Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0008031 (chest pain)
 17,248 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Streptokinase is well established as an effective thrombolytic. Anistreplase, a new thrombolytic drug, is a complex of streptokinase and acylated human plasminogen that can be administered by intravenous bolus and activates plasminogen at the clot site. Although both streptokinase and anistreplase are effected in treating myocardial infarction (MI), they have different pharmacologic properties. This study was designed to identify short- and long-term differences in their clinical effectiveness, safety in use, and survival rates in patients with acute MI. One hundred ten successive patients under seventy years of age admitted within three hours after onset of sustained chest pain suggestive of acute MI were randomized to receive either 30 units of anistreplase intravenously over five minutes or intravenous injection of 750,000 units of streptokinase over thirty to sixty minutes. Reperfusion was achieved in 34 of the 52 (65%) patients treated with anistreplase and in 41 of the 58 (71%) patients treated with streptokinase (p = NS). The two drugs were equally effective in preserving left ventricular ejection fraction, which was found to be significantly better in patients with anterior wall MI who had achieved reperfusion than it was in those who did not (p less than 0.02). One-month, twelve-month, and thirty-six-month survival rates were high (96% to 88%) with no significant difference between the two treatment groups. The authors conclude that the two drugs are equally effective thrombolytic agents but that anistreplase has the advantage that it can be administered as a bolus injection.
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PMID:Short- and long-term comparative study of anistreplase versus streptokinase in acute myocardial infarction. 162 35

Twenty-nine patients with acute myocardial infarction were given recombinant tissue plasminogen activator (tPA) within 6 hr after onset of chest pain (mean: 3.2 hr) with a total dose of 100mg iv drip given within 3hr for thrombolytic therapy. Serial determinations of total FDP, FDP D-Dimer (specific for FbDP), fibrinogen (Fg), PT, APTT, reptilase time (RT), plasminogen, alpha 2-antiplasmin (AAP), euglobulin lysis time (ELT) and antithrombin III (ATIII) were performed before and 1, 2, 4, 6, 12, 24, 48 hr after initiation of tPA injection in the 29 patients in order to evaluate the hemostatic changes after thrombolytic therapy. Decreases of plasminogen, Fg, AAP & ELT were found from 1 hr after therapy and persisted to 24, 12, 24 & 12 hr, respectively, with the maximum decrease usually between 1-4 hr. Increases of FDP, FDP D-dimer, PT, APTT & RT were found from 1, 1, 2, 1 & 1 hr after therapy, respectively, and sustained to 24, 12, 12, 24 & 12 hr, respectively, with maximum increases between 1-4 hr. No significant changes of ATIII were noted during the 48-hr study-period. 4 of these 29 patients (13.79%) had the complication of localized bleeding, 1 of them needed 1 unit of packed red blood cell transfusion. All thrombolysis-related changes recovered within 24 hr after tPA therapy. No parameter we have studied so far could be used for the prediction of the possibility of coronary patency after tPA therapy. But markedly elevated FDP was found to be associated with high risk of bleeding complication. As the coagulation changes persist for 24 hr or longer, careful monitoring of the coagulation tests and close observation of clinical bleeding signs up to 48 hr are necessary in patients treated with tPA.
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PMID:Serial thrombolysis-related changes after thrombolytic therapy with TPA in patients with acute myocardial infarction. 169 93

Unstable angina is a clinical syndrome of recurrent myocardial ischemia. In some cases, this reflects episodic platelet activation and coronary thrombosis. Thus, the biosynthesis of thromboxane A2, which is largely derived from activated platelets, is increased, often coincident with chest pain. The major role of platelets in unstable angina may influence the response to plasminogen activators. Platelets increase the resistance of thrombi to lysis, by inducing clot retraction and cross-linking and by releasing inhibitors. Thus, coronary thrombi in unstable angina may be resistant to lysis. Furthermore, both t-PA and streptokinase cause platelet activation and thrombin formation in vivo, possibly via plasmin. Plasmin can activate platelets and factor V directly. These prothrombotic effects of plasminogen activators may limit their activity in unstable angina. At the very least, their therapeutic efficacy may be highly dependent on the coadministration of potent antiplatelet agents and anticoagulants.
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PMID:Platelet activation in the pathogenesis of unstable angina: importance in determining the response to plasminogen activators. 189 67

The percentage of patients with acute myocardial infarction (AMI) who were eligible for thrombolytic therapy was evaluated prospectively, with analysis of the causes for exclusion, in 857 patients with AMI hospitalized in the Chaim Sheba Medical Center, Tel-Hashomer, in 1988. Thrombolytic therapy was given to 127 patients (14.8%); 99 patients were treated with tissue plasminogen activating factor and 28 patients received streptokinase. Three hundred and sixty patients (42.0%) were rejected because of age (greater than 72 years). Other reasons for exclusion were duration of pain lasting for more than 4 h (28.5%), unknown time of onset of the chest pain (9.7%), absence of ST elevation on admission ECG (8.1%), systemic hypertension (4.4%), and presence of severe congestive heart failure upon admission (10.1%). Restricting thrombolytic therapy only to patients less than 72 years old with chest pain duration of 4 h limits the impact of this treatment on the general welfare of patients with AMI. By raising the age limit and extending the time interval between pain onset and treatment initiation, adding newer indications, and enhancing public awareness for early arrival to hospital, the benefit of thrombolytic therapy may be made available to more patients with AMI.
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PMID:Incidence of and reasons for excluding patients with acute myocardial infarction from thrombolytic therapy. 190 38

