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[Clinico-experimental study of the possibility of the use of immobilized enzymes for local thrombolysis and thromboformation]

https://arctichealth.org/en/permalink/ahliterature55823
Source
Ukr Biokhim Zh. 1983;55(3):311-7
Publication Type
Article
Date
1983
Author
V N Smirnov
V P Torchilin
A V Mazaev
L A Suvorova
Iu I Voronkov
Source
Ukr Biokhim Zh. 1983;55(3):311-7
Date
1983
Language
Ukrainian
Publication Type
Article
Keywords
Animals
Blood Coagulation
Dogs
Embolization, Therapeutic - methods
English Abstract
Enzymes, Immobilized - administration & dosage
Hemorrhage - drug therapy
Humans
Injections, Intra-Arterial
Injections, Intravenous
Microspheres
Myocardial Infarction - blood - drug therapy
Plasmin - administration & dosage
Streptokinase - administration & dosage
Thrombin - administration & dosage
Thrombosis - drug therapy
Abstract
Fibrinolysin immobilized by a solid polysaccharide carrier capable of controllable biodegradation is shown to exert a local effective thrombolyzing action. Certain results of clinical studies of immobilized streptase (streptodecase) are presented. They show essential advantages of the new preparation over the known native enzymes. Experiments with animals show that the immobilized thrombin may be applied in therapeutic embolization for the hemorrhage cessation.
PubMed ID
6223428 View in PubMed
Less detail

Coronary thrombolysis--clinical guidelines and public policy: results of an Ontario practitioner survey.

https://arctichealth.org/en/permalink/ahliterature229068
Source
CMAJ. 1990 May 15;142(10):1069-76
Publication Type
Article
Date
May-15-1990
Author
C D Naylor
A A Hollenberg
A M Ugnat
A. Basinski
Author Affiliation
Clinical Epidemiology Unit, Toronto Hospital, Ont.
Source
CMAJ. 1990 May 15;142(10):1069-76
Date
May-15-1990
Language
English
Publication Type
Article
Keywords
Attitude of Health Personnel
Cardiology
Fibrinolytic Agents - administration & dosage
Financing, Government
Health Policy
Humans
Internal Medicine
Myocardial Infarction - drug therapy
Ontario
Physicians
Questionnaires
Societies, Medical
Streptokinase - administration & dosage
Tissue Plasminogen Activator - administration & dosage
Abstract
The Ontario Medical Association (OMA) guidelines for intravenous thrombolysis in acute myocardial infarction were released in March 1988 and contributed to a government decision against special per-case funding to assist hospitals using tissue-type plasminogen activator (tPA). In October 1988, 1512 cardiologists, internists and physician-administrators who were OMA members were mailed a questionnaire seeking their views on the OMA guidelines and related issues. Of the 419 questionnaires (28%) that were returned, 392 contained usable responses. Among the respondents 268 (68%) had used thrombolytic drugs in the preceding 12 months; the mean number of cases was 10.6 (standard deviation 12.9). A strong or a mild preference for tPA over streptokinase was registered by 64% of the respondents; 28% had no preference. However, the self-reported ratio of actual streptokinase:tPA use was about 3:1, and 73% indicated that the government's funding policy had limited the availability of tPA in their hospital. The respondents were almost equally divided as to whether the policy should be changed. The guidelines were deemed helpful by 85% of the noncardiologists, as opposed to 52% of the cardiologists (p less than 0.005). OMA involvement in developing and circulating such guidelines was supported by 74% of the respondents and opposed by 18%; opposition was more likely to come from those who found the guidelines unhelpful (p less than 0.001). Support for involvement by the College of Physicians and Surgeons of Ontario was much weaker (supported by 32%, opposed by 62%). Overwhelming opposition to government involvement was evident.
Notes
Cites: Lancet. 1988 Sep 3;2(8610):525-302900919
Cites: Nature. 1988 Apr 14;332(6165):5773128738
Cites: CMAJ. 1989 Jun 1;140(11):1289-992497946
Cites: CMAJ. 1989 Nov 1;141(9):861-62804833
Cites: Lancet. 1985 Apr 13;1(8433):842-72858711
PubMed ID
2110859 View in PubMed
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Evaluation of in vivo immune complex formation and complement activation in patients receiving intravenous streptokinase.

