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

Ventricular arrhythmias during thrombolysis for acute myocardial infarction and their relation to coronary artery patency were examined. Twenty-four-hour Holter monitoring was begun 3.1 +/- 0.2 hours after onset of pain in 40 patients (age 54 +/- 1.6 years; anterior infarction 42.5%) treated with streptokinase (42.5%) or recombinant tissue-type plasminogen activator (57.5%) (delay from pain 3.3 +/- 0.2 hours). A Marquette 8000 computer was used for Holter analysis. The infarct-related artery was considered as patent (72.5%) or non-patent (27.5%) according to coronary angiography (delay from pain 26.7 +/- 2.5 hours; 60% less than 24 hours). Ventricular arrhythmias were present in all patients. Tolerance was good (1 cardioversion for ventricular fibrillation). The incidence of accelerated idioventricular rhythm was not different between patients with a patent and nonpatent artery (90 vs 82%), nor for ventricular tachycardia (VT) (83 vs 73%). Coronary artery patency was associated with a 14-, 13- and 32-fold increase of ventricular premature complexes, VT and accelerated idioventricular rhythms, respectively. The increased incidence of sustained VT (patent 38%; nonpatent 0%; p less than 0.05) and early (before the first 6 hours) accelerated idioventricular rhythm (patent 76%; nonpatent 18%; p less than 0.01) associated with artery patency suggests that these arrhythmias may be noninvasive diagnostic criteria for reperfusion (sensitivity 38 vs 76%, and specificity 100 vs 82%). A positive correlation was found between the frequency of ventricular premature complexes and VT, and peak creatine kinase.
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PMID:Holter recording of ventricular arrhythmias during intravenous thrombolysis for acute myocardial infarction. 173 50

Continuous electrocardiography during the first 24 hours of a stay in a coronary care unit was used to record ventricular arrhythmias during treatment with alteplase (recombinant tissue plasminogen activator) or placebo. Recordings were made on 378 of the 436 patients admitted to a double blind trial of alteplase or placebo in one participating centre of the Anglo-Scandinavian study of early thrombosis (ASSET), patients being selected according to the availability of recorders. Of these, 309 (158 given alteplase and 151 placebo) had greater than 5 hours of analysable data. Most of the arrhythmias were recorded in patients with an in hospital diagnosis of myocardial infarction. Ventricular couplets and ventricular tachycardia were significantly more common in the patients treated with alteplase. Further, in patients with myocardial infarction who had ventricular extrasystoles, couplets, or ventricular tachycardia type a, the number of hours in which each arrhythmia was recorded was significantly higher in the alteplase group. The various ventricular arrhythmias in the alteplase group tended to cluster in the first 4-12 hours of the recordings. During the first 24 hours admission there were four episodes of ventricular fibrillation in the alteplase group and five in the placebo group of taped patients. By one month there had been 18 deaths in these 309 patients (alteplase four, placebo 14). These bore no relation to any recorded arrhythmia. Clinical records for the patients with no or minimal tape data yielded six further episodes of ventricular fibrillation during the first 24 hours (three in the alteplase group and three in the placebo group). Of the total 436 patients, 10 of the 218 patients in the alteplase group had died by one month compared with 22 of the 218 patients treated with placebo. The use of alteplase increases the incident of non-life threatening ventricular arrhythmias. These results, however suggest that arrhythmia after thrombolysis in the pre-hospital phase may be less of a problem than it is perceived to be.
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PMID:Ventricular arrhythmias during treatment with alteplase (recombinant tissue plasminogen activator) in suspected acute myocardial infarction. 189 82

