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)

ELISA using the test systems and a complex of equipment manufactured by Flow Company was employed to study over time the content of fibronectin, fibrinogen, products of its degradation and myoglobin in 178 patients suffering from coronary heart disease (stable and progressive angina pectoris, acute myocardial infarction). The concentration of myoglobin, fibronectin, fibrinogen and products of its degradation was established to depend on the gravity of coronary heart disease and the tame elapsed since the disease onset. In patients with progressive disease, there was an increased consumption of fibronectin which may be due both to its expenditure during blood coagulation and fulfillment of angioprotective function because of exacerbation of systemic atherosclerosis.
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PMID:[The content of fibronectin, fibrinogen, its degradation products and myoglobin in patients with ischemic heart disease]. 209

The peroxidase-immunoperoxidase immunocytochemical method was used on 27 saphenous vein coronary artery bypass grafts, which had been resected because of recurrent angina, to identify in situ cellular and humoral elements possibly associated with graft occlusion. Immunostaining was performed on paraffin wax embedded control saphenous vein and graft sections incubated directly with primary antibodies against von Willebrand antigen (vWFAg), fibronectin, fibrinogen, leucocyte common antigen (LCA), lysozyme, vimentin, desmin, platelet factor 4, and thrombospondin. Antigens were visualised by a chromogen providing an orange-red immunoprecipitate at the site of epitope localisation. The intraluminal, amorphous exudate present in most grafts was not composed simply of fibrin or fibrinogen, as previously thought, but was a multiprotein complex including wWFAg, fibronectin, thrombospondin and platelet factor 4. Along with macrophages, these components probably enter the graft after haemodynamic, physical, and chemical injury to, and disruption of, the endothelial cell. Progressive myointimal proliferation and fibrosis of these grafts may be local repetitive responses to macrophages and platelets, cells previously known to participate in vascular disease.
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PMID:Immunocytochemical features of obstructed saphenous vein coronary artery bypass grafts. 265 29

The fibronectin level in the blood of patients with myocardial infarction was measured at varying times from the onset of an angina pectoris attack in order to elucidate the diagnostic importance of blood fibronectin. At the same time these patients were examined over time for the blood content of myoglobin, MB creatine kinase protein and C-reactive protein playing a well-known role in the diagnosis. The blood concentrations of these substances reached the maximal values at different times of myocardial infarction. The mean concentrations of fibronectin in the blood of patients with myocardial infarction ranged within normal starting from the first till the 28th day since the onset of an angina pectoris attack. Moreover, the mean blood fibronectin level in myocardial infarction patients did not differ within the first-third days since the disease onset from that in patients with a clinical picture of unstable angina pectoris which was not accompanied by the development of myocardial infarction. Based on the data obtained it is concluded that measurement of blood fibronectin level does not play any diagnostic role in myocardial infarction. On the other hand, progressive increase in blood fibronectin level throughout 4 weeks starting from the 3d day of the disease and a significantly higher fibronectin content on the 28th day as compared with that on the 3d day is likely to mirror the activity of repair processes occurring in the myocardium.
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PMID:[Dynamics of blood fibronectin level in myocardial infarction]. 402 41

Patients with coronary heart disease and angina pectoris were examined. The blood outflowing from the myocardium at the height of ischemia induced by atrial stimulation was found to have lower levels of fibronectin. Ten minutes after the stimulation discontinuation the concentration of fibronectin returned to baseline. A reduction in the fibronectin content during myocardial ischemia seems to be related to its consumption as a result of maintaining antithrombotic function.
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PMID:[Fibronectin level in coronary sinus blood in myocardial ischemia caused by atrial stimulation]. 652 Nov 78

Several studies indicate that thrombosis plays an important role in the pathogenesis of coronary heart disease (CHD). Fibronectin is a multifunctional protein in plasma, other body fluids, and cell surface and plays an important role in platelet functions, including mediation of cell-cell and cell-surface interactions. Sialic acid is a regular constituent of glycoproteins and gangliozides in the outer cell membrane of mammalian cells. Therefore, the sialic acid content of platelets, which are characterized by their ability to aggregate with each other, can be important in leading to thrombus formation. In this study, platelet fibronectin, sialic acid-, and adenosine diphosphate (ADP)-induced platelet aggregation levels were determined in patients with CHD. Platelet sialic acid concentrations were determined by Warren's method. Platelet aggregation tests with ADP in platelet-rich plasma (PRP) were analyzed by use of an aggregometer. Platelet homogenate fibronectin levels were determined by ELISA. Total protein levels were determined by Lowry method. Our results indicate that, in patients with no vessel disease (patients with no obstructed vessel but suffering from chest pain, like angina pectoris) platelet fibronectin levels were significantly lower than the total of the other patients (patients with 1, 2, or 3 obstructed coronary vessels) (p<0.05). Sialic acid levels in patients with no vessel disease were significantly lower than the total of the patient group (p<0.05). There was significant (+) correlation between platelet aggregation, platelet fibronectin, platelet sialic acid, and severity of disease (p<0.05). Our preliminary findings suggest that, especially platelet fibronectin levels potentially represent a pathogenic factor for CHD.
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PMID:Preliminary study showing the relationship between platelet fibronectin, sialic acid, and ADP-induced aggregation levels in coronary heart disease. 1763 93

