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 Progetto Lombardo Atero-Trombosi (PLAT) Study was a prospective, multicenter, multidisciplinary study of the association among hemostatic variables, conventional risk factors, and atherothrombotic events in four groups of patients with preexisting vascular ischemic disease (335 myocardial infarction survivors, 123 patients with stable angina pectoris, 160 with transient ischemic attacks, and 335 with peripheral vascular disease). In the myocardial infarction group, univariate analysis showed that atherothrombotic events were associated with high fibrinogen (p = 0.001), factor VIII:C (p less than 0.001), and von Willebrand factor antigen (vWF:Ag) (p = 0.004) levels and with low high density lipoprotein cholesterol (p = 0.043), factor VII (p = 0.019), and protein C (p = 0.044) levels; multivariate analysis produced associations with high fibrinogen and factor VIII:C levels and low protein C levels. By both univariate and multivariate analysis, events in the angina pectoris group were associated with high vWF:Ag (p = 0.026) and leukocyte (p = 0.033) levels and the presence of carotid arterial stenosis (p = 0.063); associations with high leukocyte (p = 0.037) and factor VIII:C (p = 0.186) levels, family history (p = 0.031), and diabetes (p = 0.061) were also found in the group with transient ischemic attacks. In those with peripheral vascular disease, events were associated with Fontaine stage greater than or equal to IIB (p = 0.024), high factor VIII:C levels (p = 0.073), and low protein C (p = 0.028), fibrinogen (p = 0.030), antithrombin III (p = 0.054), and factor VII (p = 0.057) levels by univariate analysis and with Fontaine stage and low fibrinogen levels by multivariate analysis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The PLAT Study: hemostatic function in relation to atherothrombotic ischemic events in vascular disease patients. Principal results. PLAT Study Group. Progetto Lombardo Atero-Trombosi (PLAT) Study Group. 152 21

The activity of tissue plasminogen activator (TPA), its rapid inhibitor (TPAL), C protein (Cp), plasminogen, alpha 2-antiplasmin, antithrombin III was evaluated and the levels of fibrinogen-fibrin degradation products and fibrinogen (F) were measured in 51 males with persistent coronary heart disease (CHD) and 16 without coronary atherosclerosis and atherosclerosis of other sites, which were matched for age and CHD risk factors. The patients were found to have elevated TRAI levels (17.3 +/- 1.2 IU/ml versus 12.2 +/- 2.2 IU/ml in the controls; p less than 0.05), increased TPA release (75.5 +/- 9.2 IU/ml versus 47.5 +/- 7.9 IU/ml in the controls; p less than 0.03) in response to venous occlusion, and lower Cp levels (-7.7 +/- 2.5%; p less than 0.01). The level of F correlated with the severity of coronary atherosclerosis. The patients with primary angina pectoris displayed higher TPA release than did those with chronic CHD. The presented facts are associated with overt changes occurring in the response of the endothelium in the patients, primarily, in early CHD.
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PMID:[Tissue plasminogen activator, its inhibitor and other factors of the blood fibrinolytic system in stable coronary heart disease]. 152 46

18 type II diabetes mellitus patients with coronary artery disease (CAD) have been studied. Tissue plasminogen activator (t-PA) antigen and activity, plasminogen activator inhibitor (PAI) antigen and activity, thrombin-antithrombin III (TAT) complexes were determined in blood samples. Diabetic CAD patients showed higher TAT levels with clearly increased PAI levels whereas t-PA levels levels were similar in patients and controls. Long term defibrotide treatment induced marked changes in fibrinolytic parameters of these diabetic patients with CAD with increased t-PA activity, that could be related to an evident reduction of PAI antigen and activity. Drugs able to modulate PAI activity may be useful in clinical conditions at high risk of thrombotic vascular complications like diabetics with stable angina.
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PMID:Effects of defibrotide on fibrinolytic activity in diabetic patients with stable angina pectoris. 157 96

