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Query: UMLS:C0002962 (angina)
 21,142 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

The structural homology between plasminogen and apolipoprotein (a), the specific glycoprotein of Lp(a) lipoprotein, raises the possibility of a relationship between this lipoprotein and the plasma fibrinolytic system. The present study examines this proposal by studying 66 patients with angina pectoris. As compared to normal controls, the patients had raised concentrations of Lp(a): B lipoprotein particles. No correlation was found between circulating Lp(a): B and the fibrinolytic system. The pathogenic role of Lp(a): B lipoprotein seems therefore not mediated by its effect on the plasma fibrinolytic system.
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PMID:The increased plasma Lp(a): B lipoprotein particle concentration in angina pectoris is not associated with hypofibrinolysis. 214 23

A consensus group convened under the auspices of the Ontario Medical Association produced guidelines for the use of intravenous thrombolytic agents in acute myocardial infarction. The guidelines, updated to December 1988, include the following points. 1) Any hospital that routinely accepts the responsibility for looking after patients with acute myocardial infarction could offer thrombolytic therapy if monitoring facilities are available and if the staff are experienced in the treatment of cardiac rhythm disturbances. 2) Before treatment, all patients must be carefully screened for factors predisposing to hemorrhagic complications. 3) A physician should be clearly designated as responsible for the care of the patient receiving an infusion and be available in the event of problems. 4) For the two approved agents the usual dosages are as follows: streptokinase, 1.5 million units given over 1 hour; and tissue-type plasminogen activator (tPA), 100 mg over 3 hours, delivered as 60 mg in the first hour (of which 6 to 7 mg should be given as a bolus in the first 1 to 2 minutes) and then an infusion of 20 mg/h over the next 2 hours. 5) Intravenous thrombolytics should be considered for any patient with presumed acute myocardial infarction, as suggested by prolonged chest pain or other appropriate symptoms and typical electrocardiographic changes. Expeditious treatment is critical, since myocardial necrosis occurs within hours. 6) Emergency angiography is indicated for patients with hemodynamic compromise and no apparent response to streptokinase or tPA and in those with recurrent chest pain suggestive of acute myocardial infarction despite an apparent response to intravenous thrombolysis. Angiography before discharge is recommended for patients with postinfarction angina or evidence from noninvasive testing of significant residual ischemic risk. 7) There is insufficient evidence to choose between streptokinase and tPA on the basis of the two most important outcome measures: patient survival and myocardial preservation. More conclusive evidence comparing tPA, streptokinase and another promising agent, acylated plasminogen-streptokinase activator complex, will be available in 1989-90.
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PMID:Guidelines for the use of intravenous thrombolytic agents in acute myocardial infarction. Ontario Medical Association Consensus Group on Thrombolytic Therapy. 249 46

Combined assessment of some parameters related to hemostasis and blood plasminogen-plasmin and kinin systems and their inhibitors was carried out in 150 patients with stable angina and postinfarction cardiosclerosis during rationed exercise (bicycle ergometry). Patients with low stress tolerance showed considerably activated kallikrein-kinin system, depressed total fibrinolytic activity, elevated trypsin and enhanced platelet adhesive properties, while their inhibitor activities were reduced. Postmyocardial infarction patients showed a more dramatic increase in free kinins, coupled with depressed inhibitor proteinases and kininase activities, and a slight increment in fibrinolytic activity, as compared to patients having to history of myocardial infarction. The magnitude of free kinins and trypsin rise and kininase fall increases with age in these patients.
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PMID:[Various indicators of hemostasis, plasminogen-plasmin and kinin systems of the blood and their inhibitors in patients with stable angina pectoris and post-infarction cardiosclerosis after graded physical load]. 295 50