https://arctichealth.org/en/permalink/ahliterature54973
Source
Clin Exp Immunol. 1993 Nov;94(2):286-90
Publication Type
Article
Date
Nov-1993
Author
J. Freysdottir
S. Ormarsdottir
A. Sigfusson
Author Affiliation
Department of Immunology, National University Hospital, Reykjavik, Iceland.
Source
Clin Exp Immunol. 1993 Nov;94(2):286-90
Date
Nov-1993
Language
English
Publication Type
Article
Keywords
Antibodies - blood
Antigen-Antibody Complex - biosynthesis
Complement Activation - drug effects
Complement C3 - metabolism
Complement C3d - metabolism
Complement C4 - metabolism
Complement C4b
Erythrocytes - immunology
Humans
Infusions, Intravenous
Myocardial Infarction - drug therapy
Peptide Fragments - metabolism
Receptors, Complement 3b - metabolism
Streptokinase - administration & dosage - adverse effects - immunology
Abstract
The usefulness of several different methods for detecting immune complex formation and complement activation in the circulation were applied to samples from patients receiving intravenous Streptokinase therapy for myocardial infarction. Streptokinase is a foreign antigen and can cause immune reactions. We collected samples from 13 patients, before Streptokinase administration (baseline), at the end of infusion (1 h), 12 h later and on day 7. We measured IgG containing immune complexes (IgG-IC), free C3d and antibodies to Streptokinase by ELISA, and CR1, C3d and C4d on erythrocytes by flow cytometric assay. Antibodies to Streptokinase are common, as all but two of the patients had measurable antibody levels. During Streptokinase treatment there was a drop in antibody levels, most prominent in those patients who had high baseline levels. At the same time increased levels of free C3d and erythrocyte-bound C3d were observed. After 12 h free C3d was usually back to baseline level, but C3d on erythrocytes was still raised. These data indicate the formation of Streptokinase immune complexes in patients with high Streptokinase antibody levels, and show that these complexes are cleared rapidly from the circulation, leaving more persistent signs of complement activation. We conclude that free C3d is a good indicator of ongoing complement activation, whereas C3d on erythrocytes indicates that complement activation has recently taken place.
PubMed ID
8222319 View in PubMed
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Guidelines for the use of intravenous thrombolytic agents in acute myocardial infarction. Ontario Medical Association Consensus Group on Thrombolytic Therapy.