The authors examined the activities of plasminogen activator, its inhibitor, the levels of C protein, antithrombin III, alpha 2-antiplasmin, plasminogen, fibrinogen, fibrinogen/fibrin degradation products in 22 patients with unstable angina by using the vein occlusive test. No significant differences were found in the examined parameters while comparing the group of stable angina patients and healthy subjects. It was concluded that thrombogenesis disturbances in unstable angina were regional and the recording of peripheral blood fibrinolytic parameters failed to detect any changes characteristic of unstable angina.
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PMID:[Unstable angina: tissue plasminogen activator, tissue plasminogen activator inhibitors, protein C and other factors of the blood fibrinolytic system]. 167 68

Estimation of antithrombin III, alpha 2 macroglobulin and alpha 1 antitrypsin in patients with stable and unstable angina and acute myocardial infarction (15 cases each) were carried out. Twenty age, sex and weight matched healthy subjects were included as controls. Mean platelet factor 4(PF4) levels measured in 10 cases of each subgroup were significantly elevated in myocardial infarction (MI) (48.4 +/- 15.16 ng/ml) and III unstable angina patients (44.7 +/- 15.9 ng/ml) as compared to controls (25.42 +/- 12.47 ng/ml; P less than 0.01). Mean antithrombin III (AT III) levels were markedly reduced in all patients with MI (39.65 +/- 12.8% of normal pooled plasma) and unstable angina (37.9 +/- 16.6% of normal pooled plasma) and in 9 patients with stable angina. Alpha I antitrypsin and alpha 2 macroglobulin levels in these cases showed no significant difference compared to normals. Reduced AT III in coronary artery disease suggests a prethrombotic tendency in these patients. Raised PF4 levels in acute phase of the disease suggests heightened platelet activation.
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PMID:Evaluation of factors predisposing to arterial thrombosis in coronary artery disease. 171 6

PAI-1 antigen, tPA antigen and thrombin - antithrombin III complexes (TAT) levels were measured in 10 males with stable angina and type-II diabetes mellitus and in 16 males with stable angina without diabetes or other risk factors (hyperfibrinogenaemia, hyperlipidaemia, diabetes, hypertension, smoking and obesity) known to increase PAI levels. Ten healthy men of equivalent age served as controls. Because only diabetics with coronary artery disease (CAD) showed a decreased fibrinolytic capacity, a second study was performed on the 16 non-diabetic CAD patients to determine whether submaximal workload induces significant changes of tPA and PAI levels. TAT levels were increased in CAD, and significantly so in the diabetic group. tPA levels were increased only in the CAD patients without diabetes. PAI levels were significantly increased in diabetic CAD patients (5.26 +/- 1.96 ng/ml) but not in the stable angina patients without diabetes (2.97 +/- 1.44 ng/ml). Immunologically-reactive tPA released after exercise was higher in the 16 CAD patients without diabetes than in controls. Our data could indicate that in stable angina without diabetes there is no chronic latent activation of the clotting system, with no impairment of fibrinolytic activity. On the other hand, the presence of diabetes mellitus seems to influence the fibrinolytic capacity in CAD, particularly increasing PAI levels.
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PMID:Increased plasminogen activator inhibitor antigen levels in diabetic patients with stable angina. 177 97

Hemostatic disorders in coronary heart disease and cerebrovascular disease patients were examined by studying two groups of prothrombotic and prethrombotic markers. Sixty subjects (28 male, 32 female aged 64 +/- 6 years) were included in the study of which 30 suffered from coronary heart disease and 30 from cerebral vascular disease; the first group was subdivided into those subjects with quiescent preinfarction angina (21 cases) and those with acute myocardial infarction (9 cases), whereas the second group was subdivided into subjects with cerebral stroke (20 cases) and those with TIA (10 cases). Each subject underwent an assay to assess fasting blood levels of fibrinogen, factor VII, antithrombin III (using a chromogenic method), plasminogen tissue activator, beta-thromboglobulin and dimer-D (ELISA method) 24 hours after being admitted to hospital. From an analysis of results it was observed that of the four prothrombotic markers used, fibrinogen and factor VII showed a generic increase in comparison to coronary heart disease and cerebrovascular disease patients; this was paralleled by significant reduction of antithrombin III; differences were even more marked and significant in acute thrombo-occlusive (infarction, stroke) compared to functional forms (angina, TIA). In line with other studies, the Authors favour an irritative type endothelial response leading to a marked and surprising increase of tPA. The two prothrombotic markers (BTG, D-D) also showed a thrombotic development in the two groups of patients examined with more significant findings in the occlusive forms (infarction, stroke) in comparison to transitory forms. On the basis of these and other published results the Authors confirm the usefulness of monitoring prothrombotic markers (fibrinogen, factor VII, AT III) in apparently normal subjects with or without risk factors or with slight initial signs of arteriosclerotic disease; these call for longitudinal or cross-sectional studies of an epidemiology type, in addition to isolated assay for a generic assessment of the patient's biological status, even if it is not yet possible to elaborate a protocol for the certain and specific diagnosis of a thrombophilic condition. The value of prethrombotic markers is apparent in the acute occlusive stage of the disease as a form of prognostic and therapeutic monitoring, and in preinfarction and above all silent transitory forms where, together with the use of other techniques (Holter), it provides interesting openings for confirming the diagnosis of an in vivo microthrombotic genesis and the consequent introduction of antithrombotic drug therapy.
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PMID:[The thrombophilic status and ischemic cardiopathy]. 195 44

