1101 56

Evidence suggesting the involvement of activated monocytes and T-lymphocytes in the acute phase of coronary artery disease (CAD) has been increasing. But a detailed analysis of a correlation between monocyte and T-lymphocyte activation markers in CAD has not yet been done. We analyzed plasma C-reactive protein (CRP) levels and the expression levels of CD14 and CD11b on monocytes and the percentage of HLA-DR T-lymphocytes in 25 patients with acute coronary syndrome (ACS), 12 stable angina (SA) patients, and 23 control subjects using flow-cytometry. The expression of CD14 by monocytes was increased significantly in ACS patients (activation index 38.7 +/- 2.5, mean +/- SEM) in comparison to the control subjects (8.0 +/- 1.9) and the SA patients (16.9 +/- 3.9) (p < 0.001 and p < 0.01, respectively). The expression of CD11b by monocytes of ACS patients (4.6 +/- 0.6) was also increased significantly in comparison to control subjects (2.2 +/- 0.1) and the SA patients (2.2 +/- 0.3) (p < 0.001 for both). Also, a significantly higher percentage of HLA-DR positive T-lymphocytes (19.2 +/- 1.8 vs 13.5 +/- 1.2%, p < 0.05) was observed among ACS patients in comparison to control subjects. Significant increases in plasma CRP levels were also detected in ACS patients. Furthermore, there were statistically significant correlations among these activation markers. These results indicate that activation of inflammatory cells may play a role in the pathogenesis of ACS. The correlation between the activation status of monocytes and T-lymphocytes indicates that the activation of these immune cells is linked in such a way that activation of one type of cell may lead to the activation of another type of cell.
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PMID:Correlation between monocyte and T-lymphocyte activation markers in patients with acute coronary syndrome. 1113 67

The instability of coronary lesions was evaluated in 30 patients with stable angina and 60 patients with unstable angina. The grade of instability of coronary lesions as predicted by the increases in C-reactive protein induced by PTCA and/or stenting was closely correlated with Braunwald's classification of unstable angina.
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PMID:Instability of coronary lesions in unstable angina assessed by C-reactive protein values following coronary interventions. 1115 46

We studied the role of various markers of lipid metabolism, hemostasis and inflammation in a two year follow-up of 3,000 patients with angina pectoris, during which time 106 patients experienced myocardial infarction or sudden coronary death. Low levels of high density lipoprotein (HDL) cholesterol and of apolipoprotein (apo) A-I were most strongly associated with increased coronary risk. The relative risk per standard deviation increase was 0.68 for HDL cholesterol (95% confidence interval 0.55 to 0.84) and 0.66 for apoA-I (0.54 to 0.81). These associations were independent of other coronary risk factors, other lipid measurements, hemostatic factors, and C-reactive protein (CRP). The associations of total and LDL cholesterol, triglycerides, apoB, and lipoprotein(a) with coronary events were not independent of HDL cholesterol or hemostatic factors. We conclude that HDL cholesterol or apoA-I, hemostatic risk factors, and CRP are important prognostic markers of coronary events in secondary prevention.
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PMID:Short-term prognostic value of lipid measurements in patients with angina pectoris. The ECAT Angina Pectoris Study Group: European Concerted Action on Thrombosis and Disabilities. 1115 40

The present study investigated the relationship between myocardial damage and C-reactive protein (CRP) levels, with no increase in creatine kinase (CK) activity, immediately after the onset of acute myocardial infarction (AMI) in 85 patients with their first reperfused anterior AMI without CK elevation on admission and no ischemic events during hospitalization. Patients were classified into those with low levels (<0.3 mg/dl) of CRP (Group L; n=67) and those with high levels (> or =0.3 mg/dl) of CRP (Group H; n=18). Group H had a higher proportion of patients with a history of preinfarction angina (89 vs 55%, p<0.01), especially unstable angina. SigmaST in leads V1-6 on admission ECG was lower in Group H than in Group L (14+/-7 vs 21+/-13 mm, p<0.05). Predischarge left ventriculography showed that the left ventricular global ejection fraction (55+/-11 vs 48+/-10%, p<0.01) and SD/chord at the left anterior descending artery lesion (-1.7+/-0.9 vs -2.3+/-0.9, p<0.01) were better in Group H. Multivariate analysis demonstrated that both CRP on admission (p=0.011) and preinfarction angina (p=0.002) were independently associated with better regional wall motion (SD/chord >-2.0) before discharge. These results suggest that the clinical situation of elevated CRP immediately after onset is associated with less myocardial damage and better left ventricular function in reperfused anterior AMI.
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PMID:Relationship between myocardial damage and C-reactive protein levels immediately after onset of acute myocardial infarction. 1121 27

The present study determined the white blood cell (WBC) count and the serum C-reactive protein (CRP) level in 27 patients with coronary spastic angina, 16 with Braunwald class IB unstable angina (UA) and 13 with Braunwald class IIIB. The relationship between the clinical presentation of UA and the requirement for emergency percutaneous transluminal coronary angioplasty (PTCA) was examined, and in patients with medically refractory angina, the determining factor among the clinical manifestations of angina was also investigated. In the acute phase, the WBC count and the serum CRP level were significantly higher in patients with Braunwald class IIIB than in those with coronary spastic angina or Braunwald class IB UA (p<0.001). In the Braunwald class IIIB group, a significantly higher rate of patients required emergency PTCA than that of the coronary spastic angina group (p<0.01). Patients with medically refractory angina had a significantly higher WBC count and higher serum CRP level on admission, and the WBC count on admission was independently associated with medically refractory angina by multivariate analysis (p<0.05). Inflammation may play a major pathological role in the rapid development of acute coronary syndrome.
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PMID:Is inflammation related to the clinical severity of unstable angina? 1134 45


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