Blood samples were taken for haemostatic analysis from 225 patients with angina pectoris who were admitted to hospital for coronary angiography. beta thromboglobulin, platelet factor 3, platelet factor 4, factor VII:C, factor VIII:C, von Willebrand factor antigen, activated partial thromboplastin time, fibrinogen, antithrombin III, protein C:Ag, plasminogen, and antiplasmin were measured before angiography. Patients who had had a myocardial infarction in the two months before the investigation were excluded from the study. Multiple linear regression analysis showed that none of the haemostatic variables contributed independently to the prediction of an angiographic score that indicated the extent of coronary atherosclerosis. History of myocardial infarction, male sex, worsening of angina pectoris, serum triglycerides, and ejection fraction were independently associated with the angiographic score. There were some significant correlations between haemostatic variables and conventional risk factors for coronary heart disease. Thus data obtained from haemostatic analyses of peripheral venous blood do not permit the presence or the extent of atherosclerosis in coronary arteries to be predicted.
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PMID:Lack of association between haemostatic variables and the presence or the extent of coronary atherosclerosis. 325 21

Acute myocardial infarction is caused by thrombotic occlusion of a coronary vessel. Mortality and quality of life are both determined by the extent of infarction. It is possible to interrupt the development of necrosis by early fibrinolytic therapy. If reperfusion is initiated within three to six hours, a significant reduction in mortality is likely. Currently available fibrin-unspecific plasminogen activators such as streptokinase and urokinase are effective thrombolytic agents but do not fulfill all the criteria of an ideal plasminogen activator. Recanalisation rates are relatively low after intravenous administration, since the agents are not fibrin-specific and because the effect is delayed. Serious hemorrhagic complications may occur, since therapeutically effective dosage results in a hemostatic defect. The possible advantages of reduction in blood viscosity for collateral circulation in the ischemic region and a possible antithrombotic effect have not been defined. A complex strategy is necessary for optimal treatment of acute myocardial infarction. Early intervention is decisive in regard to recanalisation rate, infarct size, left ventricular function and mortality, while delayed interventions serve to maintain the advantages of early recanalisation by limiting angina pectoris and preventing reinfarction. Therefore, a combination of early intravenous administration of a fibrinolytic agent with subsequent invasive intervention appears reasonable and advantageous. Progress in the treatment of acute myocardial infarction will depend on development of effective plasminogen activators capable of achieving rapid and complete recanalisation without major side effects after intravenous administration.
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PMID:[Results and limits of fibrin-unspecific thrombolysis in acute myocardial infarct]. 327 57

The fate of circulating inactive prorenin was examined in patients and volunteers. Prorenin was activated either by acid-dialysis with warming at pH 3.3 or with trypsin. The results were similar but omission of warming reduced the value by 13%. In 6 volunteers, 20 min forearm venous occlusion raised regional total (T) and inactive (I) plasma renin concentration (PRC) by 51% and 48% without change of active (A) renin. During intense forearm exercise the ratio APRC: IPRC did not change in muscle or skin venous blood. Body anaerobic exercise increased APRC 3.7-fold without change in IPRC. These procedures activate plasminogen but are without effect on prorenin. In 18 patient with stable angina, TPRC was lower in coronary sinus than arterial blood (p less than 0.001) but APRC was not affected. A-V differences were not detected across the leg. Prorenin is apparently stable in the circulation but extracted by the heart.
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PMID:Potential functions of plasma prorenin; regional activation and tissue extraction. 330 99

