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Thrombolytic therapy in acute myocardial infarction : Comparison of procoagulant effects of streptokinase and alteplase regimens with focus on the Kallikrein system and plasmin
Thrombolytic therapy in patients with acute myocardial infarction (AMI) is hampered by procoagulant effects. In vitro studies have indicated that plasmin stimulation activates the kallikrein-contact-phase system, resulting in thrombin activation. This prospective comparative study was designed to ex...
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| Published in: | Circulation (New York, N.Y.) N.Y.), 1998-12, Vol.98 (23), p.2527-2533 |
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| container_end_page | 2533 |
| container_issue | 23 |
| container_start_page | 2527 |
| container_title | Circulation (New York, N.Y.) |
| container_volume | 98 |
| creator | HOFFMEISTER, H. M SZABO, S KASTNER, C BEYER, M. E HELBER, U KAZMAIER, S WENDEL, H. P HELLER, W SEIPEL, L |
| description | Thrombolytic therapy in patients with acute myocardial infarction (AMI) is hampered by procoagulant effects. In vitro studies have indicated that plasmin stimulation activates the kallikrein-contact-phase system, resulting in thrombin activation. This prospective comparative study was designed to examine the procoagulant effects of streptokinase or alteplase in AMI.
Sixty-one patients with AMI received 1.5 million U of streptokinase or front-loaded alteplase (up to 100 mg) and systemic heparin. Twenty-four patients with AMI and no thrombolytic therapy and 30 control subjects were examined for comparison. Molecular markers of thrombin, plasmin activation, and coagulation activities were determined before therapy and serially for up to 10 days. Moderate thrombin (initial thrombin-antithrombin [TAT] complex 18+/-5 versus 4+/-0.3 microg/L, P |
| doi_str_mv | 10.1161/01.CIR.98.23.2527 |
| format | article |
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Sixty-one patients with AMI received 1.5 million U of streptokinase or front-loaded alteplase (up to 100 mg) and systemic heparin. Twenty-four patients with AMI and no thrombolytic therapy and 30 control subjects were examined for comparison. Molecular markers of thrombin, plasmin activation, and coagulation activities were determined before therapy and serially for up to 10 days. Moderate thrombin (initial thrombin-antithrombin [TAT] complex 18+/-5 versus 4+/-0.3 microg/L, P<0.05) and kallikrein (up to 45+/-4 versus 30+/-1 U/L at 3 hours, P<0.01) activation occurs in patients with AMI. D-Dimers are increased (P<0.01), and plasmin is stimulated (P<0.01). Streptokinase and alteplase increase TAT to 50+/-17 and 51+/-18 microg/L at 3 hours and to 50+/-17 and 33+/-14 microg/L at 6 hours, respectively (P<0.01). Kallikrein activity is elevated (P<0. 01) to 76+/-5 and 71+/-7 U/L at 3 hours and 64+/-6 and 47+/-5 U/L by streptokinase and alteplase, respectively, at 6 hours. Reductions in fibrinogen and increases in D-dimers and plasmin-antiplasmin complexes are more marked (P<0.05 and 0.01) after streptokinase versus alteplase. Correlations were found among TAT, kallikrein activity, and plasmin activation (P<0.01).