The current revolution in the treatment of acute myocardial infarction by means of thrombolytic therapy has as its underlying strategy three aims: early restoration of the blood flow in order to salvage jeopardized but still viable tissues; limitation of acute consequences of ischemic heart disease, such as infarct size, ventricular fibrillation, and pericardial effusion; and preservation, as far as possible, of ventricular function. It is also hoped that these three achievements will result in reduced short- as well as long-term mortality rates. The techniques employed in this overall strategy are still under investigation, and several leading pharmacological compounds vie for supremacy: streptokinase (SK) and its anisoylated form (APSAC), recombinant technique tissue type plasminogen activator (rt-PA), and urokinase (UK) with or without prourokinase (PUK). Other pharmacological agents, such as angiotensin converting enzyme (ACE) inhibitors, beta-blockers, Ca2+ antagonists, and O2 radical scavengers, might find here their "finest hour" yet. In addition, the underlying anatomy may require early or, where needed, delayed PTCA, backed up by coronary artery bypass grafting. Thus, the tactics of the intervention may vary from case to case and indeed from center to center depending on experience and facilities, but the strategic conclusion is clearly the same: early reperfusion is a must if one wishes to save ischemic but still viable tissue.
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PMID:Acute consequences of ischemic myocardial damage. 248 24

The complications of IV recombinant tissue-type plasminogen activator (rtPA) have not been previously reported specifically for the first hours after initiation of the therapy when patients are often in emergency departments or in transport. The charts of 124 patients who received rtPA between April 1986 and December 1987 were retrospectively reviewed for reactions associated with rtPA infusion occurring in the first ten hours after the onset of rtPA administration. Minor bleeding developed in 19% of the patients, and life-threatening bleeding in 3%. Half of the life-threatening bleeding episodes were not predictable by history or physical examination. Arrhythmias were frequent despite the fact that all patients were maintained on IV lidocaine. New premature ventricular contractions occurred in 67%, accelerated idioventricular rhythm in 34%, ventricular tachycardia in 30%, and ventricular fibrillation in 2%. Many of the arrhythmias other than ventricular fibrillation had little hemodynamic consequence and did not require treatment. Neurologic episodes occurred in 3%, including two patients with intracerebral bleeding (1.5%); hypotension requiring treatment developed in 3%; and minor symptoms of allergy in 2%. Administration of rtPA in the ED requires careful patient selection to avoid bleeding complications and close monitoring to detect arrhythmias and changes in vital signs.
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PMID:Associated reactions during and immediately after rtPA infusion. 249 57

A randomised trial of 367 patients with acute myocardial infarction was performed to determine whether an invasive strategy combining thrombolysis with recombinant tissue-type plasminogen activator (rTPA), heparin, and acetylsalicylic acid, and immediate percutaneous transluminal coronary angioplasty (PTCA) would be superior to a noninvasive strategy with the same medical treatment but without immediate angiography and PTCA. Intravenous infusion of 100 mg rTPA was started within 5 h after onset of symptoms (median 156 min). Angiography was performed 6-165 min later in 180 out of 183 patients allocated to the invasive strategy; 184 patients were allocated to the non-invasive strategy. Immediate PTCA reduced the percentage stenosis of the infarct-related segment, but this was offset by a high rate of transient (16%) and sustained (7%) reocclusion during the procedure and recurrent ischaemia during the first 24 h (17%). The clinical course was more favourable after non-invasive therapy, with a lower incidence of recurrent ischaemia within 24 h (3%), bleeding complications, hypotension, and ventricular fibrillation. Mortality at 14 days was lower in patients allocated to non-invasive treatment (3%) than in the group allocated to invasive treatment (7%). No difference between the treatment groups was observed in infarct size estimated from myocardial release of alpha-hydroxybutyrate dehydrogenase or in left ventricular ejection fraction after 10-22 days. Since immediate PTCA does not provide additional benefit there seems to be no need for immediate angiography and PTCA in patients with acute myocardial infarction treated with rTPA.
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PMID:Thrombolysis with tissue plasminogen activator in acute myocardial infarction: no additional benefit from immediate percutaneous coronary angioplasty. 289 37

