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Oral antiplatelet therapy for acute ischaemic stroke
In people with acute ischaemic stroke, platelets become activated and can cause blood clots to form and block an artery in the brain, resulting in damage to part of the brain. Such damage gives rise to the symptoms of stroke. Antiplatelet therapy might reduce the volume of brain damaged by ischaemia...
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Published in: | Cochrane database of systematic reviews 2014-03, Vol.2014 (3), p.CD000029 |
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creator | Sandercock, Peter A G Counsell, Carl Tseng, Mei-Chiun Cecconi, Emanuela |
description | In people with acute ischaemic stroke, platelets become activated and can cause blood clots to form and block an artery in the brain, resulting in damage to part of the brain. Such damage gives rise to the symptoms of stroke. Antiplatelet therapy might reduce the volume of brain damaged by ischaemia and also reduce the risk of early recurrent ischaemic stroke, thereby reducing the risk of early death and improving long-term outcomes in survivors. However, antiplatelet therapy might also increase the risk of fatal or disabling intracranial haemorrhage.
To assess the efficacy and safety of immediate oral antiplatelet therapy (that is started as soon as possible and no later than two weeks after stroke onset) in people with acute presumed ischaemic stroke.
We searched the Cochrane Stroke Group Trials Register (last searched 16 October 2013), the Cochrane Central Register of Controlled Trials (CENTRAL) (The Cochrane Library Issue 4, 2013), MEDLINE (June 1998 to May 2013), and EMBASE (June 1998 to May 2013). In 1998, for a previous version of this review, we searched the register of the Antiplatelet Trialists' Collaboration, MedStrategy and contacted relevant drug companies.
Randomised trials comparing oral antiplatelet therapy (started within 14 days of the stroke) with control in people with definite or presumed ischaemic stroke.
Two review authors independently applied the inclusion criteria and assessed trial quality. For the included trials, they extracted and cross-checked the data.
We included eight trials involving 41,483 participants. No new trials have been added since the last update.Two trials testing aspirin 160 mg to 300 mg once daily, started within 48 hours of onset, contributed 98% of the data. The risk of bias was low. The maximum follow-up was six months. With treatment, there was a significant decrease in death or dependency at the end of follow-up (odds ratio (OR) 0.95, 95% confidence interval (CI) 0.91 to 0.99). For every 1000 people treated with aspirin, 13 people would avoid death or dependency (number needed to treat 79). Antiplatelet therapy was associated with a small but definite excess of symptomatic intracranial haemorrhages, but this small hazard was significantly outnumbered by the benefit, the reduction in recurrent ischaemic stroke and pulmonary embolus.
Antiplatelet therapy with aspirin 160 mg to 300 mg daily, given orally (or by nasogastric tube or per rectum in people who cannot swallow) and started within 48 hours of onset |
doi_str_mv | 10.1002/14651858.CD000029.pub3 |
format | article |
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To assess the efficacy and safety of immediate oral antiplatelet therapy (that is started as soon as possible and no later than two weeks after stroke onset) in people with acute presumed ischaemic stroke.
We searched the Cochrane Stroke Group Trials Register (last searched 16 October 2013), the Cochrane Central Register of Controlled Trials (CENTRAL) (The Cochrane Library Issue 4, 2013), MEDLINE (June 1998 to May 2013), and EMBASE (June 1998 to May 2013). In 1998, for a previous version of this review, we searched the register of the Antiplatelet Trialists' Collaboration, MedStrategy and contacted relevant drug companies.
Randomised trials comparing oral antiplatelet therapy (started within 14 days of the stroke) with control in people with definite or presumed ischaemic stroke.
Two review authors independently applied the inclusion criteria and assessed trial quality. For the included trials, they extracted and cross-checked the data.