The data indicate a more marked procoagulant action of the streptokinase regimen compared with front-loaded alteplase, thus supporting the hypothesis of a plasmin-mediated kallikrein activation with consecutive procoagulant action in vivo.]]></description><identifier>ISSN: 0009-7322</identifier><identifier>EISSN: 1524-4539</identifier><identifier>DOI: 10.1161/01.CIR.98.23.2527</identifier><identifier>PMID: 9843458</identifier><identifier>CODEN: CIRCAZ</identifier><language>eng</language><publisher>Hagerstown, MD: Lippincott Williams & Wilkins</publisher><subject>Acute Disease ; Adult ; Aged ; Aged, 80 and over ; Biological and medical sciences ; Blood. Blood coagulation. Reticuloendothelial system ; Female ; Fibrinolysin - analysis ; Fibrinolytic Agents - administration & dosage ; Fibrinolytic Agents - therapeutic use ; Humans ; Kallikreins - analysis ; Male ; Medical sciences ; Middle Aged ; Myocardial Infarction - blood ; Myocardial Infarction - drug therapy ; Pharmacology. Drug treatments ; Streptokinase - administration & dosage ; Streptokinase - therapeutic use ; Tissue Plasminogen Activator - administration & dosage ; Tissue Plasminogen Activator - therapeutic use</subject><ispartof>Circulation (New York, N.Y.), 1998-12, Vol.98 (23), p.2527-2533</ispartof><rights>1999 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c319t-52341d40a7e81c3fcf508fca4e0e18beadb875a7ed0c6721444313c3396e23543</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1611378$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9843458$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>HOFFMEISTER, H. M</creatorcontrib><creatorcontrib>SZABO, S</creatorcontrib><creatorcontrib>KASTNER, C</creatorcontrib><creatorcontrib>BEYER, M. E</creatorcontrib><creatorcontrib>HELBER, U</creatorcontrib><creatorcontrib>KAZMAIER, S</creatorcontrib><creatorcontrib>WENDEL, H. P</creatorcontrib><creatorcontrib>HELLER, W</creatorcontrib><creatorcontrib>SEIPEL, L</creatorcontrib><title>Thrombolytic therapy in acute myocardial infarction : Comparison of procoagulant effects of streptokinase and alteplase regimens with focus on the Kallikrein system and plasmin</title><title>Circulation (New York, N.Y.)</title><addtitle>Circulation</addtitle><description><![CDATA[Thrombolytic therapy in patients with acute myocardial infarction (AMI) is hampered by procoagulant effects. In vitro studies have indicated that plasmin stimulation activates the kallikrein-contact-phase system, resulting in thrombin activation. This prospective comparative study was designed to examine the procoagulant effects of streptokinase or alteplase in AMI.
Sixty-one patients with AMI received 1.5 million U of streptokinase or front-loaded alteplase (up to 100 mg) and systemic heparin. Twenty-four patients with AMI and no thrombolytic therapy and 30 control subjects were examined for comparison. Molecular markers of thrombin, plasmin activation, and coagulation activities were determined before therapy and serially for up to 10 days. Moderate thrombin (initial thrombin-antithrombin [TAT] complex 18+/-5 versus 4+/-0.3 microg/L, P<0.05) and kallikrein (up to 45+/-4 versus 30+/-1 U/L at 3 hours, P<0.01) activation occurs in patients with AMI. D-Dimers are increased (P<0.01), and plasmin is stimulated (P<0.01). Streptokinase and alteplase increase TAT to 50+/-17 and 51+/-18 microg/L at 3 hours and to 50+/-17 and 33+/-14 microg/L at 6 hours, respectively (P<0.01). Kallikrein activity is elevated (P<0. 01) to 76+/-5 and 71+/-7 U/L at 3 hours and 64+/-6 and 47+/-5 U/L by streptokinase and alteplase, respectively, at 6 hours. Reductions in fibrinogen and increases in D-dimers and plasmin-antiplasmin complexes are more marked (P<0.05 and 0.01) after streptokinase versus alteplase. Correlations were found among TAT, kallikrein activity, and plasmin activation (P<0.01).