To examine the outcome of patients with persistent coronary artery occlusion despite treatment with intravenous tissue-type plasminogen activator (t-PA), the clinical course of 96 patients with persistent occlusion after 90 min of therapy was evaluated. All patients underwent cardiac catheterization 90 min after initiation of intravenous t-PA. Immediate coronary angioplasty (PTCA) was attempted when the infarct-related artery failed to reperfuse unless the vessel was technically unsuitable or the infarct was thought to be small. No baseline differences could be found between these 96 patients and 288 patients who achieved perfusion with the same protocol. Although patients with and without successful perfusion after t-PA had similar clinical courses before cardiac catheterization, those without perfusion had more complications (ventricular fibrillation, severe bradycardia, hypotension) during catheterization. PTCA achieved reperfusion with less than 50% residual stenosis in 73% of the 86 patients in whom it was attempted, while 16% were left with a high-grade (greater than 50%) residual stenosis and PTCA failed in 11%. Mortality was highest in the nine patients with complete PTCA failure (44%), compared with a 6% mortality in the 63 patients with an insignificant residual stenosis after PTCA and a 14% mortality in the 14 patients with reperfusion, but a greater than 50% residual stenosis after PTCA. In 10 patients with small infarcts (six), unsuitable anatomy (two), or "spontaneous" drug induced (but later) opening before contemplated PTCA (two), PTCA was not attempted and no mortality occurred. The in-hospital reocclusion rate after successful PTCA was 29%, despite the use of heparin and antiplatelet agents.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Characteristics and outcome of patients in whom reperfusion with intravenous tissue-type plasminogen activator fails: results of the Thrombolysis and Angioplasty in Myocardial Infarction (TAMI) I trial. 296 16

A new European Cooperative Study Group trial of 721 patients has recently found recombinant tissue-type plasminogen activator (rt-PA) to positively affect infarct size, left ventricular function, cardiovascular morbidity and early survival. In this 26 center trial, patients were randomized to receive either placebo or 100 mg rt-PA intravenously over 3 h. Heparin (5,000 U bolus injection and then 1,000 U/h) and aspirin (250 mg initially, then 75 to 125 mg every other day) were given to all patients until angiography was performed (10 to 22 days after allocation). Enzymatic infarct size was found to be 20% smaller in the rt-PA group (2p = 0.0018) than in the control group. At angiography, 83% of rt-PA-treated patients had a patent infarct-related vessel compared with 77% of the placebo-treated patients. Ejection fraction was 2.2% points higher (2p = 0.04) and end-diastolic and end-systolic volumes were +/- 6 ml smaller (2p = 0.003) than in the control group, indicating an improved left ventricular pump function in the thrombolysis group. Cardiovascular complications such as shock, ventricular fibrillation and pericarditis were markedly fewer in patients treated with rt-PA, but bleeding complications occurred more frequently. An intracranial hemorrhage within 3 days after the infusion of rt-PA was observed in five patients (1.4%). None of these bleeding episodes was causally related to death. Although this European Cooperative trial was not designed primarily as a mortality study, important reductions in early mortality rates were observed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Lessons from the European Cooperative recombinant tissue-type plasminogen activator (rt-PA) versus placebo trial. 314 43

The potential use of ancrod, a purified isolate from the venom of the Malaysian pit viper, Agkistrodon rhodostoma, in decreasing the frequency of cyclic flow variations in severely stenosed canine coronary arteries and causing thrombolysis of an acute coronary thrombus induced by a copper coil was evaluated. Open-chest, anesthetized dogs were used. Ancrod was given intravenously (8 U/kg) over 1 hour and caused a significant reduction in the frequency of cyclic flow variations (5.8 +/- 0.7 to 3.6 +/- 0.8 cyclic flow variations per 30 minutes, p less than 0.05), whereas control animals failed to decrease the frequency of their cyclic flow variations over the same time period (5.3 +/- 0.3 to 5.0 +/- 0.4 cyclic flow variations per 30-minute period). Twenty-seven dogs had a coronary thrombus induced by a copper coil positioned directly in a major coronary artery; of these, four died of ventricular fibrillation prior to treatment, eight received an infusion of saline and showed no thrombolysis over 5 hours, and three died of ventricular fibrillation during the initial part of an intravenous infusion of ancrod. The remaining 12 dogs received ancrod intravenously (16 U/kg); six demonstrated lysis of the coronary thrombus (mean time to lysis, 65 +/- 20 minutes). The concentrations of ancrod used in these studies produced a severe decrease in systemic fibrinogen concentration and a significant decrease in the inhibitor of plasminogen activator levels. Thus, ancrod decreases the frequency of cyclic flow variations in stenosed canine coronary arteries and may cause coronary thrombolysis in approximately 50% of animals within 65 +/- 20 minutes of its intravenous administration.
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PMID:Ancrod decreases the frequency of cyclic flow variations and causes thrombolysis following acute coronary thrombosis. 356 40