The European Multicentre Study (EMS) assessed coronary reperfusion, functional outcome and safety of anistreplase (anisoylated plasminogen streptokinase activator complex = APSAC) compared to a control group treated with heparin alone in patients with a clinical diagnosis of acute myocardial infarction (AMI). In the Belgian subset of data (n = 103) the reperfusion results, based on non-invasive clinical parameters, were significantly better in the APSAC group: 66% versus 18% in the heparin group (P less than 0.0001). No significant difference was found between the two treatment groups with respect to left ventricular function and adverse events. The purpose of the present study was to analyse the indicative value of ST-segment changes as a possible predictor of reperfusion in threatened myocardial tissue. Two scoring systems were used: the first was based on the combined evaluation of three clinical non-invasive parameters (course of chest pain, ECG evaluation of ST segment changes, reperfusion arrhythmias); the second was based on the changes of the sum of the ST-segment (sigma-ST) evaluations on consecutive 12-lead ECGs. There was a good correlation between the combined clinical scoring system and the residual stenosis on coronary angiography (P less than 0.05) and early CK peak (P less than 0.0001). Analysis of the ECG data revealed that a decrease of greater than or equal to 50% of the sum of ST-elevations (sigma-ST) at 2 h post-treatment in both limb and precordial leads is a fairly useful predictor of reperfusion (sensitivity = 73%, specificity = 63%, predictive value = 88%).
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PMID:ST-segment analysis: a useful marker for reperfusion after thrombolysis with APSAC? The Belgian EMS Study Group. 204 Mar 18

Recombinant tissue-type plasminogen activator (rt-PA), streptokinase (SK), and anisoylated plasminogen-streptokinase activator complex (APSAC) have salutary effects on mortality when administered to patients with evolving acute myocardial infarction (MI). Studies suggest that intravenous rt-PA is more effective in reperfusing occluded infarct-related arteries than SK, and the results of ongoing studies directly comparing the influence of SK and rt-PA on mortality are awaited. The clinical role of agents such as APSAC, urokinase, and pro-urokinase, used alone or in combination, remains to be determined. It is evident that a variety of thrombolytic agents will be effective, and variables such as ease of administration, pharmacokinetics, fibrin specificity, effects on blood viscosity, and incidence of adverse effects need to be assessed to determine which agents are the most suitable for clinical use. There is an increased risk of bleeding at vascular puncture sites with all thrombolytic agents. Current indications for thrombolytic therapy include ischemic chest pain of at least 30 min duration that is unrelieved by nitroglycerin and is associated with ST-segment elevations of at least 0.1 mV in two contiguous electrocardiographic leads. Such therapy is usually reserved for patients less than 75 years old who are not at increased risk for bleeding and whose chest pain began less than 4-6 prior to treatment. Trials are under way to determine whether patients with shorter pain duration, transient ST-segment changes (ie, unstable angina patients), chest pain associated with ST-segment depressions or T-wave inversions (ie, non-Q-wave infarction patients), or patients whose pain began more than 4 to 6 h earlier will benefit from early thrombolytic therapy. Other factors such as patient age, the likelihood of the diagnosis of MI, and the estimated risk of bleeding should also be considered. The findings of available major randomized trials indicate that early invasive procedures are generally unnecessary and that meticulous care must be exercised in the selection and management of patients subjected to thrombolytic therapy.
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PMID:Thrombolytic therapy in acute myocardial infarction. 210 51

Thrombolytic agents administered intravenously have been shown to have a salutary effect in the early management of acute myocardial infarction. However, a debate still is pending over the definite choice of an ideal thrombolytic agent. In our 83-bed community hospital, from January 1986 to September 1988, we treated 19 patients (n = 19) with acute myocardial infarction (average one patient every six weeks) with either intravenous streptokinase (IV STK) or intravenous tissue plasminogen (IV TPA) with a mean follow-up of 20.2 months. We compared both groups in terms of clinical reperfusion, morbidity and mortality, cost-effectiveness and long-term functional disability. Our results showed that most patients received their respective agents within four hours of the onset of chest pain (81% in the STK group, n = 11, versus 75% of the tPA group, n = 8). In the STK group, 90.9% showed clinical evidence of reperfusion compared to 87.5% in the TPA one, the difference not being statistically significant. Two patients in the STK group developed a treatable bradycardia, and one showed a junctional rhythm that was corrected. One patient in the TPA subset encountered a reversible ventricular tachycardia. However, we didn't note any bleeding complication in either group.
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PMID:Thrombolytic therapy in acute coronary thrombosis. 211 80