The data indicate a more marked procoagulant action of the streptokinase regimen compared with front-loaded alteplase, thus supporting the hypothesis of a plasmin-mediated kallikrein activation with consecutive procoagulant action in vivo.]]></description><subject>Acute Disease</subject><subject>Adult</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Biological and medical sciences</subject><subject>Blood. Blood coagulation. Reticuloendothelial system</subject><subject>Female</subject><subject>Fibrinolysin - analysis</subject><subject>Fibrinolytic Agents - administration & dosage</subject><subject>Fibrinolytic Agents - therapeutic use</subject><subject>Humans</subject><subject>Kallikreins - analysis</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Myocardial Infarction - blood</subject><subject>Myocardial Infarction - drug therapy</subject><subject>Pharmacology. Drug treatments</subject><subject>Streptokinase - administration & dosage</subject><subject>Streptokinase - therapeutic use</subject><subject>Tissue Plasminogen Activator - administration & dosage</subject><subject>Tissue Plasminogen Activator - therapeutic use</subject><issn>0009-7322</issn><issn>1524-4539</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1998</creationdate><recordtype>article</recordtype><recordid>eNpFUcFu1DAQtRCobAsfwAHJB8Qtix07icMNrYBWVEJC5WzNOuOuqRMH2xHKX_GJOHQFp9GbN-_NjB4hrzjbc97yd4zvDzff9r3a12JfN3X3hOx4U8tKNqJ_SnaMsb7qRF0_J5cp_SiwFV1zQS56JYVs1I78vjvFMB6DX7MzNJ8wwrxSN1EwS0Y6rsFAHBz40rMQTXZhou_pIYwzRJcKCJbOMZgA94uHKVO0Fk1OWz_liHMOD26ChBSmgYLPOPsNRbx3I06J_nL5RG0wS5FM2wX0C3jvHiKWK9KaMo5_pZtsdNML8syCT_jyXK_I908f7w7X1e3XzzeHD7eVEbzPVVMLyQfJoEPFjbDGNkxZAxIZcnVEGI6qawo7MNN2NZdSCi6MEH2LtWikuCJvH33Lcz8XTFmPLhn05UcMS9Id41yxTpVB_jhoYkgpotVzdCPEVXOmt5Q047qkpHula6G3lIrm9dl8OY44_FOcYyn8mzMPyYC3ESbj0n_jlnNRVv8B0s-e9w</recordid><startdate>19981208</startdate><enddate>19981208</enddate><creator>HOFFMEISTER, H. M</creator><creator>SZABO, S</creator><creator>KASTNER, C</creator><creator>BEYER, M. E</creator><creator>HELBER, U</creator><creator>KAZMAIER, S</creator><creator>WENDEL, H. P</creator><creator>HELLER, W</creator><creator>SEIPEL, L</creator><general>Lippincott Williams & Wilkins</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>19981208</creationdate><title>Thrombolytic therapy in acute myocardial infarction : Comparison of procoagulant effects of streptokinase and alteplase regimens with focus on the Kallikrein system and plasmin</title><author>HOFFMEISTER, H. M ; SZABO, S ; KASTNER, C ; BEYER, M. E ; HELBER, U ; KAZMAIER, S ; WENDEL, H. P ; HELLER, W ; SEIPEL, L</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c319t-52341d40a7e81c3fcf508fca4e0e18beadb875a7ed0c6721444313c3396e23543</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1998</creationdate><topic>Acute Disease</topic><topic>Adult</topic><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>Biological and medical sciences</topic><topic>Blood. Blood coagulation. Reticuloendothelial system</topic><topic>Female</topic><topic>Fibrinolysin - analysis</topic><topic>Fibrinolytic Agents - administration & dosage</topic><topic>Fibrinolytic Agents - therapeutic use</topic><topic>Humans</topic><topic>Kallikreins - analysis</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Myocardial Infarction - blood</topic><topic>Myocardial Infarction - drug therapy</topic><topic>Pharmacology. Drug treatments</topic><topic>Streptokinase - administration & dosage</topic><topic>Streptokinase - therapeutic use</topic><topic>Tissue Plasminogen Activator - administration & dosage</topic><topic>Tissue Plasminogen Activator - therapeutic use</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>HOFFMEISTER, H. M</creatorcontrib><creatorcontrib>SZABO, S</creatorcontrib><creatorcontrib>KASTNER, C</creatorcontrib><creatorcontrib>BEYER, M. E</creatorcontrib><creatorcontrib>HELBER, U</creatorcontrib><creatorcontrib>KAZMAIER, S</creatorcontrib><creatorcontrib>WENDEL, H. P</creatorcontrib><creatorcontrib>HELLER, W</creatorcontrib><creatorcontrib>SEIPEL, L</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Circulation (New York, N.Y.