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PubMed1990

The safety of anistreplase from the placebo-controlled AIMS study (anistreplase Intervention Mortality Study). The AIMS Study Group.

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)

Acute Disease↗
PubMed1991

Angiographically assessed coronary arterial patency and reocclusion in patients with acute myocardial infarction treated with anistreplase: results of the anistreplase reocclusion multicenter study (ARMS).

In this open multicenter study, 156 patients with acute myocardial infarction received 30 U of anistreplase intravenously over 5 minutes within 4 hours of the onset of chest pain. The patency of the infarct-related vessel was determined by coronary angiography 90 minutes after anistreplase treatment, and also 24 hours after treatment, in patients with a patent infarct-related vessel at 90 minutes, to assess the reocclusion rate. The investigators categorized the infarct-related vessel as patent or occluded, and 2 independent cardiologists graded the infarct-related vessel according to the Thrombolysis in Myocardial Infarction (TIMI) perfusion criteria. At the 90-minute assessment, 106 of 145 evaluable patients (73%) had patent infarct-related vessels, and 39 of 145 (27%) had occluded infarct-related vessels. Of the 139 independently assessed patients, 98 (71%) had TIMI grades 2 or 3 and 41 (29%) had TIMI grades 0 or 1. At the 24-hour assessment, 98 of 102 patients (96%) had a patent infarct-related vessel, and reocclusion had occurred in 4 of 102 patients (4%). Of the 94 independently assessed patients 90 (96%) had TIMI grades 2 or 3, and 4 (4%) had TIMI grades 0 or 1. The reliability of noninvasive parameters as indicators of achieved patency of the infarct-related vessel was estimated by means of correlation with patency assessed by coronary angiography. A significant correlation of 0.62 was found. The patency rate of 71 to 73% after use of anistreplase in patients with acute myocardial infarction corresponds with findings in earlier studies. The low reocclusion rate of 4% after use of anistreplase probably reflects the prolonged action of anistreplase.

Adult↗
PubMed1992

Coronary reperfusion rates in acute myocardial infarction patients after thrombolytic treatment with anistreplase: correlation with the delay from onset of symptoms to treatment: a review of 424 case records of patients admitted to coronary reperfusion studies with anistreplase.

The individual data for 424 acute myocardial infarction patients from 15 reperfusion studies conducted with anistreplase were reviewed to assess the correlation between the delay onset of symptoms to treatment and reperfusion of the coronary artery. The patients had a mean age of 56 years and 85.4% were male. All patients had a baseline angiogram showing an occluded coronary artery. Anistreplase was given in doses ranging from 3.75 to 35 IU (60% of patients received 30 IU). The mean delay between onset of symptoms to treatment was 3 h 29 min and reperfusion was observed in a total of 61.1% of patients. There was a highly significant correlation between reperfusion and the delay from onset of symptoms to treatment (p less than 0.001). A multivariate logistic regression was performed adjusting for age, sex, location of infarct, dose, and concomitant treatment. The only remaining statistically significant prediction factor for reperfusion was the delay between onset of symptoms to treatment (p less than 0.001). In conclusion, the ability of anistreplase to cause the lysis of coronary thrombi appears to be increasingly important as the delay from onset of symptoms to treatment is decreased. This may contribute to the lower mortality rate observed with early fibrinolytic treatment.

Acute Disease↗
PubMed1990

Anistreplase: a new thrombolytic for the treatment of acute myocardial infarction.

