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Query: UNIPROT:P00750 (PLA)
 16,800 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The blood content of soluble fibrin and D and E fibrinogen fragments, the protamine sulfate test and the activity of plasmin and plasminogen activator were studied in patients with macrofocal myocardial infarction. It was established that the content of soluble fibrin in blood considerably increases in the first days of the disease, and the level of products of fibrinogen D and E disintegrationand the value of the protamine sulfate test increase in the 2nd--3rd week of the disease. The appearance in the blood of fibrinogen derivates was attended by low activity of plasmin and plasminogen activator in blood. The highest content of fibrinogen derivates and low activity of plasmin and plasminogen activator were noted in patients with arrhythmias and congestive circulatory insufficiency. It is suggested that the appearance in circulation of high-molecular fibrinogen compounds is important in the development of rheological disorders.
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PMID:[Content of fibrinogen degradation products, soluble fibrin and the fibrinolytic activity of blood in myocardial infarct]. 49 64

Plasma von Willebrand factor, plasminogen activator inhibitor activity and C-reactive protein were assessed as markers of coronary recanalisation in 30 patients with acute myocardial infarction receiving tissue-type plasminogen activator (t-PA). Blood samples were taken before t-PA (time 0), 4-hourly for 24 h and daily up to 72 h. A continuous electrocardiogram was recorded in the first 24 h. Coronary arteriography was performed 90 min and 24 h after the start of t-PA. Patients with a patent infarct artery (n = 17), compared to those with occluded artery (n = 13), showed a fall in von Willebrand factor from 0 to 24 h (p = 0.001), a greater fall in plasminogen activator inhibitor from 24 to 48 h (p = 0.04) and a fall in C-reactive protein from 48 to 72 h (p = 0.002). The accuracy of these indices compared favourably with time to peak plasma MB creatine kinase and > or = 50% resolution of maximal ST-deviation on the electrocardiogram. Thus, changes in plasma von Willebrand factor, plasminogen activator inhibitor and C-reactive protein during the first 3 days of myocardial infarction are indicative of thrombolytic efficacy. Their concordant behaviour may reflect a common regulatory mechanism.
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PMID:Von Willebrand factor, plasminogen activator inhibitor-1 and C-reactive protein are markers of thrombolytic efficacy in acute myocardial infarction. 128 82

This 6-month follow-up of the patients recruited into the GISSI-2 Study and the International Study substantially confirmed the in-hospital results. The aim was to compare the effectiveness and safety of alteplase (tPA) and streptokinase (SK), and of heparin and no heparin, in patients with acute myocardial infarction in an open multicentre randomized trial with a 2 x 2 factorial study design. Six-months' mortality rates were similar for patients randomized to tPA or SK (12.3% vs 11.7%, RR = 1.06, 95% CI 0.97-1.15) and for patients randomized to heparin or no heparin (11.9% vs 12.1%, RR = 0.98, 95% CI 0.90-1.07). Mortality rates were also similar between randomized treatments in the pre-defined subgroups: sex, age above and below 70 years, with and without previous myocardial infarction, Killip class at entry and randomization within 3 h or between 3 and 6 h from onset of symptoms. Reinfarction and cerebrovascular accidents were similar in all treatment groups. Adjusted analysis (Cox model) indicated that age and higher Killip class were the most important predictors of a poor prognosis. Previous myocardial infarction, female sex and longer delay from onset of symptoms were also indicators. Patients treated with SK plus heparin have a statistically significant better survival than the others, although the statistical significance of the remaining absolute difference disappears once the substantial proportion of patients dying in the first 12 h is excluded, when, by design, no heparin was given.
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PMID:Six-month survival in 20,891 patients with acute myocardial infarction randomized between alteplase and streptokinase with or without heparin. GISSI-2 and International Study Group. Gruppo Italiano per lo Studio della Sopravvivenza nell'Infarto. 128 1

