Depressed platelet status in an elderly patient with hemorrhagic stroke after thrombolysis for acute myocardial infarction
Background —Impaired platelet function has been reported in acute myocardial infarction (AMI) and stroke. However, prospective data on the changes of platelet status in patients before the occurrence of hemorrhagic stroke after thrombolytic therapy are unavailable. Case Description —An 86-year-old m...
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Veröffentlicht in: | Stroke (1970) 1998, Vol.29 (1), p.235-238 |
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container_title | Stroke (1970) |
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creator | SEREBRUANY, V. L GURBEL, P. A SHUSTOV, A. R DALESANDRO, M. R GUMBS, C. I GRABLETZ, L. B BAHR, R. D OHMAN, E. M TOPOL, E. J |
description | Background
—Impaired platelet function has been reported in acute myocardial infarction (AMI) and stroke. However, prospective data on the changes of platelet status in patients before the occurrence of hemorrhagic stroke after thrombolytic therapy are unavailable.
Case Description
—An 86-year-old male patient was among the 23 AMI patients enrolled in the platelet study for the GUSTO-III trial. He received 325 mg of aspirin daily for at least 6 years, suffered an AMI, and was successfully reperfused with alteplase, but after 44 hours developed a large hemorrhagic stroke resulting in paraplegia. Platelet aggregation and receptor expression were measured by flow cytometry and ELISA before thrombolysis and at 3, 6, 12, and 24 hours thereafter. The percentage of platelet aggregation was lower in the stroke patient at every time point when induced by 5 μmol/L of ADP, by 10 μmol/L of ADP, and by thrombin than in the rest of the AMI group. Ristocetin and collagen-induced aggregability were within the group range. Decreased platelet glycoprotein Ib, IIb, IIIa, and IIb/IIIa and vitronectin receptor expression were observed in the stroke patient. No other differences in p24 (CD9), very late antigen-2, P-selectin, and platelet/endothelial cell adhesion molecule-1 expression were determined.
Conclusions
—Profound depression of platelet status preceded the occurrence of hemorrhagic stroke in an elderly long-term aspirin user treated with thrombolytic therapy. Initial “exhausted” platelets may be responsible for the increased risk for hemorrhagic stroke after coronary thrombolysis. |
doi_str_mv | 10.1161/01.STR.29.1.235 |
format | Article |
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—Impaired platelet function has been reported in acute myocardial infarction (AMI) and stroke. However, prospective data on the changes of platelet status in patients before the occurrence of hemorrhagic stroke after thrombolytic therapy are unavailable.
Case Description
—An 86-year-old male patient was among the 23 AMI patients enrolled in the platelet study for the GUSTO-III trial. He received 325 mg of aspirin daily for at least 6 years, suffered an AMI, and was successfully reperfused with alteplase, but after 44 hours developed a large hemorrhagic stroke resulting in paraplegia. Platelet aggregation and receptor expression were measured by flow cytometry and ELISA before thrombolysis and at 3, 6, 12, and 24 hours thereafter. The percentage of platelet aggregation was lower in the stroke patient at every time point when induced by 5 μmol/L of ADP, by 10 μmol/L of ADP, and by thrombin than in the rest of the AMI group. Ristocetin and collagen-induced aggregability were within the group range. Decreased platelet glycoprotein Ib, IIb, IIIa, and IIb/IIIa and vitronectin receptor expression were observed in the stroke patient. No other differences in p24 (CD9), very late antigen-2, P-selectin, and platelet/endothelial cell adhesion molecule-1 expression were determined.