The chemistry, pharmacology, pharmacokinetics, clinical efficacy, adverse effects, and dosage and administration of anistreplase in the treatment of acute myocardial infarction (AMI) are reviewed. Anistreplase is an acylated form of the streptokinase-plasminogen complex. Acylation makes the complex temporarily inactive but protects it from neutralization by plasmin inhibitors. After deacylation, which begins immediately after injection, the streptokinase-plasminogen complex promotes thrombolysis by speeding the conversion of plasminogen to plasmin. Like other thrombolytic agents, anistreplase induces a systemic fibrinogenolytic state. The plasma half-life of anistreplase, 88-112 minutes, is longer than that of the other thrombolytic drugs marketed in the United States. Anistreplase lyses coronary artery thrombi when given by the intracoronary or i.v. route. I.V. anistreplase is comparable in efficacy to i.v. streptokinase but has not been directly compared with i.v. alteplase. Anistreplase therapy in patients with AMI may help preserve left ventricular function and prolong survival. Anistreplase is comparable in safety to other thrombolytic drugs. Although bleeding has occurred in 4-47% of patients treated with anistreplase, most episodes have been clinically unimportant and have occurred at a vascular puncture site; intracranial hemorrhage has occurred in less than 1% of patients. Cardiac arrhythmia and transient hypotension are common after anistreplase administration. Anistreplase is easy to administer and may be appropriate for use in patients with suspected AMI before hospital admission. The recommended dose is 30 units i.v. given over two to five minutes. Anistreplase is similar in efficacy and safety to other thrombolytic agents in the treatment of AMI. The drug's ease of administration may be an important clinical consideration.

Acute Disease↗
PubMed1991

Invasive reperfusion study. II. Multicentre European randomized trial of anistreplase vs streptokinase in acute myocardial infarction.

IRS II (Invasive reperfusion study II) was a multicentre randomized trial comparing the efficacy of a 2-5-min 30 U anistreplase intravenous injection with a 1,500,000 U 60-min streptokinase (SK) intravenous infusion in acute myocardial infarction. 116 patients were randomized within 6 h of onset of symptoms. Early coronary patency was assessable in 107 patients by coronary angiogram performed 102 min after thrombolytic treatment (range: 30-297 min) in the anistreplase group and 93 min (range: 22-330 min) in the SK group. The early coronary patency rate was significantly higher in the anistreplase group than in the SK group: respectively, 70% (38/54) and 51% (27/53), P less than 0.05). Fifty patients had assessable coronary angiograms at 90 min and 24 h. The 24-h patency rate was 92.3% (24/26) in the anistreplase group vs 87.5% (21/24) in the SK group. No early reocclusion occurred in the anistreplase group vs 15.4% (2/13) in the SK group (NS). Fibrinogen fell to 13.2 +/- 19.8% on anistreplase vs 9.4 +/- 10.3% on SK (NS). Bleeding complications occurred in 12% (7/58) of treated patients in the anistreplase group vs 20.7% (13/58) in the SK group (NS). Two cerebrovascular accidents occurred after thrombolytic treatment with anistreplase (3.4%) vs one after SK (1.7%) (NS). Thus, anistreplase is more effective than intravenous SK and easier to administer.

Adult↗
PubMed1991

Multicenter patency trial of intravenous anistreplase compared with streptokinase in acute myocardial infarction. The TEAM-2 Study Investigators.

Thrombolytic therapy has been shown to improve clinical outcome when administered early after the onset of symptoms of acute myocardial infarction; the mechanism of benefit is believed to be reestablishment and maintenance of coronary artery patency. Anistreplase is a second generation thrombolytic agent that is easily administered and has a long duration of action. To compare anistreplase (30 units/2-5 min) and therapy with the Food and Drug Administration-approved regimen of intravenous streptokinase (1.5 million units/60 min), a randomized, double-blind, multicenter patency trial was undertaken in 370 patients less than 76 years of age with electrocardiographic ST segment elevation who could be treated within 4 hours of symptom onset. Coronary patency was determined by reading, in a blinded fashion, angiograms obtained early (90-240 minutes; mean, 140 minutes) and later (18-48 hours; mean, 28 hours) after beginning therapy. Early total patency (defined as Thrombolysis in Myocardial Infarction grade 2 or 3 perfusion) was high after both anistreplase (132/183 = 72%) and streptokinase (129/176 = 73%) therapy, and overall patency patterns were similar, although patent arteries showed "complete" (grade 3) perfusion more often after anistreplase (83%) than streptokinase (72%) (p = 0.03). Similarly, residual coronary stenosis, determined quantitatively by a validated computer-assisted method, was slightly less in patent arteries early after anistreplase (mean stenosis diameter, 74.0%) than streptokinase (77.2%, p = 0.02). In patients with patent arteries without other early interventions, reocclusion risk within 1-2 days was defined angiographically and found to be very low (anistreplase = 1/96, streptokinase = 2/94). Average coronary perfusion grade was greater, and percent residual stenosis was less, at follow-up than on initial evaluation and did not differ between treatment groups. Enzymatic and electrocardiographic evolution was not significantly different in the two groups. Despite rapid injection, anistreplase was associated with only a small (4-5 mm Hg), transient (at 5-10 minutes) mean differential fall in blood pressure. In-hospital mortality rates were comparable for anistreplase and streptokinase (5.9%, 7.1%). Stroke occurred in one (0.5%) and three (1.6%) patients, respectively; one stroke was hemorrhagic. Other serious bleeding events and adverse experiences occurred uncommonly and with similar frequency in the two groups. Thus, for the end points of our study (patency, safety), anistreplase and streptokinase showed overall favorable and relatively comparable outcomes, with a few differences.(ABSTRACT TRUNCATED AT 400 WORDS)