https://arctichealth.org/en/permalink/ahliterature230736
Source
CMAJ. 1989 Jun 1;140(11):1289-99
Publication Type
Article
Date
Jun-1-1989
Author
C D Naylor
P W Armstrong
Author Affiliation
Thrombolysis Guidelines, Ontario Medical Association, Toronto.
Source
CMAJ. 1989 Jun 1;140(11):1289-99
Date
Jun-1-1989
Language
English
Publication Type
Article
Keywords
Angiography
Cost-Benefit Analysis
Hemorrhage - prevention & control
Humans
Injections, Intravenous
Myocardial Infarction - drug therapy - radiography
Ontario
Physicians
Risk factors
Streptokinase - administration & dosage - adverse effects - therapeutic use
Time Factors
Tissue Plasminogen Activator - administration & dosage - adverse effects - therapeutic use
Abstract
A consensus group convened under the auspices of the Ontario Medical Association produced guidelines for the use of intravenous thrombolytic agents in acute myocardial infarction. The guidelines, updated to December 1988, include the following points. 1) Any hospital that routinely accepts the responsibility for looking after patients with acute myocardial infarction could offer thrombolytic therapy if monitoring facilities are available and if the staff are experienced in the treatment of cardiac rhythm disturbances. 2) Before treatment, all patients must be carefully screened for factors predisposing to hemorrhagic complications. 3) A physician should be clearly designated as responsible for the care of the patient receiving an infusion and be available in the event of problems. 4) For the two approved agents the usual dosages are as follows: streptokinase, 1.5 million units given over 1 hour; and tissue-type plasminogen activator (tPA), 100 mg over 3 hours, delivered as 60 mg in the first hour (of which 6 to 7 mg should be given as a bolus in the first 1 to 2 minutes) and then an infusion of 20 mg/h over the next 2 hours. 5) Intravenous thrombolytics should be considered for any patient with presumed acute myocardial infarction, as suggested by prolonged chest pain or other appropriate symptoms and typical electrocardiographic changes. Expeditious treatment is critical, since myocardial necrosis occurs within hours. 6) Emergency angiography is indicated for patients with hemodynamic compromise and no apparent response to streptokinase or tPA and in those with recurrent chest pain suggestive of acute myocardial infarction despite an apparent response to intravenous thrombolysis. Angiography before discharge is recommended for patients with postinfarction angina or evidence from noninvasive testing of significant residual ischemic risk. 7) There is insufficient evidence to choose between streptokinase and tPA on the basis of the two most important outcome measures: patient survival and myocardial preservation. More conclusive evidence comparing tPA, streptokinase and another promising agent, acylated plasminogen-streptokinase activator complex, will be available in 1989-90.
Notes
Cites: Prog Cardiovasc Dis. 1988 Jan-Feb;30(4):235-663275989
Cites: Lancet. 1988 Jan 30;1(8579):197-2032893037
Cites: N Engl J Med. 1988 Mar 3;318(9):576-92963215
Cites: Eur Heart J. 1988 Feb;9(2):197-83127215
Cites: N Engl J Med. 1988 Apr 7;318(14):923-43352678
Cites: Ann Intern Med. 1988 May;108(5):658-623128953
Cites: N Engl J Med. 1988 Jun 9;318(23):1512-203285216
Cites: Circulation. 1977 Nov;56(5):786-94912839
Cites: Lab Invest. 1979 Jun;40(6):633-44449273
Cites: N Engl J Med. 1980 Oct 16;303(16):897-9027412821
Cites: Am J Cardiol. 1982 Nov;50(5):933-77137045
Cites: Am J Cardiol. 1984 May 1;53(9):1209-166711421
Cites: Circulation. 1984 Dec;70(6):1012-76388898
Cites: Lancet. 1985 Apr 13;1(8433):842-72858711
Cites: Lancet. 1985 Sep 14;2(8455):578-822863596
Cites: Eur Heart J. 1985 Jul;6(7):556-853899654
Cites: J Am Coll Cardiol. 1985 Nov;6(5):957-624045046
Cites: Lancet. 1985 Nov 2;2(8462):965-92865502
Cites: N Engl J Med. 1985 Nov 28;313(22):1384-94058533
Cites: Circulation. 1985 Dec;72(6):1321-64064276
Cites: CMAJ. 1986 Feb 15;134(4):333-403080215
Cites: Circulation. 1986 Feb;73(2):347-523080262
Cites: N Engl J Med. 1986 Aug 14;315(7):417-233736619
Cites: Circulation. 1987 Feb;75(2):420-82948735
Cites: Am J Cardiol. 1987 Mar 1;59(6):501-43548298
Cites: Circulation. 1987 Apr;75(4):817-293103950
Cites: Circulation. 1987 Jun;75(6):1192-93105913
Cites: J Am Coll Cardiol. 1987 Jun;9(6):1205-132953770
Cites: Circulation. 1987 Jul;76(1):142-543109764
Cites: N Engl J Med. 1987 Sep 3;317(10):624-62956517
Cites: Am J Cardiol. 1987 Aug 1;60(4):231-73113222
Cites: J Am Coll Cardiol. 1987 Sep;10(3):479-903114349
Cites: N Engl J Med. 1987 Oct 1;317(14):850-52888018
Cites: J Am Coll Cardiol. 1987 Nov;10(5 Suppl B):75B-78B2959717
Cites: J Am Coll Cardiol. 1987 Nov;10(5 Suppl B):79B-90B2959718
Cites: J Am Coll Cardiol. 1987 Nov;10(5 Suppl B):91B-95B3117861
Cites: J Am Coll Cardiol. 1987 Dec;10(6):1173-73119685
Cites: Lancet. 1987 Nov 28;2(8570):12782890891
Cites: N Engl J Med. 1987 Dec 24;317(26):1613-82960897
Cites: CMAJ. 1988 Sep 15;139(6):487-933044553
Cites: Circulation. 1988 Sep;78(3):546-563136953
Cites: Lancet. 1988 Sep 3;2(8610):525-302900919
Cites: JAMA. 1988 Oct 14;260(14):2088-932901501
Cites: Lancet. 1988 Nov 19;2(8621):1187-82903390
Cites: Lancet. 1988 Nov 19;2(8621):1188-92903391
Cites: Circulation. 1988 Dec;78(6):1345-512973377
Cites: J Am Coll Cardiol. 1988 Dec;12(6 Suppl A):58A-68A3057037
Cites: Ann Intern Med. 1988 Dec 15;109(12):970-802973762
Cites: N Engl J Med. 1989 Feb 2;320(5):318-92911329
Erratum In: Can Med Assoc J 1989 Jul 15;141(2):104
PubMed ID
2497946 View in PubMed
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Impact of intravenous thrombolysis on short-term coronary revascularization rates. A meta-analysis.