We included eight trials involving 41,483 participants. No new trials have been added since the last update.Two trials testing aspirin 160 mg to 300 mg once daily, started within 48 hours of onset, contributed 98% of the data. The risk of bias was low. The maximum follow-up was six months. With treatment, there was a significant decrease in death or dependency at the end of follow-up (odds ratio (OR) 0.95, 95% confidence interval (CI) 0.91 to 0.99). For every 1000 people treated with aspirin, 13 people would avoid death or dependency (number needed to treat 79). Antiplatelet therapy was associated with a small but definite excess of symptomatic intracranial haemorrhages, but this small hazard was significantly outnumbered by the benefit, the reduction in recurrent ischaemic stroke and pulmonary embolus.
Antiplatelet therapy with aspirin 160 mg to 300 mg daily, given orally (or by nasogastric tube or per rectum in people who cannot swallow) and started within 48 hours of onset of presumed ischaemic stroke, reduced the risk of early recurrent ischaemic stroke without a major risk of early haemorrhagic complications; long-term outcomes were improved.</description><identifier>ISSN: 1469-493X</identifier><identifier>EISSN: 1469-493X</identifier><identifier>DOI: 10.1002/14651858.CD000029.pub3</identifier><identifier>PMID: 24668137</identifier><language>eng</language><publisher>England: John Wiley & Sons, Ltd</publisher><subject>Aspirin - therapeutic use ; Brain Ischemia - drug therapy ; Brain Ischemia - prevention & control ; Dipyridamole - therapeutic use ; Heart & circulation ; Humans ; ISCHAEMIC/UNSPECIFIED STROKE, TRANSIENT ISCHAEMIC ATTACK ; Neurology ; Platelet Aggregation Inhibitors - adverse effects ; Platelet Aggregation Inhibitors - therapeutic use ; Randomized Controlled Trials as Topic ; Risk ; Stroke - drug therapy ; Stroke - prevention & control ; Ticlopidine - therapeutic use ; Time-to-Treatment</subject><ispartof>Cochrane database of systematic reviews, 2014-03, Vol.2014 (3), p.CD000029</ispartof><rights>Copyright © 2019 The Cochrane Collaboration. Published by John Wiley & Sons, Ltd.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5393-d30ebe918f1fde397dcaa5704aaeacc26677a5dd47ebd2cbb32c9d2e72296ad23</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,776,780,881,27903,27904</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24668137$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Sandercock, Peter A G</creatorcontrib><creatorcontrib>Counsell, Carl</creatorcontrib><creatorcontrib>Tseng, Mei-Chiun</creatorcontrib><creatorcontrib>Cecconi, Emanuela</creatorcontrib><title>Oral antiplatelet therapy for acute ischaemic stroke</title><title>Cochrane database of systematic reviews</title><addtitle>Cochrane Database Syst Rev</addtitle><description>In people with acute ischaemic stroke, platelets become activated and can cause blood clots to form and block an artery in the brain, resulting in damage to part of the brain. Such damage gives rise to the symptoms of stroke. Antiplatelet therapy might reduce the volume of brain damaged by ischaemia and also reduce the risk of early recurrent ischaemic stroke, thereby reducing the risk of early death and improving long-term outcomes in survivors. However, antiplatelet therapy might also increase the risk of fatal or disabling intracranial haemorrhage.
To assess the efficacy and safety of immediate oral antiplatelet therapy (that is started as soon as possible and no later than two weeks after stroke onset) in people with acute presumed ischaemic stroke.
We searched the Cochrane Stroke Group Trials Register (last searched 16 October 2013), the Cochrane Central Register of Controlled Trials (CENTRAL) (The Cochrane Library Issue 4, 2013), MEDLINE (June 1998 to May 2013), and EMBASE (June 1998 to May 2013). In 1998, for a previous version of this review, we searched the register of the Antiplatelet Trialists' Collaboration, MedStrategy and contacted relevant drug companies.
Randomised trials comparing oral antiplatelet therapy (started within 14 days of the stroke) with control in people with definite or presumed ischaemic stroke.
Two review authors independently applied the inclusion criteria and assessed trial quality. For the included trials, they extracted and cross-checked the data.