Anistreplase↗
PubMed1990

Effects on infarct size and left ventricular function of early intravenous injection of anistreplase in acute myocardial infarction. The APSIM Study Investigators.

A total of 231 patients suffering from a first acute myocardial infarction were randomly allocated within 4 hours following the onset of symptoms either to anistreplase or anisoylated plasminogen streptokinase activator complex (APSAC), 30 U over 5 minutes, or to conventional heparin therapy, 5000 IU in bolus injection. Heparin was reintroduced in both groups 4 h after initial therapy at a dosage of 500 IU/kg per day. A total of 112 patients received anistreplase and 119 received heparin within a mean period of 188 +/- 62 min following the onset of symptoms. Infarct size was estimated from single photon emission computerized tomography and expressed in percentage of the total myocardial volume. The patency rate of the infarct-related artery was 77% in the anistreplase group and 36% in the heparin group (p less than 0.001). Left ventricular ejection fraction determined from contrast angiography was significantly higher in the anistreplase group than in the heparin group (6 absolute percentage point difference). A significant 31% reduction in infarct size was found in the anistreplase group (33% for the anterior wall infarction subgroup [p less than 0.05] and 16% for the inferior wall infarction subgroup, NS). A close inverse relation was found between the values of left ventricular ejection fraction and infarct size (r = -.73, p less than 0.01). In conclusion, early infusion of anistreplase in acute myocardial infarction produced a high early patency rate, a significant limitation of infarct size, and a significant preservation of left ventricular systolic function, mainly in the anterior wall infarctions.

Acute Disease↗
PubMed1990

French multicenter trial of anistreplase versus heparin in acute myocardial infarction.

Eighty-four patients aged less than 71 years with less than 4-hour duration acute myocardial infarction (AMI) were randomized in a multicenter study to 30 U anistreplase or heparin (single injection of 6500 IU followed by 1000 IU/hr). Early reperfusion was assessed from ECG changes (50% of sum ST decrease 2 hours postdosing) and the CK release profile (CK peak less than 16 hours after onset of symptoms, CK slope greater than 10%/hr). Reperfusion rates in patients meeting at least two criteria of reperfusion were 62.5% on anistreplase versus 27.5% on heparin. On delayed angiogram (13.7 +/- 3.4 days), patency rates were 66% with anistreplase versus 47% (NS) with heparin in 76 patients. Global LVF was similar in both groups. With anistreplase, the mean lowest fibrinogen level was 0.43 +/- 0.55 g/l, plasminogen was 20 +/- 9%, and the highest F.D.P. was 1447 +/- 548 micrograms/ml. All values recovered by hour 48. In-hospital and 1-year follow-up mortality was 7.2% (three patients) with anistreplase versus 10.2% (four patients) with heparin. Bleeding occurred in 9.7% and 5.1% of the patients (NS), respectively. No intracranial hemorrhage occurred. Thus, with combined clinical criteria or reperfusion, anistreplase is twice as efficient as heparin, has a good tolerance, and is easy to use as a single injection.

Anistreplase↗
PubMed1992

Lack of influence of pretreatment antistreptokinase antibody on efficacy in a multicenter patency comparison of intravenous streptokinase and anistreplase in acute myocardial infarction.