https://arctichealth.org/en/permalink/ahliterature228591
Source
JAMA. 1990 Aug 8;264(6):697-702
Publication Type
Article
Date
Aug-8-1990
Author
C D Naylor
S B Jaglal
Author Affiliation
Clinical Epidemiology Unit, Sunnybrook Health Science Centre, North York, Canada.
Source
JAMA. 1990 Aug 8;264(6):697-702
Date
Aug-8-1990
Language
English
Publication Type
Article
Keywords
Angiography - statistics & numerical data - utilization
Angioplasty, Balloon, Coronary - statistics & numerical data - utilization
Canada
Fibrinolytic Agents - administration & dosage
Health planning
Humans
Infusions, Intravenous
Meta-Analysis as Topic
Multicenter Studies as Topic
Myocardial Infarction - drug therapy
Myocardial Revascularization - statistics & numerical data - utilization
Randomized Controlled Trials as Topic
Streptokinase - administration & dosage
Thrombolytic Therapy
Tissue Plasminogen Activator - administration & dosage
Abstract
Evidence of the potential impact of intravenous thrombolytic therapy on short-term revascularization rates among patients with acute myocardial infarction was sought. Because nonrandomized comparisons with conventional treatment would be subject to various confounders, a meta-analysis of randomized controlled trials was performed. Seven trials were included, applying standard doses of either tissue plasminogen activator or streptokinase without an aggressive revascularization protocol. Follow-up ranged from 14 to 30 days. The revascularization rates among treated patients in all trials were lower than in the conservative arm of the Thrombolysis in Myocardial Infarction Phase II trial, which established the current procedural benchmarks for postthrombolysis management. However, the aggregate volume of bypass surgery and angioplasty in patients treated with tissue plasminogen activator was more than double that of controls (odds ratio, 2.25; 95% confidence interval, 1.31 to 3.94), with a smaller but still significant increase for streptokinase-treated patients (odds ratio, 1.66; 95% confidence interval, 1.08 to 2.59). Combining all trials, the increase in mechanical revascularization was 80% (95% confidence interval, 33% to 144%). Thus, for patterns of practice currently accepted in North America, intravenous thrombolysis for myocardial infarction leads to a significant short-term increase in clinical and angiographic indications for revascularization as compared with conventional treatment.
Notes
Comment In: JAMA. 1991 Jan 2;265(1):28-91898523
Comment In: JAMA. 1990 Aug 8;264(6):738-92142742
PubMed ID
2142741 View in PubMed
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Plasminogen depletion during streptokinase treatment or two-chain urokinase incubation correlates with decreased clot lysability ex vivo and in vitro.

