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

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

Blood coagulation and fibrinolysis were studied at rest and during bicycle ergometry in 45 patients with angina of new onset (ANO). Fourteen chronic coronary patients and 20 subjects, free of coronary heart disease or coronary atherosclerosis, were taken as controls. Fibrinolysis tended to be depressed in resting ANO patients. Potential fibrinolysis depended on the clinical pattern of the disease and was particularly depressed in patients with severe ANO. Stress did not activate fibrinolysis in patients with vasospastic angina and high basal plasminogen activator level at rest.
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PMID:[Initial-onset stenocardia: characteristics of the blood coagulation system and fibrinolysis as reaction to physical exertion]. 341 63

Early postinfarction angina implies an unfavorable prognosis. Most published information on this outcome represents data collected in the prethrombolytic era, in which definitions and populations differed considerably. Our purpose was to evaluate the incidence and importance of recurrent ischemia after administration of thrombolytic therapy. We studied patients enrolled in the Thrombolysis and Angioplasty in Myocardial Infarction studies. Patients were enrolled into 5 studies with similar entry criteria; 552 patients were treated with tissue plasminogen activator (t-PA), 293 were treated with urokinase, and 385 received both thrombolytic agents. Recurrent ischemia was defined as symptoms in association with electrocardiographic changes; reinfarction was defined as a reelevation of creatine kinase myocardial band isoenzyme in an appropriate clinical setting. Both recurrent ischemia and reinfarction occurred in 42 patients (3.4%), recurrent ischemia alone occurred in 226 (18%), whereas neither occurred in 964 (78%). Although baseline characteristics were similar among the 3 groups, in-hospital cardiac events (total 73 deaths, 253 heart failure episodes) were not: in-hospital mortality in patients with reinfarction was 21%; with recurrent ischemia, 11%; and with neither event, 4% (p < 0.0001). The in-hospital heart failure rate of patients with reinfarction was 50%; with recurrent ischemia alone, 31%; and with neither event, 17% (p < 0.0001). As expected, median in-hospital costs were highest in patients with reinfarction ($26,802), intermediate for those with recurrent ischemia alone ($18,422), and lowest in patients with neither event ($15,623). Recurrent myocardial ischemia after thrombolytic therapy is a frequent, important, and expensive adverse clinical outcome, making it a critical target for therapeutic intervention.
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PMID:Frequency, significance, and cost of recurrent ischemia after thrombolytic therapy for acute myocardial infarction. TAMI Study Group. 748 52

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

Among endothelial secretogogues prostacyclin (PGI2), nitric oxide (NO) and tissue plasminogen activator (t-PA) play a crucial role in maintaining thromboresistance, tone and structure of the vascular wall. Most receptor agonists, such as B2 kinin receptor agonists, or shear force produce a coupled release of all three secretogogues, and therefore interactions between them are to be expected. Essentially, PGI2 is a platelet suppressant, NO a vasodilator and t-PA a fibrinolytic agent. These and other properties of endothelial secretogogues supplement each other in protecting the cardiovascular system from injuries. It is not surprising that disturbances of the secretory function of endothelial cells are associated with atherosclerosis, diabetes, thrombosis or hypertension. Traditionally, PGI2, NO, t-PA or their substitutes are used individually for the treatment of peripheral arterial disease, angina pectoris or acute myocardial infarction. In light of recent findings, their joint administration can be advocated. For instance, NO donors will potentiate platelet-suppressant action of PGI2 analogues, whereas exogenous PGI2 or TXA2 synthase inhibitors (i.e. following increase in endogenous PGI2) will abolish a paradox of prothrombotic action of t-PA or streptokinase. The replacement therapy with PGI2, NO or t-PA should match as closely as possible the physiologically coupled release of these secretogogues.
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PMID:Interactions between endothelial secretogogues. 754 32

Among patients with recent-onset unstable angina and evidence of ischemia or coronary artery disease, the incidence of subsequent cardiovascular events is high. The aim of this study was to investigate, in this high-risk population, whether unstable angina was associated with abnormalities of tissue-type plasminogen activator (t-PA) or plasminogen activator inhibitor (PAI) activities and whether, in a prospective study, any of these parameters would identify patients with an adverse cardiovascular prognosis. A group of 22 high-risk patients with unstable angina (64% event rate at 3 months) was studied prospectively for 12 weeks, and the fibrinolytic parameters measured at presentation were related to subsequent cardiovascular progress. A group of 20 age- and sex-matched healthy subjects acted as control subjects. Patients who had subsequent cardiovascular events (acute myocardial infarction or severe recurrent angina +/- intervention) had significantly elevated PAI activity at presentation compared with both those who remained event-free (p < 0.05) or with control subjects (p < 0.02). In addition, basal activation of fibrinolysis was demonstrated in unstable angina at presentation; this persisted at 9 weeks in patients with a favorable outcome (p < 0.02 vs control subjects), whereas it was no longer evident in those who developed cardiac events. These findings suggest that measurements of t-PA/PAI activity may reflect the underlying pathophysiologic state and relate to subsequent cardiovascular events in unstable angina.
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PMID:Tissue-type plasminogen activator and plasminogen activator inhibitor activities as predictors of adverse events in unstable angina. 805 19