Conclusions
—Profound depression of platelet status preceded the occurrence of hemorrhagic stroke in an elderly long-term aspirin user treated with thrombolytic therapy. Initial “exhausted” platelets may be responsible for the increased risk for hemorrhagic stroke after coronary thrombolysis.</description><identifier>ISSN: 0039-2499</identifier><identifier>EISSN: 1524-4628</identifier><identifier>DOI: 10.1161/01.STR.29.1.235</identifier><identifier>CODEN: SJCCA7</identifier><language>eng</language><publisher>Hagerstown, MD: Lippincott Williams & Wilkins</publisher><subject>Biological and medical sciences ; Drug toxicity and drugs side effects treatment ; Medical sciences ; Pharmacology. Drug treatments ; Toxicity: nervous system and muscle</subject><ispartof>Stroke (1970), 1998, Vol.29 (1), p.235-238</ispartof><rights>1998 INIST-CNRS</rights><rights>Copyright American Heart Association, Inc. Jan 1998</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c330t-3b0a861e1cee7aabcc605cd252e9ea7a2ca7aedf139591e0bfc6d9cb27f03d643</citedby><cites>FETCH-LOGICAL-c330t-3b0a861e1cee7aabcc605cd252e9ea7a2ca7aedf139591e0bfc6d9cb27f03d643</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>309,310,314,780,784,789,790,3687,4050,4051,23930,23931,25140,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=2135727$$DView record in Pascal Francis$$Hfree_for_read</backlink></links><search><creatorcontrib>SEREBRUANY, V. L</creatorcontrib><creatorcontrib>GURBEL, P. A</creatorcontrib><creatorcontrib>SHUSTOV, A. R</creatorcontrib><creatorcontrib>DALESANDRO, M. R</creatorcontrib><creatorcontrib>GUMBS, C. I</creatorcontrib><creatorcontrib>GRABLETZ, L. B</creatorcontrib><creatorcontrib>BAHR, R. D</creatorcontrib><creatorcontrib>OHMAN, E. M</creatorcontrib><creatorcontrib>TOPOL, E. J</creatorcontrib><title>Depressed platelet status in an elderly patient with hemorrhagic stroke after thrombolysis for acute myocardial infarction</title><title>Stroke (1970)</title><description>Background
—Impaired platelet function has been reported in acute myocardial infarction (AMI) and stroke. However, prospective data on the changes of platelet status in patients before the occurrence of hemorrhagic stroke after thrombolytic therapy are unavailable.
Case Description
—An 86-year-old male patient was among the 23 AMI patients enrolled in the platelet study for the GUSTO-III trial. He received 325 mg of aspirin daily for at least 6 years, suffered an AMI, and was successfully reperfused with alteplase, but after 44 hours developed a large hemorrhagic stroke resulting in paraplegia. Platelet aggregation and receptor expression were measured by flow cytometry and ELISA before thrombolysis and at 3, 6, 12, and 24 hours thereafter. The percentage of platelet aggregation was lower in the stroke patient at every time point when induced by 5 μmol/L of ADP, by 10 μmol/L of ADP, and by thrombin than in the rest of the AMI group. Ristocetin and collagen-induced aggregability were within the group range. Decreased platelet glycoprotein Ib, IIb, IIIa, and IIb/IIIa and vitronectin receptor expression were observed in the stroke patient. No other differences in p24 (CD9), very late antigen-2, P-selectin, and platelet/endothelial cell adhesion molecule-1 expression were determined.
Conclusions
—Profound depression of platelet status preceded the occurrence of hemorrhagic stroke in an elderly long-term aspirin user treated with thrombolytic therapy. Initial “exhausted” platelets may be responsible for the increased risk for hemorrhagic stroke after coronary thrombolysis.</description><subject>Biological and medical sciences</subject><subject>Drug toxicity and drugs side effects treatment</subject><subject>Medical sciences</subject><subject>Pharmacology. Drug treatments</subject><subject>Toxicity: nervous system and muscle</subject><issn>0039-2499</issn><issn>1524-4628</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1998</creationdate><recordtype>article</recordtype><recordid>eNo9kE2LFDEQhoMoOI6evQbx2j2pZPojR9kPXVgQdDyH6nTFydrTaSsZZPz1tuyyl3ovz_sUvEK8B1UDtLBTUH8_fKu1raHWpnkhNtDofbVvdf9SbJQyttJ7a1-LNzk_KKW06ZuN-HtNC1PONMplwkITFZkLlnOWcZY4S5pG4ukiFyyR5iL_xHKURzol5iP-jH6lOf0iiaEQy3LkdBrSdMkxy5BYoj8XkqdL8shjxGm1BmRfYprfilcBp0zvnnIrftzeHK6-VPdfP99dfbqvvDGqVGZQ2LdA4Ik6xMH7VjV-1I0mS9ih9uuhMYCxjQVSQ_DtaP2gu6DM2O7NVnx49C6cfp8pF_eQzjyvLx3Yrgfb63aFdo-Q55QzU3ALxxPyxYFy__d1Cty6r9PWgVv3XRsfn7SYPU6BcfYxP9c0mKbTnfkH3zJ-9w</recordid><startdate>1998</startdate><enddate>1998</enddate><creator>SEREBRUANY, V. L</creator><creator>GURBEL, P. A</creator><creator>SHUSTOV, A. R</creator><creator>DALESANDRO, M. R</creator><creator>GUMBS, C. I</creator><creator>GRABLETZ, L. B</creator><creator>BAHR, R. D</creator><creator>OHMAN, E. M</creator><creator>TOPOL, E. J</creator><general>Lippincott Williams & Wilkins</general><general>American Heart Association, Inc</general><scope>IQODW</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>K9.