https://arctichealth.org/en/permalink/ahliterature54955
Source
Thromb Haemost. 1993 Dec 20;70(6):998-1004
Publication Type
Article
Date
Dec-20-1993
Author
P T Onundarson
H M Haraldsson
L. Bergmann
C W Francis
V J Marder
Author Affiliation
Department of Hematology, Landspítalinn University Hospital, Reykjavík, Iceland.
Source
Thromb Haemost. 1993 Dec 20;70(6):998-1004
Date
Dec-20-1993
Language
English
Publication Type
Article
Keywords
Amino Acid Sequence
Comparative Study
Humans
In Vitro
Infusions, Intravenous
Iodine Radioisotopes - diagnostic use
Molecular Sequence Data
Myocardial Infarction - blood - complications - drug therapy
Plasminogen - drug effects
Research Support, Non-U.S. Gov't
Streptokinase - administration & dosage
Thrombolytic Therapy
Thrombophlebitis - blood - complications - drug therapy
Urinary Plasminogen Activator - blood - drug effects
Abstract
The relationship between lytic state variables and ex vivo clot lysability was investigated in blood drawn from patients during streptokinase administration for acute myocardial infarction. A lytic state was already evident after 5 min of treatment and after 20 min the plasminogen concentration had decreased to 24%, antiplasmin to 7% and fibrinogen 0.2 g/l. Lysis of radiolabeled retracted clots in the patient plasmas decreased from 37 +/- 8% after 5 min to 21 +/- 8% at 10 min and was significantly lower (8 +/- 9%, p
PubMed ID
8165625 View in PubMed
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[Prognosis of return to work after streptokinase-treated acute myocardial infarction]

https://arctichealth.org/en/permalink/ahliterature54601
Source
Ugeskr Laeger. 1996 Nov 11;158(46):6620-2
Publication Type
Article
Date
Nov-11-1996
Author
J H Christensen
L. Ravn
S E Rasmussen
H T Sørensen
Author Affiliation
Kardiologisk afdeling, Aalborg Sygehus Syd.
Source
Ugeskr Laeger. 1996 Nov 11;158(46):6620-2
Date
Nov-11-1996
Language
Danish
Publication Type
Article
Keywords
Adult
Cohort Studies
Comparative Study
Denmark
English Abstract
Fibrinolytic Agents - administration & dosage
Humans
Middle Aged
Myocardial Infarction - drug therapy - rehabilitation
Prognosis
Questionnaires
Research Support, Non-U.S. Gov't
Streptokinase - administration & dosage
Thrombolytic Therapy
Time Factors
Work
Abstract
In order to assess the impact of thrombolytic therapy on return to work 18 months after a first myocardial infarction 32 patients treated with streptokinase were compared to 30 patients not treated with streptokinase. The study was designed as a historical cohort study. The patients in both groups had continuous chest pain of less than six hours prior to admission and electrocardiographic changes consistent with acute myocardial infarction. The two groups were comparable with respect to medical variables related to their myocardial infarction and to educational level. A total of 17 patients (53%) in the streptokinase group and 16 (53%) among controls had stopped working 18 months after their MI. An association between the treatment and the working status could not be found (relative risk = 1.0) nor could it be found if the figures were corrected for deaths and retirements because of age. In conclusion, this study could not demonstrate any beneficial effect of thrombolytic therapy on the return to work 18 months after an initial myocardial infarction.
PubMed ID
8966830 View in PubMed
Less detail

Streptokinase resistance in medical patients in Oslo.