Intracoronary thrombus formation has been thought to play an important role in the genesis of acute myocardial infarction an unstable angina. To examine whether the coagulation and fibrinolytic systems are altered in such ischemic heart diseases, the plasma levels of fibrinopeptide A (FPA) and plasminogen activator (PAI) were measured. The plasma level of FPA was increased in patients with variant angina as compared with those with stable exertional angina and there was a significant circadian variation in the plasma level of FPA in parallel with that of the frequency of the attacks with the peak level occurring from midnight to early morning in patients with variant angina. The plasma FPA level increased in patients with coronary spastic angina after the ischemic attack induced by hyperventilation. Furthermore, FPA was released into the coronary circulation after the anginal attack induced by intracoronary injection of acetylcholine. These findings suggest that the coronary artery spasm may induce thrombin generation and trigger thrombus formation in the coronary artery. On the other hand, the plasma level of PAI activity was higher in patients with unstable angina and coronary spastic angina than in those with stable exertional angina. Moreover, the PAI activity in patients with unstable angina decreased to the level in patients with stable exertional angina after the stabilization of their symptoms by drugs. Our findings suggest that the increased plasma PAI activity may reduce fibrinolytic activity and attenuate removal of the thrombus and may ultimately lead to acute myocardial infarction in some patients with unstable angina and coronary spastic angina.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Blood coagulation and fibrinolysis in ischemic heart disease]. 810 82

To examine whether ischemic attack induced by coronary spasm changes fibrinolytic activity, we examined plasma levels of tissue-plasminogen activator antigen and plasminogen activator inhibitor activity before and after hyperventilation test in patients with variant angina and in control subjects. In 12 patients with variant angina, ischemic attack associated with ST-segment elevation on the electrocardiogram was induced by hyperventilation and plasma plasminogen activator inhibitor activity levels increased significantly 15 min after the attacks (pre, 5.1 +/- 0.8; immediately after, 5.8 +/- 1.1; and 15 min after, 7.2 +/- 0.9 IU/ml, P < 0.01). In 12 control subjects, plasminogen activator inhibitor activity levels did not change. Plasma tissue-plasminogen activator antigen levels did not change in both two groups. We conclude that coronary artery spasm increases plasma plasminogen activator inhibitor activity and that it may thereby lead to the coronary thrombus formation.
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PMID:Increased plasma plasminogen activator inhibitor activity after coronary spasm. 822 69

In our study, we measured resting tissue-type plasminogen activator(t-PA) activity and resting plasminogen activator inhibitor-1 (PAI-1) activity in 15 healthy men and in 20 patients (male) with coronary heart disease in the morning and evening. Resting t-PA activity was lower (P < 0.05) in controls and was significantly lower (P < 0.001) in patients in the morning compared with that in the evening. In contrast, PAI-1 activity was significantly higher (P < 0.001) in controls and was also significantly higher (P < 0.001) in patients in the morning compared with that in the evening. t-PA activity in patients compared with that in controls was significantly lower (P < 0.05) in the morning and the evening; PAI-1 activity in patients compared with that in controls was significantly higher (P < 0.001) in the morning and the evening. However, t-PA activity was significantly lower (P < 0.05) and PAI-1 activity was significantly higher (P < 0.05) in patients with myocardial infarction compared with anginal patients in the morning. Applying this clinical phenomenon that myocardial infarction and angina have often occurred in the morning, the relationship between time of onset of myocardial infarction and circadian variation of t-PA and PAI-1 was discussed.
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PMID:[A study on the circadian variation of tissue-type plasminogen activator and its rapid inhibitor in patients with coronary heart disease]. 824 32

Fluctuations in tissue plasminogen activator (t-PA) activity, t-PA antigen, and plasminogen activator inhibitor-I (PAI-1) antigen levels were evaluated in blood samples obtained from 84 patients with initial uneventful acute myocardial infarction (AMI) and 35 patients with reinfarction and fatal infarction (patients with bad prognoses). Patients with initial AMI had significantly higher levels of t-PA activity than those of 14 patients with angina pectoris. Tissue plasminogen activator activity peaked between day 7 and 19 after the initial attack of AMI. Plasminogen activator inhibitor-I antigen level decreased significantly between day 2 and 19, then returned to the baseline levels of patients with angina pectoris nearly 4 weeks later. The t-PA activity levels of patients with reinfarction were significantly lower than those in patients without events between day 0 and 3 and between day 7 and 19. The percentage stenosis in the coronary arteries measured by coronary angiography was negatively correlated with t-PA activity. This information may help in selecting aggressive treatments such as thrombolysis by recombinant t-PA and predicting the prognosis for patients with AMI.
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PMID:Evaluation of tissue plasminogen activator and plasminogen activator inhibitor-I levels in acute myocardial infarction. 864 3


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