Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P00750 (PLA)
 16,800 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A blinded, randomized trial compared the effects of front-loaded streptokinase with those of the conventional dose of intravenous recombinant tissue-type plasminogen activator (rt-PA) on left ventricular (LV) function after acute myocardial infarction (AMI). Thrombolytic therapy was administered in the emergency departments of 30 community hospitals in central Illinois, and subsequent studies were performed at 1 tertiary referral center. Patients aged < or = 75 years with a first AMI who could be treated within 4 hours of the onset of chest pain were randomly assigned to receive either streptokinase (375,000 IU bolus, followed by 1,125,000 IU over 1 hour) or rt-PA (10 mg bolus, followed by 50 mg in the first hour, and 20 mg/hour for the next 2 hours). All patients were treated with aspirin (325 mg) and intravenous heparin. Patients were transferred for angiography within 24 hours. During the 30-month study, 253 patients were treated with intravenous thrombolytic therapy 2.4 +/- 1.0 hour after the onset of AMI. In patients with anterior wall AMI (n = 90), global LV ejection fraction measured by angiography within 24 hours was 45 +/- 12% with rt-PA, and 39 +/- 13% with streptokinase (p < 0.03). Convalescent radionuclide angiography documented a persistent beneficial effect of rt-PA on LV regional wall contractility, but not global ejection fraction. There were no differences between rt-PA and streptokinase in preserving global or regional LV function in patients with inferior wall AMI.
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PMID:A difference between front-loaded streptokinase and standard-dose recombinant tissue-type plasminogen activator in preserving left ventricular function after acute myocardial infarction (the Central Illinois Thrombolytic Therapy Study). 821 79

Patients who have chest pain occurring at rest are at a significant risk of myocardial infarction and or sudden death. Most trials enter patients with anginal rest pain after an initial screening period. Thus, the clinical efficacy of early thrombolytic treatment for patients with rest pain remains unproven. Eighty patients with chest pain at rest and with ECG changes of ST depression of at least 1 mm in any ECG lead, were randomized to alteplase 100 mg infused over 3 h, or placebo. Concomitantly, all patients received intravenous heparin and 300 mg of aspirin daily (unless contra-indicated). Seventy-four patients had coronary angiography (the majority within 72 h of admission) of which 73 were assessable. The patency of the ischaemia-related vessel was not significantly greater in the alteplase treated group (81% vs 78%, P = 0.82). The culprit lesion morphology tended to be more concentric in the alteplase treated group (84% vs 56%, P = 0.06) although alteplase treatment was not associated with a significant reduction in the severity of the culprit lesion stenosis. Intra-coronary thrombi were detected in 7% of patients (3% placebo, 11% alteplase, P = 0.35). The mean left ventricular ejection fraction or the alteplase-treated group was 49 +/- 3% and for the placebo-treated patients 56 +/- 3% (P = 0.05). There was no difference in the total in-hospital cardiac event rate i.e. cardiac death, myocardial infarction and coronary revascularization between patients receiving alteplase (10%, 63%, and 38%) and those receiving placebo (8%, 65%, and 30%) respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Double-blind randomized trial of alteplase versus placebo in patients with chest pain at rest. 829 37

We carried out a prospective survey of the outcome of patients with 'suspected myocardial infarction', in order to determine where they should be nursed. The delay between onset, admission, transfer to the CCU, the sequelae and side-effects of thrombolytic therapy were noted and were documented prospectively. Of 217 admissions to CCU with a history of chest pain and suspected acute myocardial infarction during a four-month period (mean age was 62.8 years range 31 to 86 years) 202 fulfilled the criteria for suspected myocardial infarction. Streptokinase was given in 129 and alteplase in one patient. The delay between onset of pain and admission was < 4 h in 73, 4 to 12 h in 30 and > 12 h in 23. Elderly patients were just as likely as younger ones to receive thrombolytic therapy (Chi 2 = 3.6; P = 0.6). An eventual diagnosis of acute myocardial infarction was made in 133 of whom 100 received streptokinase. Dysrhythmia or shock was encountered in one-third of those given streptokinase and a quarter of the remainder. Reactions to streptokinase were recorded in 32 mainly hypotension or bradycardia alone or in combination. Forty-five per cent experienced either cardiac complications or drug reactions or both. During one month there were 57 admissions, 50 of whom arrived by ambulance. The mean delay between call out and arrival in the A&E department was 55 min. We concluded patients who are given thrombolytic therapy need close supervision and they should be nursed in a CCU or its equivalent.
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PMID:Coronary care follow-up study: acute care required immediately following thrombolytic therapy. 831 24