We included eight trials involving 41,483 participants. No new trials have been added since the last update.Two trials testing aspirin 160 mg to 300 mg once daily, started within 48 hours of onset, contributed 98% of the data. The risk of bias was low. The maximum follow-up was six months. With treatment, there was a significant decrease in death or dependency at the end of follow-up (odds ratio (OR) 0.95, 95% confidence interval (CI) 0.91 to 0.99). For every 1000 people treated with aspirin, 13 people would avoid death or dependency (number needed to treat 79). Antiplatelet therapy was associated with a small but definite excess of symptomatic intracranial haemorrhages, but this small hazard was significantly outnumbered by the benefit, the reduction in recurrent ischaemic stroke and pulmonary embolus.
Antiplatelet therapy with aspirin 160 mg to 300 mg daily, given orally (or by nasogastric tube or per rectum in people who cannot swallow) and started within 48 hours of onset of presumed ischaemic stroke, reduced the risk of early recurrent ischaemic stroke without a major risk of early haemorrhagic complications; long-term outcomes were improved.</description><subject>Aspirin - therapeutic use</subject><subject>Brain Ischemia - drug therapy</subject><subject>Brain Ischemia - prevention & control</subject><subject>Dipyridamole - therapeutic use</subject><subject>Heart & circulation</subject><subject>Humans</subject><subject>ISCHAEMIC/UNSPECIFIED STROKE, TRANSIENT ISCHAEMIC ATTACK</subject><subject>Neurology</subject><subject>Platelet Aggregation Inhibitors - adverse effects</subject><subject>Platelet Aggregation Inhibitors - therapeutic use</subject><subject>Randomized Controlled Trials as Topic</subject><subject>Risk</subject><subject>Stroke - drug therapy</subject><subject>Stroke - prevention & control</subject><subject>Ticlopidine - therapeutic use</subject><subject>Time-to-Treatment</subject><issn>1469-493X</issn><issn>1469-493X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><recordid>eNpVkFtLw0AQhRdRbK3-hZJHXxL3kt3NvghSr1Doi4JvYbI7sdHczG6E_nsDVqnzMgNn-M6cIWTJaMIo5VcsVZJlMktWt3QqbpJ-LMQRmU-CiVMjXo8P5hk58_6dUmEYy07JjKdKZUzoOUk3A9QRtKHqawhYY4jCFgfod1HZDRHYMWBUebsFbCob-TB0H3hOTkqoPV7s-4K83N89rx7j9ebhaXWzjq0URsROUCzQsKxkpUNhtLMAUtMUAMFarpTWIJ1LNRaO26IQ3BrHUXNuFDguFuT6hztla9BZbMN0bd4PVQPDLu-gyv8rbbXN37qvXClluKYT4HIPGLrPEX3ImykL1jW02I0-Z5JxKY00alpdHnr9mfy-SnwD_VRvUg</recordid><startdate>20140325</startdate><enddate>20140325</enddate><creator>Sandercock, Peter A G</creator><creator>Counsell, Carl</creator><creator>Tseng, Mei-Chiun</creator><creator>Cecconi, Emanuela</creator><general>John Wiley & Sons, Ltd</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20140325</creationdate><title>Oral antiplatelet therapy for acute ischaemic stroke</title><author>Sandercock, Peter A G ; Counsell, Carl ; Tseng, Mei-Chiun ; Cecconi, Emanuela</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5393-d30ebe918f1fde397dcaa5704aaeacc26677a5dd47ebd2cbb32c9d2e72296ad23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Aspirin - therapeutic use</topic><topic>Brain Ischemia - drug therapy</topic><topic>Brain Ischemia - prevention & control</topic><topic>Dipyridamole - therapeutic use</topic><topic>Heart & circulation</topic><topic>Humans</topic><topic>ISCHAEMIC/UNSPECIFIED STROKE, TRANSIENT ISCHAEMIC ATTACK</topic><topic>Neurology</topic><topic>Platelet Aggregation Inhibitors - adverse effects</topic><topic>Platelet Aggregation Inhibitors - therapeutic use</topic><topic>Randomized Controlled Trials as Topic</topic><topic>Risk</topic><topic>Stroke - drug therapy</topic><topic>Stroke - prevention & control</topic><topic>Ticlopidine - therapeutic use</topic><topic>Time-to-Treatment</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Sandercock, Peter A G</creatorcontrib><creatorcontrib>Counsell, Carl</creatorcontrib><creatorcontrib>Tseng, Mei-Chiun</creatorcontrib><creatorcontrib>Cecconi, Emanuela</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Cochrane database of systematic