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>HOFFMEISTER, H. M</au><au>SZABO, S</au><au>KASTNER, C</au><au>BEYER, M. E</au><au>HELBER, U</au><au>KAZMAIER, S</au><au>WENDEL, H. P</au><au>HELLER, W</au><au>SEIPEL, L</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Thrombolytic therapy in acute myocardial infarction : Comparison of procoagulant effects of streptokinase and alteplase regimens with focus on the Kallikrein system and plasmin</atitle><jtitle>Circulation (New York, N.Y.)</jtitle><addtitle>Circulation</addtitle><date>1998-12-08</date><risdate>1998</risdate><volume>98</volume><issue>23</issue><spage>2527</spage><epage>2533</epage><pages>2527-2533</pages><issn>0009-7322</issn><eissn>1524-4539</eissn><coden>CIRCAZ</coden><abstract><![CDATA[Thrombolytic therapy in patients with acute myocardial infarction (AMI) is hampered by procoagulant effects. In vitro studies have indicated that plasmin stimulation activates the kallikrein-contact-phase system, resulting in thrombin activation. This prospective comparative study was designed to examine the procoagulant effects of streptokinase or alteplase in AMI.
Sixty-one patients with AMI received 1.5 million U of streptokinase or front-loaded alteplase (up to 100 mg) and systemic heparin. Twenty-four patients with AMI and no thrombolytic therapy and 30 control subjects were examined for comparison. Molecular markers of thrombin, plasmin activation, and coagulation activities were determined before therapy and serially for up to 10 days. Moderate thrombin (initial thrombin-antithrombin [TAT] complex 18+/-5 versus 4+/-0.3 microg/L, P<0.05) and kallikrein (up to 45+/-4 versus 30+/-1 U/L at 3 hours, P<0.01) activation occurs in patients with AMI. D-Dimers are increased (P<0.01), and plasmin is stimulated (P<0.01). Streptokinase and alteplase increase TAT to 50+/-17 and 51+/-18 microg/L at 3 hours and to 50+/-17 and 33+/-14 microg/L at 6 hours, respectively (P<0.01). Kallikrein activity is elevated (P<0. 01) to 76+/-5 and 71+/-7 U/L at 3 hours and 64+/-6 and 47+/-5 U/L by streptokinase and alteplase, respectively, at 6 hours. Reductions in fibrinogen and increases in D-dimers and plasmin-antiplasmin complexes are more marked (P<0.05 and 0.01) after streptokinase versus alteplase. Correlations were found among TAT, kallikrein activity, and plasmin activation (P<0.01).
The data indicate a more marked procoagulant action of the streptokinase regimen compared with front-loaded alteplase, thus supporting the hypothesis of a plasmin-mediated kallikrein activation with consecutive procoagulant action in vivo.]]></abstract><cop>Hagerstown, MD</cop><pub>Lippincott Williams & Wilkins</pub><pmid>9843458</pmid><doi>10.1161/01.CIR.98.23.2527</doi><tpages>7</tpages></addata></record> |
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| ispartof | Circulation (New York, N.Y.), 1998-12, Vol.98 (23), p.2527-2533 |
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| source | Free E-Journal (出版社公開部分のみ） |
| subjects | Acute Disease Adult Aged Aged, 80 and over Biological and medical sciences Blood. Blood coagulation. Reticuloendothelial system Female Fibrinolysin - analysis Fibrinolytic Agents - administration & dosage Fibrinolytic Agents - therapeutic use Humans Kallikreins - analysis Male Medical sciences Middle Aged Myocardial Infarction - blood Myocardial Infarction - drug therapy Pharmacology. Drug treatments Streptokinase - administration & dosage Streptokinase - therapeutic use Tissue Plasminogen Activator - administration & dosage Tissue Plasminogen Activator - therapeutic use |
| title | Thrombolytic therapy in acute myocardial infarction : Comparison of procoagulant effects of streptokinase and alteplase regimens with focus on the Kallikrein system and plasmin |
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