We report the use of centrally administered tissue-type plasminogen activator for three patients who presented with massive pulmonary embolism to the emergency department. In all patients, rapid improvement of pulmonary arterial pressures ensued by the end of the drug infusion, while the presenting symptoms of chest pain and shortness of breath subsided.
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PMID:Treatment of massive pulmonary embolism with centrally administered tissue-type plasminogen activator. 833 42

We describe an autopsy case of severe intracranial hemorrhage which occurred during the infusion of tissue plasminogen activator (t-PA) for acute myocardial infarction. A 75-year-old man was admitted with substernal chest pain of 3-h duration and electrocardiographic changes consistent with an acute inferior myocardial infarction. Physical examination was unremarkable, except for an initial blood pressure reading of 160/96 mmHg. The patient received 3,000 IU intravenous heparin followed by a 2.4 x 10(6) IU bolus dose of tissue plasminogen activator (t-PA) (Alteplase). This was followed by a drip infusion of 21.6 x 10(6) IU of t-PA over 1 h (total dose 41 mg). Thirty minutes after the infusion of t-PA was initiated, the patient suddenly lost consciousness and began to have violent convulsions, followed by cardiac arrest. Autopsy revealed massive hemorrhage in the bilateral cerebrum and brain stem. To our knowledge, this is the first case of sudden death during t-PA infusion therapy.
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PMID:An autopsy case of intracranial hemorrhage during tissue plasminogen activator infusion. 840 27

Recurrent chest pain with new ST-segment elevation was observed in 26 of 652 patients (4%) with myocardial infarction in a clinical trial of alteplase (recombinant tissue-type plasminogen activator; 100 mg) and aspirin with or without heparin. Clinical and electrocardiographic signs of reocclusion were treated with a second dose of alteplase: 50 mg in 20 patients with signs of reocclusion < or = 24 hours after initial therapy, and 100 mg in 5 patients with signs between 24 and 77 hours, and in 1 patient with early signs of reocclusion. Pain and ST changes disappeared within 100 minutes (median 50). D-dimer determinations in 15 patients were increased, indicating activation of the coagulation system. Signs of reocclusion occurred despite adequate anticoagulation with heparin in 5 of 11 patients in whom coagulation measurements were available. No excess bleeding was observed in patients who received a second dose of alteplase. Retreatment with alteplase is feasible and provides an alternative for angioplasty in patients with clinical and electrocardiographic signs of reocclusion early after thrombolytic therapy.
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PMID:Retreatment with alteplase for early signs of reocclusion after thrombolysis. The European Cooperative Study Group. 843 37

To characterize the vasospastic angina patients with exercise-induced ischemia, we measured hemostasis (platelet factor 4; PF4, fibrinopeptide A; FPA) and fibrinolytic parameters (tissue plasminogen activator antigen; t-PA, free plasminogen activator inhibitor-1 antigen; free PAI-1) in 15 normal subjects and 33 vasospastic angina patients without significant coronary artery stenosis (less than 50% stenosis). All of the vasospastic angina patients began to feel chest pain within 3 months before diagnostic coronary angiography. Blood samples were obtained from all of the study patients at 8:30-9:30 am before exercise 201Tl emission computed tomography. Vasospastic angina patients were divided into 2 groups; 15 patients with exercise-induced ischemia (group 1) and 18 patients without exercise-induced ischemia (group 2). On coronary angiography, the severity of coronary artery stenosis at the site of spasm in group 1 (34 +/- 5%) was greater than that in group 2 (18 +/- 3%). Plasma FPA and PF 4 levels in group 1 were also significantly higher than those in normal subjects and group 2. Plasma t-PA and free PAI-1 levels in group 1 were significantly higher than those in normal subjects and group 2. Plasma levels of free PAI-1 group 2 were also significantly higher than those in normal subjects. The present study demonstrated that all of the patients with vasospastic angina had impaired fibrinolysis, and these patients with exercise-induced ischemia showed enhanced platelet activation, an enhanced coagulation system, and advanced atherosclerotic lesions. These results suggest that vasospastic angina with exercise-induced ischemia puts patients at increased risk for thrombus formation.
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PMID:Characteristics of vasospastic angina with exercised-induced ischemia--analysis of parameters of hemostasis and fibrinolysis. 880 21