All thrombolytic agents convert plasminogen to plasmin, either directly, as in the case of urokinase, saruplase, and alteplase, or indirectly, as in the case of streptokinase. In the majority of recent clinical trials with streptokinase, a high-dose (0.7-1.5 million units), brief-duration (30-90 minutes) drug regimen has been used. After a mean interval of 4.2 hours from onset of chest pain to intravenous infusion of streptokinase, repeat angiography performed 60-90 minutes after the start of thrombolytic treatment gave a reperfusion rate of 43%; the corresponding figures for anistreplase, saruplase, and alteplase are 56%, 67%, and 69%. The patency rates obtained in similar studies with the same end point are 56% for streptokinase, 77% for anistreplase, 62% for urokinase, 71% for saruplase, and 75% for alteplase. The in-hospital mortality in randomized trials (six large studies in a total of 31,713 randomized patients) with intravenous high-dose streptokinase decreased from 12.0% in the control group to 9.47% in the streptokinase group. In a mortality study involving 1,258 patients randomized to intravenous anistreplase or placebo, the 30-day mortality was reduced by 47%, from 12.2% to 6.4%. In a large trial in which 5,011 patients were randomized to alteplase or placebo, the 30-day mortality was 7.2% compared with 9.8% in controls, a reduction of 27% by alteplase. In another trial, 721 patients were randomized to placebo or alteplase; all patients received acetylsalicylic acid and intravenous heparin. The 14-day mortality was only 2.8% in the alteplase group, 51% less than that in the control group. It is most important that the favorable impact on hospital survival be maintained at 1 year for any thrombolytic drug. Large-scale trials directly comparing mortality after alteplase, streptokinase, or anistreplase are being performed or are in the planning phase. The risk of bleeding exists with any thrombolytic agent; intracranial bleeding is the most serious risk. In a large trial in 5,011 patients with acute myocardial infarction, stroke occurred in 1.1% of alteplase-treated patients compared with 1.0% in placebo-treated controls. Haunting problems are residual stenosis of the coronary artery and reocclusion. Urgent angioplasty does not seem to be the right answer; more effective antithrombotic strategies have yet to be developed.
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PMID:Thrombolytic treatment in acute myocardial infarction. 211 32

In the anistreplase, or anisoylated plasminogen streptokinase activator complex (APSAC) Intervention Mortality Study (AIMS), 1,258 patients with acute myocardial infarction were randomized in a parallel, double-blind, placebo-controlled mortality study in which they received either anistreplase or placebo, followed by anticoagulation therapy. Data on all adverse clinical events were recorded, regardless of their clinical significance or possible relation to therapy. There was a similar frequency of such events in both groups (anistreplase 80.4%, placebo 76.0%, difference not significant). Cardiovascular events included more reports of bradycardia, idioventricular rhythm, and hypotension in the anistreplase group, and a higher incidence of cardiac arrest, ventricular fibrillation, complete heart block, and pericarditis in the placebo group. Hemorrhagic events occurred in 13.8% of patients in the anistreplase group compared with 4.1% of patients in the placebo group. Most of these events consisted of bleeding or bruising around the puncture sites. There was a low incidence of allergic events after administration of both anistreplase and placebo. Thirteen cerebrovascular events (8 strokes and 5 transient ischemic episodes) were reported in the anistreplase group, compared with 5 in the placebo group (5 and 0, respectively). The mean systolic and diastolic pressures were significantly lower (by 5-10 mmHg) in patients in the anistreplase group during the first 24 hours after dosing. There were no significant differences in temperature and pulse rate between the two groups. The incidence of chest pain during the first 4- to 24-h period was lower in the anistreplase-treated patients than in the placebo group. The frequency of in-hospital reinfarction was higher in anistreplase-treated patients compared with patients given placebo.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The safety of anistreplase from the placebo-controlled AIMS study (anistreplase Intervention Mortality Study). The AIMS Study Group. 218 37

Twenty-two patients were infused with 240,000 units streptokinase during a 60-minute period into the ostium of the infarct-related coronary artery (IC), and 23 patients were infused with 1,500,000 units streptokinase intravenously (IV) over 45 minutes; all infusions occurred within 12 hours of the patients' onset of chest pain. Thereafter, heparin was infused for 10 days. Serial coagulation and fibrinolytic parameters were studied over 46 to 72 hours after the streptokinase infusion. A generalized fibrinolytic state was produced in both groups as evidenced by a fall in fibrinogen and plasminogen levels, prolongation of thrombin and reptilase clotting times, a rise in fibrinogen degradation products, and a shortening of the euglobulin lysis time. Recovery to preinfusion levels was similar in both groups of patients. Hemorrhagic complications requiring blood replacement occurred in 7/23 (30%) treated IC, and 4/23 (17%) in the IV group.
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PMID:Coagulation and fibrinolytic changes in evolving acute myocardial infarction treated by high-dose, brief-duration intracoronary or intravenous streptokinase. 230 Dec 85


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