A hundred and eighty three patients with a primary myocardial infarction less than 4 hours old were included in a double blind trial versus placebo comparing an isolated plasminogen streptokinase activator complex (APSAC: 30 mu in 5 mn) and tissue type plasminogen activator (rt PA: 10 mg bolus followed by 90 mg in 130 mn). Clinical evolution, side effects, patency of the artery responsible for infarction, left ventricular contractile function (contrast angiography on the 7th day and angioscintigraphy on the 21st day) and infarct size were studied. The two groups were comparable in age (54 +/- 11 years), delay in randomisation (170 +/- 50 mn), infarct site and severity of cardiac failure. There was no significant difference in hospital mortality (7 in the rt PA group and 5 in the APSAC group) or in adverse effects (haemorrhage: rt PA: 9 patients, APSAC: 11 patients). The patency was 72% in the APSAC and 76% in the rt PA group. Left ventricular function and infarct size were comparable in the two groups: angiographic EF (0.50 +/- 0.1 in the APSAC and 0.52 +/- 0.1 in the rt PA group: NS); asynergic score (11.3 +/- 1.7 in the APSAC and 10.5 +/- 1.8 in the rt PA group: NS); infarct size (10.9 +/- 8.0 in the APSAC and 9.4 +/- 7.2 in the rt PA group: NS). This trial shows that these two thrombolytic agents have the same efficacy. The authors recommend adaptation of the dosage of rt PA to body weight.
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PMID:[Study of new thrombolytic agents in myocardial infarction: a multicenter randomized trial (APSAC versus rt-PA)]. 130 Sep 57

Thrombolysis during the early hours of a myocardial infarction significantly improves patient survival in a hospital. Beyond 6 hours, up to 24 hours, thrombolysis may still contribute to a reduction in mortality. However, further confirmation is desirable before such therapy late in the course of an evolving infarct can be routinely recommended. Although clot-specific agents such as recombinant tissue-type plasminogen activator (rt-PA) produce a higher initial patency rate, reocclusion rates are higher in the absence of the profound systemic fibrinolysis produced by agents such as streptokinase. This may explain the GISSI-2 results where 15-day survival was no different between the streptokinase- and rt-PA-treated subjects. Although the manner of heparin administration may have clouded these results, current research is directed toward looking at combinations of thrombolytic agents that would combine drugs efficient in producing early patency with those that produce a more pronounced fibrinolytic state. More effective adjunctive therapy is also under intense investigation, particularly specific antithrombin agents that would produce more effective anticoagulation following thrombolysis, and more effective antiplatelet agents that would help prevent reocclusion.
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PMID:Thrombolytic therapy for myocardial ischemia and infarction. 134 5

While it is no longer possible to imagine the treatment of an acute transmural myocardial infarction without the use of thrombolytic agents, some discussion still exists as to the choice of the thrombolytic agent. Our study concerns a group of 160 patients with an acute transmural myocardial infarction, 60 of whom were treated with anistreplase, 52 with streptokinase and 48 with alteplase. Statistically, the administration of anistreplase was associated with a significantly higher frequency of ventricular arrhythmias in comparison to the other thrombolytic agents, whereas after subsequent coronary angiography, the anistreplase group revealed a significantly lower number of completely occluded coronary arteries. The data from this study demonstrate that anistreplase is a very valuable thrombolytic agent. It may even be more effective than streptokinase and alteplase in the treatment of acute myocardial infarction when the patency of the coronary arteries 1 month after the acute coronary event is considered the primary endpoint.
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PMID:Are the various thrombolytic agents equally effective in the treatment of acute transmural myocardial infarction? 145 46