https://arctichealth.org/en/permalink/ahliterature250016
Source
Scand J Haematol. 1977 Apr;18(4):348-52
Publication Type
Article
Date
Apr-1977
Author
H. Arnesen
M. Rygh
B. Ly
E. Jakobsen
Source
Scand J Haematol. 1977 Apr;18(4):348-52
Date
Apr-1977
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Aged
Drug resistance
Female
Humans
Male
Middle Aged
Norway
Streptokinase - administration & dosage - immunology
Abstract
The streptokinase titrated initial dose (TID) was estimated in 31 2 patients consecutively admitted to a medical department in Oslo. 93% had a TID below 250,000 IU, 97% below 425,000 IU and 98.5% below 650,000 IU. No differences were found between the two sexes. The highest values were found in patients 50--60 years old. Otherwise, no differences were found between different age groups from 10 to 90 years of age. Two patients with extremely high TID values were both anamnestically prone to streptococcal infections. It is concluded that our standard initial dose of 250,000 IU of streptokinase is sufcient for the great majority of our patients. Pre-treatment test for TID is recommended only when recent streptococcal infections are suspected.
PubMed ID
857296 View in PubMed
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[Streptokinase treatment in Nordkapp]

https://arctichealth.org/en/permalink/ahliterature54371
Source
Tidsskr Nor Laegeforen. 1998 Jun 30;118(17):2632-3
Publication Type
Article
Date
Jun-30-1998
Author
H. Bjøru
E. Langfeldt
A. Løvland
B. Nordang
S. Høybjør
Author Affiliation
Nordkapp legestasjon, Honningsvåg.
Source
Tidsskr Nor Laegeforen. 1998 Jun 30;118(17):2632-3
Date
Jun-30-1998
Language
Norwegian
Publication Type
Article
Keywords
Emergency medical services
English Abstract
Family Practice
Fibrinolytic Agents - administration & dosage
Humans
Myocardial Infarction - drug therapy
Norway
Physician's Practice Patterns
Streptokinase - administration & dosage
Thrombolytic Therapy
Abstract
Since July 1994 the primary health care service in the municipality of Nordkapp has been conducting a study on the feasibility of prehospital thrombolytic treatment of acute myocardial infarction. The diagnosis of infarction was verified in all nine patients included in the study up until February 1998. In one patient the treatment was ended because of serious complications; in the other eight the treatment was without complications. There was a significant time saving for these patients compared to being given the same treatment in hospital. The authors argue that thrombolytic treatment of acute myocardial infarction should be defined in standard procedures and administered by general practitioners.
PubMed ID
9673512 View in PubMed
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[The effect of the duration of coronary occlusion on the healing of an experimental myocardial infarct]

https://arctichealth.org/en/permalink/ahliterature54131
Source
Fiziol Zh. 1999;45(6):26-30
Publication Type
Article
Date
1999
Author
D V Syroïd
V M Sokrut
I R Shvyrenko
Author Affiliation
M. Gorky Medical University, Ministry of Public Health of Ukraine, Donetsk.
Source
Fiziol Zh. 1999;45(6):26-30
Date
1999
Language
Ukrainian
Publication Type
Article
Keywords
Animals
Aspartate Aminotransferases - metabolism
Comparative Study
Coronary Disease - drug therapy - enzymology - physiopathology
Creatine Kinase - metabolism
Disease Models, Animal
Dogs
Drug Evaluation, Preclinical
English Abstract
Fibrinolytic Agents - administration & dosage
Myocardial Infarction - drug therapy - enzymology - physiopathology
Myocardial Ischemia - drug therapy - enzymology - physiopathology
Myocardium - enzymology - pathology
Necrosis
Streptokinase - administration & dosage
Thrombolytic Therapy
Time Factors
Wound Healing - physiology
Abstract
Increasing the period of myocardial ischaemia prior to conduction of reperfusion adequality induces complicated healing of experimental myocardial infarction, thereby resulting in postinfarctional aneurysm of the heart. Complicated healing of myocardial infarction upon of coronary blood re-circulation after 3 or more hours of ischaemia, happens due to disbalance of necrotic and reparative processes in the infarct zone. Conduction of reperfusion induces activation of necrotic processes with retention and slowdown of reparative processes.
PubMed ID
10687078 View in PubMed
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12 records – page 1 of 2.