</scope><scope>NAPCQ</scope></search><sort><creationdate>1998</creationdate><title>Depressed platelet status in an elderly patient with hemorrhagic stroke after thrombolysis for acute myocardial infarction</title><author>SEREBRUANY, V. L ; GURBEL, P. A ; SHUSTOV, A. R ; DALESANDRO, M. R ; GUMBS, C. I ; GRABLETZ, L. B ; BAHR, R. D ; OHMAN, E. M ; TOPOL, E. J</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c330t-3b0a861e1cee7aabcc605cd252e9ea7a2ca7aedf139591e0bfc6d9cb27f03d643</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1998</creationdate><topic>Biological and medical sciences</topic><topic>Drug toxicity and drugs side effects treatment</topic><topic>Medical sciences</topic><topic>Pharmacology. Drug treatments</topic><topic>Toxicity: nervous system and muscle</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>SEREBRUANY, V. L</creatorcontrib><creatorcontrib>GURBEL, P. A</creatorcontrib><creatorcontrib>SHUSTOV, A. R</creatorcontrib><creatorcontrib>DALESANDRO, M. R</creatorcontrib><creatorcontrib>GUMBS, C. I</creatorcontrib><creatorcontrib>GRABLETZ, L. B</creatorcontrib><creatorcontrib>BAHR, R. D</creatorcontrib><creatorcontrib>OHMAN, E. M</creatorcontrib><creatorcontrib>TOPOL, E. J</creatorcontrib><collection>Pascal-Francis</collection><collection>CrossRef</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><jtitle>Stroke (1970)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>SEREBRUANY, V. L</au><au>GURBEL, P. A</au><au>SHUSTOV, A. R</au><au>DALESANDRO, M. R</au><au>GUMBS, C. I</au><au>GRABLETZ, L. B</au><au>BAHR, R. D</au><au>OHMAN, E. M</au><au>TOPOL, E. J</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Depressed platelet status in an elderly patient with hemorrhagic stroke after thrombolysis for acute myocardial infarction</atitle><jtitle>Stroke (1970)</jtitle><date>1998</date><risdate>1998</risdate><volume>29</volume><issue>1</issue><spage>235</spage><epage>238</epage><pages>235-238</pages><issn>0039-2499</issn><eissn>1524-4628</eissn><coden>SJCCA7</coden><abstract>Background
—Impaired platelet function has been reported in acute myocardial infarction (AMI) and stroke. However, prospective data on the changes of platelet status in patients before the occurrence of hemorrhagic stroke after thrombolytic therapy are unavailable.
Case Description
—An 86-year-old male patient was among the 23 AMI patients enrolled in the platelet study for the GUSTO-III trial. He received 325 mg of aspirin daily for at least 6 years, suffered an AMI, and was successfully reperfused with alteplase, but after 44 hours developed a large hemorrhagic stroke resulting in paraplegia. Platelet aggregation and receptor expression were measured by flow cytometry and ELISA before thrombolysis and at 3, 6, 12, and 24 hours thereafter. The percentage of platelet aggregation was lower in the stroke patient at every time point when induced by 5 μmol/L of ADP, by 10 μmol/L of ADP, and by thrombin than in the rest of the AMI group. Ristocetin and collagen-induced aggregability were within the group range. Decreased platelet glycoprotein Ib, IIb, IIIa, and IIb/IIIa and vitronectin receptor expression were observed in the stroke patient. No other differences in p24 (CD9), very late antigen-2, P-selectin, and platelet/endothelial cell adhesion molecule-1 expression were determined.
Conclusions
—Profound depression of platelet status preceded the occurrence of hemorrhagic stroke in an elderly long-term aspirin user treated with thrombolytic therapy. Initial “exhausted” platelets may be responsible for the increased risk for hemorrhagic stroke after coronary thrombolysis.</abstract><cop>Hagerstown, MD</cop><pub>Lippincott Williams & Wilkins</pub><doi>10.1161/01.STR.29.1.235</doi><tpages>4</tpages></addata></record> |
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source | American Heart Association Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Journals@Ovid Complete; Alma/SFX Local Collection |
subjects | Biological and medical sciences Drug toxicity and drugs side effects treatment Medical sciences Pharmacology. Drug treatments Toxicity: nervous system and muscle |
title | Depressed platelet status in an elderly patient with hemorrhagic stroke after thrombolysis for acute myocardial infarction |
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