Two hundred five men, 40 to 70 years of age, admitted to the coronary care unit with unstable coronary artery disease (unstable angina or non-Q wave myocardial infarction), were randomized to double-blind placebo-controlled treatment with an intravenous infusion of recombinant tissue-type plasminogen activator (rTPA), 1 mg/kg body weight (maximum 100 mg) during 4 hours, in addition to aspirin, heparin, and beta-blockade. No severe complications occurred. Myocardial ischemia, defined as myocardial infarction, incapacitating angina despite medication, or signs of ischemia at the exercise test, was reduced by treatment with rTPA compared with placebo both at discharge, 53% compared with 70% (p = 0.02), and at 1 month, 61% compared with 80% (p = 0.005). Signs of myocardial ischemia during the exercise test were reduced at discharge 51.0% compared with 68% (p = 0.03) and at 1 month 48% compared with 62% (p = 0.09). Coronary angiography after 1 month showed no difference in major coronary lesions between the groups, nor was there any reduction in the number of performed coronary revascularization procedures. In conclusion, treatment with rTPA in unstable coronary artery disease in men reduced myocardial ischemia but did not significantly reduce the need for revascularization in long-term follow-up.
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PMID:Thrombolysis with recombinant human tissue-type plasminogen activator during instability in coronary artery disease: effect on myocardial ischemia and need for coronary revascularization. TRIC Study Group. 146 94

To assess the relationship between the fibrinolytic system and coronary risk factors, several fibrinolytic parameters were measured in 72 male survivors of myocardial infarction and in 53 age-matched healthy controls. The coronary patients had significantly higher plasminogen activator inhibitor (PAI) activity than the control subjects, while t-PA antigen did not differ between the groups. After stratifying the coronary patients in 14 diabetic and 58 nondiabetic patients, the elevated PAI activity remained limited to the diabetic group. PAI activity correlated significantly with systolic blood pressure, blood glucose, body mass index and LDL cholesterol. In multivariate regression analysis, significant associations persisted between PAI and diabetes, body mass index and LDL cholesterol. Coronary disease had no impact on the regression model. Our results suggest that the increased PAI-1 in selected groups of coronary patients is not a consequence of coronary disease itself, but is rather related to the metabolic risk factors of atherosclerosis, especially diabetes.
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PMID:Increased plasminogen activator inhibitor activity in survivors of myocardial infarction is associated with metabolic risk factors of atherosclerosis. 146 21

Of a total of 329 consecutive patients treated by thrombolysis with recombinant tissue-type plasminogen activator following myocardial infarction, 13 (4%) were in cardiogenic shock at the time of admission to hospital, and 4 others (1.2%) developed cardiogenic shock during their hospital stay. Overall hospital mortality for shock was high at 88% (15 of 17 patients), and shock was responsible for 57.6% (15 of 26) of all hospital deaths. Although several studies have shown that thrombolysis reduces the likelihood of cardiogenic shock developing after admission, our data confirm that it does not constitute effective treatment of established shock. More aggressive approaches, using thrombolysis together with angioplasty and mechanical ventricular assist devices, need to be evaluated.
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PMID:[Role of thrombolysis in the treatment of cardiogenic shock following myocardial infarct]. 149 39

We measured levels of tissue plasminogen activator (t-PA) antigen in 100 patients within six hours of the onset of acute myocardial infarction, in 34 patients with chronic angina but no recent infarction, and in 36 normal subjects. We also assayed von Willebrand factor in the acute patients and in the normal subjects. Measurements were repeated in 40 acute patients at three weeks after myocardial infarction. Although resting levels of t-PA antigen were not significantly different from normal during myocardial infarction, the capacity of the vascular endothelium to release t-PA after five minutes of venous occlusion was impaired (p less than 0.01). The acute phase vessel wall release of von Willebrand factor was increased during acute infarction (p less than 0.01). We conclude that impairment of t-PA production is associated with acute coronary thrombosis, although it is not possible to differentiate between a causative role or a secondary response due to exhaustion of the t-PA producing mechanism.
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PMID:Reduced synthesis of tissue plasminogen activator by vascular endothelium during acute myocardial infarction. 149 53


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