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 study of the fibrinolytic system and the activity of interleukin 1 and 2 in 75 patients with various cardial manifestations of atherosclerosis (angina of effort, angina decubitus, arrhythmia, symptomatic hypertension) revealed a decrease in the activity of plasminogen--a blood activator--in patients with angina of effort, angina decubitus and cardiac arrhythmias. In those with atherosclerotic hypertension the activatory activity was in the normal limits. A decrease in the activity of interleukin 1 and 2 was noted in all those examined.
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PMID:[Fibrinolysis, interleukins and coronary atherosclerosis]. 150 14

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

The circadian variation of angina pectoris, myocardial infarction and sudden death, with a first peak in the early morning and a second one in the late afternoon, suggests that physical activity plays an important role in triggering ischemic events by an increase of cardiac oxygen demand. But there is also evidence of decreased oxygen supply related to a paradoxical catecholamine-induced vasoconstriction which reflects the endothelial dysfunction of atherosclerotic coronary arteries. Elevated blood pressure during daytime and other mechanical factors can facilitate a plaque-rupture which triggers formation of coronary thrombosis. Hypercoagulability in the early morning hours by increased platelet aggregability and by elevated levels of plasminogen-activator inhibitors may contribute to this fatal mechanism.
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PMID:[Mechanisms of myocardial ischemia and circadian fluctuations of ischemic episodes]. 153 51

With intravenous thrombolysis mortality of acute myocardial infarction can be significantly reduced, not only in the first hours after the onset of symptoms, but also up to 24 hours. The open infarct related coronary artery is important concerning long-term clinical outcome. If thrombolysis can be administered within the first three to six hours, limitation of infarct size and preservation of left ventricular function contribute to an impressive reduction in mortality. Long-term assessments of clinical outcome have surprisingly shown that the prognosis is much more dependent upon patency of the infarct related artery than from the time to treatment. Since a correlation is suspected between the degree of residual stenosis and the clinical course, recurrence of ischemia, reinfarction, hemodynamic instability and death, and the fact that mortality is highest within the first three days after thrombolysis the emphasis of numerous investigations has been on possibilities of PTCA in the acute stage of myocardial infarction. The application of interventional techniques was tested at different times within the progression of myocardial infarction. PTCA can be applied as primary, direct therapy without thrombolysis, immediately and during intravenous thrombolysis, following successful pharmacological recanalisation, as rescue-PTCA for failed thrombolytic therapy, delayed and as a prophylactic measure up to until days after the infarction or later when accompanied by careful observation of the patient, when limited to few indications with spontaneous or stress-related angina pectoris, hemodynamic instability or predetermined angiographic criteria. Important results have been gathered by the larger studies of the last few years, TAMI, ECSG, and TIMI as well as by numerous smaller investigations, about the pathophysiology and treatment of myocardial infarction. Despite different study design, the three larger trials have come to the same conclusion regarding PTCA and rt-PA thrombolysis, early PTCA is without advantage compared to a deferred treatment; the acute results are usually worse and the clinical course more complicated. It must be mentioned however, that major problems still remain unresolved: primary or direct angioplasty, PTCA in combination with non-fibrin specific plasminogen activators, as well as rescue-PTCA after failed thrombolysis. Specially, 90 minutes after thrombolysis 23 to 44% of the coronaries are still occluded, depending on the plasminogen activator, and there is no non-invasive procedure to detect this patient-group and to advise further treatment. Due to the high mortality rate within the first three days attempts of treatment are concentrated on this time-span.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[PTCA in acute myocardial infarct: primary, immediate, delayed or elective?]. 154 50

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

Lipoprotein (a) [Lp(a)] appears to be involved in atherogenesis and in vitro studies have suggested that it may interfere with thrombolysis. In this study, Lp(a) serum levels were determined by radioimmunoassay in 124 patients with ischemic heart disease. Of these, 47 had acute myocardial infarction, 13 had unstable angina, and 64 were age-matched patients with stable angina. Of the 60 patients with acute coronary artery disease, 34 received thrombolysis and 26 did not. In addition to Lp(a), serum plasminogen, alpha 2 antiplasmin, fibrinogen, and D-dimer (cross-linked fibrin degradation products) levels were measured. These tests were repeated after 6 hours in patients with myocardial infarction and unstable angina. No significant difference was found for admission Lp(a) levels among patients with myocardial infarction (0.324 +/- 0.047 g/liter), unstable angina (0.435 +/- 0.123 g/liter) and stable angina (0.431 +/- 0.023 g/liter), between patients with myocardial infarction with or without thrombolytic treatment, nor between late and early measurements in patients with unstable angina and acute myocardial infarction. Plasminogen, alpha 2 antiplasmin and fibrinogen values decreased significantly after thrombolytic treatment. The size of this decrease correlated positively with higher Lp(a) blood levels (p less than 0.05). Patients with Lp(a) greater than 0.25 g/liter had a 66% decrease in fibrinogen and a 53% decrease in anti-plasmin, compared with 35 and 32%, respectively, in patients with Lp(a) level less than or equal to 0.25 g/liter (p less than 0.05). Plasminogen levels revealed a similar trend, with a 61% decrease for the higher values and a 45% decrease for the lower values.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Lipoprotein (a) blood levels in unstable angina pectoris, acute myocardial infarction, and after thrombolytic therapy. 153 Dec 83