reviews</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Sandercock, Peter A G</au><au>Counsell, Carl</au><au>Tseng, Mei-Chiun</au><au>Cecconi, Emanuela</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Oral antiplatelet therapy for acute ischaemic stroke</atitle><jtitle>Cochrane database of systematic reviews</jtitle><addtitle>Cochrane Database Syst Rev</addtitle><date>2014-03-25</date><risdate>2014</risdate><volume>2014</volume><issue>3</issue><spage>CD000029</spage><pages>CD000029-</pages><issn>1469-493X</issn><eissn>1469-493X</eissn><abstract>In people with acute ischaemic stroke, platelets become activated and can cause blood clots to form and block an artery in the brain, resulting in damage to part of the brain. Such damage gives rise to the symptoms of stroke. Antiplatelet therapy might reduce the volume of brain damaged by ischaemia and also reduce the risk of early recurrent ischaemic stroke, thereby reducing the risk of early death and improving long-term outcomes in survivors. However, antiplatelet therapy might also increase the risk of fatal or disabling intracranial haemorrhage.
To assess the efficacy and safety of immediate oral antiplatelet therapy (that is started as soon as possible and no later than two weeks after stroke onset) in people with acute presumed ischaemic stroke.
We searched the Cochrane Stroke Group Trials Register (last searched 16 October 2013), the Cochrane Central Register of Controlled Trials (CENTRAL) (The Cochrane Library Issue 4, 2013), MEDLINE (June 1998 to May 2013), and EMBASE (June 1998 to May 2013). In 1998, for a previous version of this review, we searched the register of the Antiplatelet Trialists' Collaboration, MedStrategy and contacted relevant drug companies.
Randomised trials comparing oral antiplatelet therapy (started within 14 days of the stroke) with control in people with definite or presumed ischaemic stroke.
Two review authors independently applied the inclusion criteria and assessed trial quality. For the included trials, they extracted and cross-checked the data.
We included eight trials involving 41,483 participants. No new trials have been added since the last update.Two trials testing aspirin 160 mg to 300 mg once daily, started within 48 hours of onset, contributed 98% of the data. The risk of bias was low. The maximum follow-up was six months. With treatment, there was a significant decrease in death or dependency at the end of follow-up (odds ratio (OR) 0.95, 95% confidence interval (CI) 0.91 to 0.99). For every 1000 people treated with aspirin, 13 people would avoid death or dependency (number needed to treat 79). Antiplatelet therapy was associated with a small but definite excess of symptomatic intracranial haemorrhages, but this small hazard was significantly outnumbered by the benefit, the reduction in recurrent ischaemic stroke and pulmonary embolus.
Antiplatelet therapy with aspirin 160 mg to 300 mg daily, given orally (or by nasogastric tube or per rectum in people who cannot swallow) and started within 48 hours of onset of presumed ischaemic stroke, reduced the risk of early recurrent ischaemic stroke without a major risk of early haemorrhagic complications; long-term outcomes were improved.</abstract><cop>England</cop><pub>John Wiley & Sons, Ltd</pub><pmid>24668137</pmid><doi>10.1002/14651858.CD000029.pub3</doi><oa>free_for_read</oa></addata></record> |
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subjects | Aspirin - therapeutic use Brain Ischemia - drug therapy Brain Ischemia - prevention & control Dipyridamole - therapeutic use Heart & circulation Humans ISCHAEMIC/UNSPECIFIED STROKE, TRANSIENT ISCHAEMIC ATTACK Neurology Platelet Aggregation Inhibitors - adverse effects Platelet Aggregation Inhibitors - therapeutic use Randomized Controlled Trials as Topic Risk Stroke - drug therapy Stroke - prevention & control Ticlopidine - therapeutic use Time-to-Treatment |
title | Oral antiplatelet therapy for acute ischaemic stroke |
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