Antistreptokinase antibodies present in patients as a result of previous streptococcal infections might theoretically influence the thrombolytic response to streptokinase or anistreplase. The potential influence of antibody, measured as antigen binding to immunoglobulin G, was investigated in a randomized, double-blind, multicenter patency comparison of intravenous streptokinase (1.5 million units/60 minutes) and intravenous anistreplase (30 units/2 to 5 minutes) in patients with acute myocardial infarction. Antibody results were evaluated in 333 patients (from a total study population of 370 patients) less than 76 years of age with ECG evidence of ST segment elevation who could be treated within 4 hours of the onset of symptoms. Variations in pretreatment circulating levels of antibody did not influence angiographically defined early coronary patency rates (Thrombolysis in Myocardial Infarction grade 2 or 3 perfusion, measured at a mean of 140 minutes after therapy was begun) for either streptokinase or anistreplase. Similarly the lytic response represented by systemic plasminogen activation and measured as changes in plasma plasminogen and fibrinogen levels after dosing (at mean times of 90 minutes and 24 hours) was not correlated with baseline antibody levels. Furthermore, pretreatment antibody was not a risk factor for poor outcome in response to streptokinase or anistreplase (reocclusion within 24 hours, in-hospital death, or stroke) and did not correlate with hypotension or allergic-type reactions recorded as adverse events. In conclusion, within the population limits defined by the inclusion and exclusion criteria of the study (patients were excluded if they had received streptokinase or anistreplase within the previous 6 months), pretreatment antistreptokinase immunoglobulin G is not a significant determinant of the efficacy response to streptokinase or anistreplase.

Anistreplase↗
PubMed1990

Anistreplase: a novel thrombolytic agent for acute myocardial infarction.

Anistreplase, a modified congener of streptokinase, is a recently approved thrombolytic agent used in the treatment of acute myocardial infarction (AMI). Clinical studies have demonstrated anistreplase to be equally efficacious as intracoronary streptokinase when given within four hours of the onset of chest pain. Thirty units, given as a single bolus intravenous injection, result in reperfusion rates of approximately 60-70 percent. The adverse-effect profile of anistreplase compares favorably with that of streptokinase, with hemorrhagic complications being the most serious. Anistreplase has two distinct advantages over both streptokinase and alteplase: (1) it can be administered as a single bolus intravenous injection and (2) it has a longer half-life which may result in decreased reocclusion rates. Anistreplase therapy is associated with reductions in both short- and long-term mortality and has been shown to preserve left ventricular function. A large, long-term, comparative clinical trial (Third International Study of Infarct Survival or ISIS-III) investigating morbidity and mortality rates with streptokinase, alteplase, and anistreplase is ongoing, as is a direct comparative study against alteplase alone (TEAM-3, Multicenter Thrombolytic Trials of Eminase in Acute Myocardial Infarction).

Anistreplase↗
PubMed1990

A systemic non-lytic state and local thrombolytic failure of anistreplase (anisoylated plasminogen streptokinase activator complex, APSAC) in acute myocardial infarction.

The relation between coronary thrombolysis and coagulation variables after administration of anistreplase (anisoylated plasminogen streptokinase activator complex, APSAC) was studied in patients with an acute myocardial infarction. Fifty eight consecutive patients with acute myocardial infarction were given 30 U of anistreplase intravenously within 4 hours of the onset of symptoms. A fall in the plasma concentration fibrinogen to less than 1.0 g/l 90 minutes after administration of anistreplase was considered to reflect a systemic lytic state. Coronary angiography was performed 48 hours after thrombolytic treatment. The overall patency rate was 74% (43/58). Patency rates were significantly different in patients with a systemic lytic (83% (43/52)) and a systemic non-lytic state (0% (0/6)). The absence of a systemic lytic state after anistreplase administration seemed to be highly predictive of the failure of coronary thrombolysis. Coagulation studies showed evidence of inhibition of anistreplase induced fibrinolytic activity which may explain the failure of thrombolytic treatment in patients with evidence of a systemic non-lytic state.

Adult↗
PubMed1992

Monitoring of streptokinase resistance titre in acute myocardial infarction patients up to 30 months after giving streptokinase or anistreplase and related studies to measure specific antistreptokinase IgG.