Clinical experience with the use of intracoronary tissue plasminogen activator (t-PA) is limited. We therefore undertook this study to document current clinical usage of intracoronary t-PA during a 2-yr period in a multicenter registry. Intracoronary t-PA was utilized on 206 occasions in 198 patients (154 men and 44 women; mean age, 59 +/- 12 yr). The mean dose of intracoronary t-PA was 31 +/- 15 mg. Indications for use included acute myocardial infarction (MI) (n = 83), preexisting thrombus with (n = 49) or without (n = 41) percutaneous transluminal coronary angioplasty (PTCA), unstable angina (n = 14), abrupt vessel closure (n = 11), and post-PTCA "clean-up" (n = 8). The Thrombolysis in Myocardial Infarction (TIMI Phase I) criteria were used to assess perfusion and degree of thrombus formation. Overall, the mean TIMI flow grade increased from 1.2 +/- 1.1 before treatment to 2.3 +/- 1.0 after treatment (P < 0.0001); the mean TIMI thrombus grade decreased from 3.2 +/- 1.0 before treatment to 1.6 +/- 1.4 after treatment (P < 0.0001). Complications included bleeding (9.2%), MI (17.6%), need for coronary artery bypass grafting (CABG) (9.2%), need for repeat PTCA/atherectomy/stents (4.9%), and ventricular fibrillation (1.7%, all associated with opening totally occluded vessels). There were 14 subsequent in-hospital deaths: 13 of the patients who died had originally presented with MI; the other had experienced abrupt vessel closure during a PTCA procedure. Intracoronary t-PA appears to be effective in improving distal flow and decreasing thrombus burden; however, intracoronary delivery of t-PA has associated risks.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Clinical experience with intracoronary tissue plasminogen activator: results of a multicenter registry. Intracoronary t-PA Registry Investigators. 749 84

In a canine copper coil-induced coronary thrombosis model, the differences in frequency of reperfusion arrhythmias (premature ventricular complexes: PVC) and mortality rate after thrombolysis by intravenous bolus injection of a novel modified tissue-type plasminogen activator (t-PA), E6010, and by continuous intravenous infusion of native t-PA or urokinase were evaluated. Rapid coronary occlusion and reperfusion were produced with a balloon catheter in another group of dogs, and the findings were compared with those in the thrombolysis groups. Reperfusion occurred gradually after the administration of E6010, but was significantly more rapid after administration of native t-PA and urokinase (P < 0.05). PVC were observed more frequently in native t-PA, urokinase and balloon occlusion-reperfusion groups than in the E6010 group. The mortality rate due to ventricular fibrillation was 0.0% in the E6010 group, 50.0% in the native t-PA and balloon occlusion-reperfusion groups, and 33.3% in the urokinase group. These results suggest that the more gradual reperfusion of the coronary artery at an earlier period after drug administration led to the lower frequency of reperfusion arrhythmias and low mortality rate in the E6010 group than in the native t-PA, urokinase and balloon occlusion-reperfusion groups.
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PMID:A novel modified tissue-type plasminogen activator (t-PA), E6010, gradually increases coronary blood flow after thrombolysis compared with native t-PA, urokinase and balloon catheter occlusion-reperfusion. 753 43


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