This study assesses the effects of invasive procedures, hemostatic and clinical variables, and doses of recombinant tissue plasminogen activator (t-PA) on hemorrhagic events in the thrombolysis in myocardial ischemia (TIMI), phase 1B clinical trial (n = 1,425). Patients seen within 24 hours of the onset of ischemic chest pain at rest were randomized using a 2 x 2 factorial design for comparison of: (1) t-PA versus placebo as initial therapy, and (2) an early invasive (coronary arteriography with percutaneous angioplasty, if feasible) versus an early conservative strategy (coronary arteriography followed by revascularization if initial medical therapy failed). All patients received conventional medication for acute ischemic syndromes, including heparin, aspirin, beta blockers, nitrates, and calcium antagonists. The total dose of t-PA or placebo was 0.8 mg/kg, up to a maximum dose of 80 mg. In patients treated with t-PA, major and minor hemorrhagic events were more common than among those assigned to placebo (p < 0.001). Patients assigned to the invasive strategy arm had a higher hemorrhagic event rate than the noninvasive strategy, although the difference was not significant (p = 0.026). Patients > 75 years of age had higher intracranial hemorrhage rates than those < 75 years of age (6.7% vs 0.2%, respectively, p = 0.01). Major hemorrhagic events were more common in patients with higher heparin levels (p < 0.001), higher peak D-dimer levels (p = 0.007), and lower nadir fibrinogen levels (p = 0.005). Thus, increased morbidity due to hemorrhagic complications is associated with the use of t-PA, increased age, and selected hemostatic measures. Comparison to TIMI II demonstrates a significant association between the dose of t-PA and hemorrhagic complications.
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PMID:Hemorrhagic events during therapy with recombinant tissue plasminogen activator, heparin, and aspirin for unstable angina (Thrombolysis in Myocardial Ischemia, phase IIIB trial). 905 37

The use of outcome markers other than mortality reduction alone for evaluating thrombolytic agents in patients with acute myocardial infarction (AMI) is discussed. Mortality has been a primary endpoint in clinical trials evaluating thrombolytic agents for treatment of AMI. However, differences in mortality rates among thrombolytics are 1% or less and require tens of thousands of patients to detect. Broadening the endpoints studied will allow for more extensive data collection and more comprehensive cost-effectiveness analysis, enabling clinicians to make better decisions. The Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary Arteries (GUSTO-1) trial measured not only mortality but issues related to the patency of the infarct-related artery and complications. Other potentially important outcome markers after AMI are left ventricular function; markers of reperfusion, such as early resolution of ST-segment elevation; and resolution of chest pain. Available long-term data show that the mortality benefit from alteplase is sustained over time and is correlated with enzymatically determined infarct size, left ventricular function, the number of diseased vessels, and Thrombolysis in Myocardial Infarction flow grade at the time of discharge from the hospital. Clinicians must also consider risk factors for stroke. Outcome measures other than mortality alone may help in determining which thrombolytic agent is most effective clinically and in financial decision-making without requiring large, expensive trials.
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PMID:Clinical trials in thrombolytic therapy, Part 1: Outcome markers that go beyond mortality reduction. 939 34

There are several opinions asserting that the accelerated t-PA is more efficient than the standard protocol of streptokinase (SK) administration in acute myocardial infarction (AMI). One hundred patients admitted within the first 6 hrs after the onset of the symptoms revealing AMI were divided in two subgroups, as follows: subgroup A (50 patients) in whom a dose of 1.5 M.U. SK was infused in 20 min (accelerated protocol) and subgroup B (50 patients) in whom the same dose was infused in 60 min (standard protocol). In order to assess the efficiency of thrombolytic therapy (TT), we used three noninvasive criteria: the rapid resolution of the chest pain, the rapid decreasing of the ST segment elevation by more than 50% from the initial value, and the rapid increasing of enzymes revealing necrosis. Using the above-mentioned criteria, we considered that coronary reperfusion appeared in 40 patients from subgroup A (80%) and in 29 patients from subgroup B (58%). The speed of coronary reperfusion was 40 +/- 26 min in patients with accelerated SK and this time was significantly shorter than the time of 60 +/- 24 min registered in the control group. No major hemorrhagic events appeared in both subgroups. Although hypotension appeared more frequently in subgroup A, this minor complication was well supported by our patients. The rapid infusion of the standard dose of SK was followed by a higher rate and speed of coronary reperfusion as compared to the standard protocol.
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PMID:Rapid infusion of streptokinase standard dose in acute myocardial infarction is followed by a higher rate of coronary reperfusion than standard protocol. 956 52


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