OBJECTIVE: To examine the induction of antistreptokinase antibodies after giving streptokinase or anistreplase to patients with acute myocardial infarction. DESIGN: Patients were randomly allocated to receive either 1.5 x 10(6) IU, streptokinase or 30U anistreplase in a double blind study. Blood samples were collected immediately before treatment and subsequently at intervals up to 30 months; plasma samples were assayed for streptokinase resistance titre (functional assay) and streptokinase binding by IgG (microradioimmunoassay). SETTING: Cardiology department in a general hospital. PATIENTS: 128 consecutive eligible patients. Samples were collected for up to one year according to a prospective design: a subsection of 47 patients was selected for intensive study over the first 14 days. After one year, all available patients (67) were sampled on one further occasion. RESULTS: Antibody responses to streptokinase and anistreplase were similar. Streptokinase resistance titres exceeded pretreatment concentrations five days after dosing, and values peaked at 14 days. By 12 months after dosing, 92% of resistance titres (n = 84) had returned to within the pretreatment range. Antistreptokinase IgG concentrations also exceeded baseline concentrations within five days and peaked at 14 days. Half of the individual values had returned to within the pretreatment range by 12 months (n = 84) and 89% by 30 months (n = 18). CONCLUSION: Although we cannot be sure of the clinical significance, because of the increased likelihood of resistance due to antistreptokinase antibody, streptokinase and anistreplase may not be effective if administered more than five days after an earlier dose of streptokinase or anistreplase, particularly between five days and 12 months, and increased antistreptokinase antibody may increase the risk of allergic-type reactions.

Adult↗
PubMed1992

Short- and long-term comparative study of anistreplase versus streptokinase in acute myocardial infarction.

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.

Aged↗
PubMed1990

Long-term effects of intravenous anistreplase in acute myocardial infarction: final report of the AIMS study. AIMS Trial Study Group.

In a randomised, double-blind study 1258 patients were allocated to receive either anistreplase (anisoylated plasminogen streptokinase activator complex [APSAC], 'Eminase') or placebo within 6 h of onset of suspected acute myocardial infarction. At 30 days, 40 (6%) of 624 patients on anistreplase had died, compared with 77 (12%) of 634 patients on placebo (odds reduction 50.5%). On long-term follow-up a survival benefit was still observed: at 12 months, 69 (11%) patients treated with anistreplase had died, compared with 113 (18%) patients given placebo (odds reduction 43%; p = 0.0007, 95% confidence interval 21-59%). This effect on mortality was not related to time between onset of symptoms and treatment or to any patient characteristic. Site of infarction and age were the most important influences on 1-year survival in both treatment groups; tachycardia (over 100 beats/min) on admission and previously diagnosed ischaemic heart disease were also associated with increased risk. Major complications of acute myocardial infarction were less frequent in patients treated with anistreplase than in controls. As for other thrombolytic agents, haemorrhage was more common, but usually minor. These findings indicate that anistreplase is an effective and acceptably safe thrombolytic with long-term survival benefits for patients with acute myocardial infarction.

Actuarial Analysis↗
PubMed1990

Angiographic patency study of anistreplase versus streptokinase in acute myocardial infarction.

128 patients with acute myocardial infarction of duration 6 h or less were randomised in double-blind fashion to receive 30 U anistreplase over 5 min or 1.5 MU streptokinase over 1 h, both intravenously. Angiographic patency was assessed 90 min and 24 h from the start of therapy. 55% of patients who received anistreplase and 53% of patients who received streptokinase had patent infarct-related arteries (TIMI grade 2-3) at 90 min (95% CI 42-68% and 40-66%, respectively). At 24 h 81% and 87.5% of arteries were patent respectively (95% CI, 71-91% and 83.5-91.5%). Time to therapy had no significant effect on patency rates. There was one early reocclusion within 24 h in each treatment group and clinical evidence of reocclusion was recorded between 24 h and hospital discharge in a further 5 patients (streptokinase 3, anistreplase 2). With these regimens, therefore, anistreplase and streptokinase gave the same patency rates.

Adult↗
PubMed1991

Anistreplase in early acute myocardial infarction and the one-year follow-up.