Fibrinolysis and lipid disturbances have been considered as independent risk factors for coronary artery disease. Besides this, lipoprotein(a), which is characterized by its homology with plasminogen may interfere with the fibrinolytic function. To evaluate the eventual correlation between fibrinolytic parameters, lipoprotein (a) and other risk factors, 46 patients with coronary artery disease (34 with chronic angina pectoris and 12 with myocardial infarction) were studied. Increased basal values of t-PA antigen (8.2 and 6.6 vs. 4.2 ng/ml) but decreased response after stimulus (2.2 and 1.8 vs. 3.8 ng/ml) and increased levels of lipoprotein(a) (24.7 and 35.9 vs. 10.5 mg/dl) were the most relevant differences between coronary artery disease patients and controls. No correlation between lipoprotein(a) and fibrinolytic parameters was found. Therefore plasma concentration of the main plasma fibrinolytic parameters and lipoprotein(a) seem to be unrelated though the relevance of this interaction at a local level needs to be studied.
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PMID:Fibrinolytic parameters and lipoprotein (a) levels in plasma of patients with coronary artery disease. 183 82

Ample evidence exists to support the major role of intracoronary thrombosis superimposed on a disrupted plaque in unstable angina. Consequently, thrombolytic treatment, already established to be highly beneficial in patients with acute myocardial infarction, might also be indicated in patients with unstable angina. The clinical response to thrombolytic treatment has been evaluated in several small-sized studies with inconsistent and somewhat deceiving results. Thus, the role of thrombolysis in the treatment of unstable angina is still controversial. Two ongoing large-scale, randomized, controlled trials, the Third Thrombolysis in Myocardial Infarction (TIMI III) in the United States testing recombinant tissue-type plasminogen activator and UNASEM in Europe testing anisoylated plasminogen-streptokinase activator complex will, it is hoped, solve the debate. At present, early thrombolysis might be considered for the treatment of the subset of patients with severe rest angina associated with transient ST-T ischemic changes.
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PMID:Thrombolysis in unstable angina: results of clinical studies. 189 74

The impact of 6-week strenuous exercise training (SET) on blood coagulative and fibrinolytic parameters (levels of fibrinogen, soluble fibrin, fibrinogen-fibrin degradation products, activities of plasminogen and plasmin) was studied in 28 patients with first angina pectoris, in 16 of whom in the first 3 months of onset of the disease, but angina pectoris lasting 3-4 prior to SET. The 6-week strenuous exercises in patients with first angina were found to cause a decrease in fibrinogen levels, exert no action on thrombin and fibrin formation. They did not diminish plasminogen activator release during exercise in patients with pre-exercise unstable angina.
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PMID:[Newly developed stenocardia: effect of intensive physical training on the indicators of the blood coagulation system and fibrinolysis]. 189 56

Using percutaneous transluminal coronary angioplasty (PTCA) as primary therapy for unstable angina is quite common. Unstable angina appears to be the indication for the procedure in approximately one third of all PTCA attempts. Considering the unstable nature of the plaque in this type of angina, and the increased risk of abrupt occlusion due to frequent intraluminal thrombus, the generally reported rate of success, approximately 85%, is highly respectable. The evidence supporting a period of pretreatment with aspirin and heparin is strong. Less certain is the value of concomitantly administering plasminogen activators. Pending data should produce important further guidelines for effective therapy. Major trials, some using fibrinolytics as well as taking an overall aggressive, interventional approach (like that taken by UNSA, TIMI-III, and others), are reaching the recruitment-completion and promulgation stages.
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PMID:The role of coronary angioplasty in the management of unstable angina pectoris. 195 Nov 5


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