The relation between fibronectin and coronary artery disease (CAD) according to previous study results is controversial. The aim of the present study is to investigate the predictive value of fibronectin in determining the presence and severity of CAD. Patients with stable angina (n=62) who had angiographically documented CAD, and control patients (n=31) who had normal coronary angiograms, were included in the study. Plasma fibronectin levels were determined in all patients. Plasma fibronectin level (milligrams per liter) in patients with CAD was higher than normal controls (364.2+/-171 vs 265.1+/-135.5, p=0.006). The severity of CAD determined according to Gensini score and fibronectin level did not show any correlation (r=0.13, p=0.311). If fibronectin level 240 mg/l was determined as cutoff, it showed 76% sensitivity, 46% specificity, 46% negative predictive value, and 72.3% positive predictive value for predicting CAD. The present study showed that plasma fibronectin level in CAD is significantly higher than normal control subjects. However, it has no role in predicting the severity of CAD.
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PMID:Diagnostic value of plasma fibronectin level in predicting the presence and severity of coronary artery disease. 1871 75

Recent clinical studies on chronic kidney disease (CKD) reported that renal dysfunction was a critical risk factor for cardiovascular events (CVE), which lead us to reconsider the effect of cardioprotective agents on the kidney. Glomerulonephritis, which is the major cause of CKD, is characterized by mesangial cell proliferation and extracellular matrix deposition. Nicorandil, a therapeutic drug for angina and acute heart failure, have been reported to show antiproliferative activity in mesangial cells. In this study, we first investigated the in vivo effects of nicorandil in anti-Thy1 nephritis rats. In male F344 rats, anti-Thy1 nephritis was induced by the injection of an anti-Thy1 antibody. From three days before induction, nicorandil (10, 30 mg/kg per day) was administered in the drinking water for 12 consecutive days. Anti-Thy1 nephritis resulted in a significant increase in proteinuria and glomerular mesangial cell proliferation. In nephritis rats, nicorandil (30 mg/kg per day) significantly suppressed increase in proteinuria, mesangial cell proliferation (the number of glomerular cell and glomerular area), and renal hypertrophy without affecting blood pressure. Nicorandil significantly prevented the overexpression of type I collagen, fibronectin, transforming growth factor (TGF)-beta, and platelet-derived growth factor (PDGF) mRNA. These results suggest that nicorandil may have renoprotective effects in mesangioproliferative glomerulonephritis.
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PMID:Nicorandil improves glomerular injury in rats with mesangioproliferative glomerulonephritis via inhibition of proproliferative and profibrotic growth factors. 1972 33

Upon activation, platelets release a host of soluble and vesicular signals, collectively termed the "platelet releasate" (PR). The contents of this PR play a significant role in haemostasis, inflammation, and pathologic sequelae. Despite this, proteomic studies investigating the PR in coronary artery disease have not been performed. Here, we undertook a comparative label-free quantitative (LFQ) proteomic profiling of the 1 U/ml thrombin-induced PR from 13 acute coronary syndrome vs. 14 stable angina pectoris patients using a tandem mass spectrometry approach. Data are available via ProteomeXchange with identifier PXD009356. 318 PR proteins were identified across both cohorts with 9 proteins found to be differentially released, including tetranectin (CLEC3B), protein disulfide-isomerase-A3 (PDIA3), coagulation factor V (F5), and fibronectin (FN1). Strikingly, these 9 differential proteins were all associated with the gene ontology cellular component term "extracellular vesicle" and reduced levels of EVs were detected in the corresponding plasma of ST-segment elevation myocardial infarction (STEMI) patients. Network analysis revealed 3 proteins either reduced (F5; FN1) or absent (CLEC3B) in the PR of STEMI patients that are strongly connected to both the clotting cascade and major druggable targets on platelets. This moderated proteomic signature may prove useful for non-invasive risk assessment of the progression of coronary artery disease. These data further contribute to the growing evidence-base of using the platelet releasate as a predictor of pathological state and disease severity.
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PMID:Comparative Platelet Releasate Proteomic Profiling of Acute Coronary Syndrome versus Stable Coronary Artery Disease. 3267 Oct 99