Of consecutive patients seen with first myocardial infarction (88 of whom were treated out-of-hospital by mobile coronary care staff), 139 received 30 units of intravenous anistreplase at a mean of 101 minutes (range 35-180) from onset of symptoms. Thrombolysis in myocardial infarction patency grade 2 or 3 was found in 76/91 (83.5%) patients. At 3-4 months after hospital discharge, the mean global left ventricular ejection fraction and mean infarct-related regional third ejection fraction declined with increasing delay to anistreplase. For the first, second and third hour administrations, global ejection fraction was 54%, 50% and 45% (P = 0.002) and for regional third ejection fractions 49%, 43% and 41% (P = 0.02) respectively. Of the patients, 130 were reviewed at approximately 1 year: reinfarction had occurred in 9, 6 had undergone coronary angioplasty and 1 had coronary arterial bypass grafting performed since discharge. Mean global left ventricular ejection fraction was 52% and mean infarct-related regional third ejection fraction was 51%. Thus, intravenous anistreplase induces high rates of arterial patency. Global and regional third ejection fractions decline with increasing delay in the time of administration of anistreplase. Mortality and morbidity is low in the first year.

Adult↗
PubMed1992

Feasibility, safety, and efficacy of domiciliary thrombolysis by general practitioners: Grampian region early anistreplase trial. GREAT Group.

OBJECTIVE: To assess the feasibility, safety, and efficacy of domiciliary thrombolysis by general practitioners. DESIGN: Randomised double blind parallel group trial of anistreplase 30 units intravenously and placebo given either at home or in hospital. SETTING: 29 rural practices in Grampian admitting patients to teaching hospitals in Aberdeen (average distance 36 (range 16-62) miles). PATIENTS: 311 patients with suspected acute myocardial infarction and no contraindications to thrombolytic therapy seen at home within four hours of onset of symptoms. MAIN OUTCOME MEASURES: Time saving, adverse events, Q wave infarction, left ventricular function. RESULTS: Anistreplase was administered at home 101 minutes after onset of symptoms, while anistreplase was given in hospital 240 minutes after onset of symptoms (median times). Adverse events after thrombolysis were infrequent and, apart from cardiac arrest, not a serious problem when they occurred in the community: seven of 13 patients were resuscitated after cardiac arrest out of hospital. By three months after trial entry the relative reduction of deaths from all causes in patients given thrombolytic therapy at home was 49% (13/163 (8.0%) v 23/148 (15.5%); difference -7.6% (95% confidence interval -14.7% to -0.4%), p = 0.04). Full thickness Q wave infarction was less common in patients with confirmed infarction receiving treatment at home (65/122 (53.3%) v 76/112 (67.9%); difference -14.6% (95% confidence interval -27.0% to -2.2%), p = 0.02). CONCLUSIONS: General practitioners provided rapid pre-hospital coronary care of a high standard. Compared with later administration in hospital, giving anistreplase at home resulted in reduction in mortality, fewer cardiac arrests, fewer Q wave infarcts, and better left ventricular function. Benefits were most marked where thrombolytic therapy was administered within two hours of the onset of symptoms.

Adult↗
PubMed1990

[Anistreplase. Pharmacology and biological data].

Anistreplase is a second generation thrombolytic agent, an equimolecular streptokinase lys-plasminogen complex the active site of which is temporarily blocked by a p-anisoyle group. Acylation enables the drug to be administered as a bolus intravenous injection over 2 to 5 minutes, and it protects anistreplase against circulating inhibitors, hence a plasma elimination half-life of 90 minutes. Deacylation is slow and progressive (deacylation half-life: 105 minutes), and it begins as soon as the product is injected. It reduces the hypotensive effect of streptokinase, permits a prolonged action in the thrombus and limits the risk of reocclusion. Using lys-plasminogen increases the affinity of the drug for fibrin and potentiates its accumulation and retention in the thrombus. In vitro studies have shown that the affinity of anistreplase for fibrin is similar to that of t-PA. In doses used for myocardial infarction, anistreplase induces a pronounced fibrinogenolysis. The effectiveness of the drug has been demonstrated on numerous animal models and subsequently by clinical trials.

Anistreplase↗