Plasma antithrombin III was measured by an immunological approach (AT III:Ag) using an antiserum developed in our laboratory and by its ability to inhibit thrombin (functional assay) using a chromogenic synthetic substrate in 12 patients with myocardial infarction, 9 patients with angina pectoris and 10 healthy control subjects. In the early stage (3 to 24 hours after the onset of pain) of an acute myocardial infarction AT III:Ag (115.67% +/- 21.23) was found to be significantly (p less than 0.01) higher than functional (free) AT III (92% +/- 10.27). This difference was less obvious 10 days later (AT III:Ag 118% +/- 18.93; functional AT III 104.94 +/- 14.45). There was also no significant difference between AT III:Ag and functional AT III in patients with angina pectoris as well as in controls. Since AT III:Ag represents total plasma AT III while functional AT III represents only free AT III the difference between these two variables could provide informations about the amount of the anticoagulant forming complexes with activated clotting factors. It is therefore considered that the significant increase in the difference between AT III:Ag and functional AT III in the early stage of acute myocardial infarction is likely to suggest an intravascular activation of coagulation.
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PMID:Functional and antigenic antithrombin III in angina pectoris and acute myocardial infarction patients. 210 Aug 76

Circulating immunoreactive endothelin (ir-ET) was measured in nine patients with acute myocardial infarction (AMI), 10 patients with stable angina pectoris (SAP), and 25 normal control subjects. In patients with AMI, the plasma ir-ET level was elevated in the acute phase and was highest on the day of onset (AMI: 3.8 +/- 1.7 pg/ml, normal control value: 0.5 +/- 0.2 pg/ml). The plasma ir-ET level showed a positive correlation with the wall motion abnormality index (rs = 0.56, p less than 0.01), thrombin-antithrombin III complex (rs = 0.55, p less than 0.01), and beta thromboglobulin (rs = 0.39, p less than 0.05). An especially high plasma ir-ET level was detected in patients in whom the Killip subset was IV. The plasma ir-ET level was not increased in patients with SAP (0.8 +/- 0.3 pg/ml). The plasma ir-ET level is increased in the acute phase of AMI. A pathophysiologic state characterized by cardiac dysfunction, an activated coagulation system, and platelet hyperactivity may be associated with this increase in plasma ir-ET.
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PMID:Circulating immunoreactive endothelin in ischemic heart disease. 213 44

The effect on plasma antithrombin III (AT III) and protein C on a supplement with polyunsaturated fatty acids (PUFA's) was investigated in a double-blind study in 36 patients with stable angina pectoris. All participants were given a supplement to their normal diets of vegetable oil (4.8 g n-6 PUFA's) for 4 weeks and were then randomized to the same oil or to fish oil (4.8 g n-3 PUFA's) for 12 weeks. Both oil supplements resulted in a statistically significant decrease in AT III activity, but there were no differences between the two different types of PUFA's. Antithrombin III antigen, protein C antigen or activity did not change significantly after either oil supplement. The background and significance for the decrease in antithrombin III activity induced by n-3 and n-6 PUFA's in patients with ischaemic heart disease is unknown.
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PMID:Antithrombin III and protein C in stable angina pectoris--influence of dietary supplementation with polyunsaturated fatty acids. 306 Sep 87


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