The paper presents an overview of the recent diagnostic and therapeutic feasibilities in acute coronary heart disease. In unstable angina the leading symptoms are new onset or increasing anginal pain or resting pain as well as ST-T-changes in the ecg without a rise in enzymes. Coronary arteriography shows double or triple vessel disease (70%), a left main stenosis (10 to 15%) or normal coronary arteries (10 to 15%). The treatment of unstable angina in the CCU consists of Nitroglycerin-infusion together with calcium channel blockers and/or betablockers. With this regimen, 80% of patients may be stabilized within 24 to 48 hours. Thereafter coronary arteriography is performed to settle the further therapeutic regimen (PTCA, CABG, medical therapy). Acute myocardial infarction is characterized by persisting (more than 30 min) pain, ST-T-changes in the ecg with or without development of Q-waves indicating irreversible myocardial damage. Angiographically, usually a subtotal or total occlusion of the corresponding artery is found. Aims of therapy in acute myocardial infarction is-besides treatment of complications like arrhythmias and left ventricular failure-reperfusion of the myocardium with reopening of the occluded vessels by intracoronary or systemic thrombolysis. Recently, also clot-specific streptokinase derivates and plasminogen activators are used with fewer bleeding complications. After recanalization of the vessel a persisting stenosis should be relieved either by PTCA or CABG to avoid reocclusion. However, these active forms of treatment can only be performed, if the patient reaches the hospital within 4 to 6 hours after the onset of ischemia.
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PMID:[Acute coronary heart disease. Current status of diagnostic and therapeutic possibilities in the intensive care station]. 372 2

The author report the case of a 48 years old patient, admitted to hospital 3 hours and a half after an anterior myocardial infarct which was well tolerated. Coronary recanalization with urokinase-plasminogen removed the obstruction of the middle part of the anterior interventricular artery 1 hour and a half after the patient's arrival. Selective left coronary angiography demonstrated a narrow stenosis, in the order of 98%, in the proximal part of the AIV artery. Angioplasty was attempted immediately, in view of the ease with which the guide wire was passed through the initial thrombosis and the good haemodynamic tolerance. The residual stenosis was estimated to be 20% after the angioplasty and at the examination 48 hours later. The ECG on discharge from hospital showed a QS appearance in V1 to V3 with R in V4. An improvement in the ejection fraction (EF) and in the end-diastolic volumes was found: EF: 48% compared to 38%, EDV (cc/m2): 79 compared to 120. The clinical course at two months is very satisfactory, with no residual angina and a negative stress test. This special procedure, combining a double therapeutic catheterization, lasted 1 hour 50 minutes and allowed the progression of the myocardial infarction to be halted and also avoided a subsequent aorto-coronary graft operation.
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PMID:[Coronary angioplasty immediately after coronary recanalization in the acute phase of myocardial infarct]. 622 68

The ECAT Angina Pectoris Study is a European multicentre study with the aim of investigating the pathogenetic and predictive role of haemostatic factors in the progression of coronary heart disease. It is the largest study performed up to now with regard to both the number of patients with angina pectoris (n = 3043) and the number of haemostasis assays (n = 23) included. The present paper presents baseline cross-sectional data with particular reference to the relationship of haemostatic factors with each other and with the coronary risk factors age, gender and acute-phase reaction (1). Two clusters of haemostatic factors could be distinguished in which each variable was correlated (P < 0.001) to every other variable: (a) Eight fibrinolysis assays including t-PA, PAI-1 and euglobulin clot lysis time (ECLT), for which PAI-1 appeared to be the dominating factor; (b) antithrombin III, protein C, alpha 2-antiplasmin and plasminogen, the interdependence of which has no obvious explanation. (2). Twelve out of the 23 haemostasis assays were associated (P < or = 0.01) with age. Except for alpha 2-antiplasmin, these relationships indicated an increased tendency to thrombosis with increasing age. (3). Gender differences found in 14 haemostasis parameters do not indicate a consistent difference in the tendency to thrombosis between men and women. Eight haemostasis parameters were on average higher in female than in male patients in the age group over 50 years. (4). C-reactive protein, an acute-phase reactant, was positively correlated (P < 0.001) with fibrinogen, factor VIIIc, von Willebrand factor, the fibrinolysis assays t-PA, PAI-1, ECLT and plasminogen.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Haemostasis factors in angina pectoris; relation to gender, age and acute-phase reaction. Results of the ECAT Angina Pectoris Study Group. 749 59


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