Aspirin Resistance in Children with Heart Disease at Risk for Thromboembolism: Prevalence and Possible Mechanisms
Aspirin is used to prevent thromboembolism in children with heart disease without evidence supporting its efficacy. Studies in adults report a 5%–51% prevalence of aspirin resistance, yet the mechanisms involved are poorly understood. Our aims were to determine its prevalence in these children and t...
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| Veröffentlicht in: | Pediatric cardiology 2008-03, Vol.29 (2), p.285-291 |
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| creator | Heistein, Lisa C. Scott, William A. Zellers, Thomas M. Fixler, David E. Ramaciotti, Claudio Journeycake, Janna M. Lemler, Matthew S. |
| description | Aspirin is used to prevent thromboembolism in children with heart disease without evidence supporting its efficacy. Studies in adults report a 5%–51% prevalence of aspirin resistance, yet the mechanisms involved are poorly understood. Our aims were to determine its prevalence in these children and to explore its possible mechanisms. One hundred twenty-three cardiac patients routinely receiving aspirin were prospectively enrolled. Platelet function was measured by Platelet Function Analyzer (PFA)-100 using epinephrine and adenosine diphosphate (ADP) agonists. Aspirin resistance was defined as failure to prolong the epinephrine closure time following aspirin administration. Urine levels of 11-dehydro-thromboxane B
2
(11-dTXB
2
) were measured to determine inhibition of the cyclo-oxygenase pathway. The prevalence of aspirin resistance was 26%. Median ADP closure time was shorter for aspirin-resistant (79.60–115 s) than for aspirin-sensitive (100.60–240 s) patients (
p |
| doi_str_mv | 10.1007/s00246-007-9098-7 |
| format | Article |
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2
(11-dTXB
2
) were measured to determine inhibition of the cyclo-oxygenase pathway. The prevalence of aspirin resistance was 26%. Median ADP closure time was shorter for aspirin-resistant (79.60–115 s) than for aspirin-sensitive (100.60–240 s) patients (
p
< 0.01). 11-dTXB
2
levels did not correlate with aspirin resistance. Aspirin-resistant patients had higher 11-dTXB
2
levels before (7297 vs. 4160 pg/mg creatinine;
p
< 0.01) and after (2153 vs. 1412 pg/mg;
p
= 0.03) aspirin, with a similar percentage decrease in thromboxane (70.5% vs. 66.1%;
p
= 0.43). Our findings suggest that resistance is not entirely due to lack of inhibition of platelet thromboxane production. Alternative sources of thromboxane and thromboxane-independent mechanisms, such as ADP-induced platelet activation, may contribute to aspirin resistance.</description><identifier>ISSN: 0172-0643</identifier><identifier>EISSN: 1432-1971</identifier><identifier>DOI: 10.1007/s00246-007-9098-7</identifier><identifier>PMID: 17896127</identifier><language>eng</language><publisher>New York: Springer-Verlag</publisher><subject>Adolescent ; Aspirin - administration & dosage ; Aspirin - therapeutic use ; Blood Platelets - drug effects ; Blood Platelets - physiology ; Cardiac Surgery ; Cardiology ; Child ; Child, Preschool ; Dose-Response Relationship, Drug ; Drug Resistance - physiology ; Female ; Follow-Up Studies ; Heart Defects, Congenital - complications ; Heart Defects, Congenital - metabolism ; Humans ; Infant ; Male ; Medicine ; Medicine & Public Health ; Original ; Platelet Aggregation Inhibitors - administration & dosage ; Platelet Aggregation Inhibitors - therapeutic use ; Prevalence ; Prognosis ; Retrospective Studies ; Risk Factors ; Texas - epidemiology ; Thromboembolism - epidemiology ; Thromboembolism - etiology ; Thromboembolism - prevention & control ; Thromboxane B2 - analogs & derivatives ; Thromboxane B2 - urine ; Vascular Surgery</subject><ispartof>Pediatric cardiology, 2008-03, Vol.29 (2), p.285-291</ispartof><rights>Springer Science+Business Media, LLC 2007</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c342t-cd921da2c245b8a25249cc9c84f62185491ef8966e8013d616d3719bb11fc593</citedby><cites>FETCH-LOGICAL-c342t-cd921da2c245b8a25249cc9c84f62185491ef8966e8013d616d3719bb11fc593</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s00246-007-9098-7$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00246-007-9098-7$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17896127$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Heistein, Lisa C.</creatorcontrib><creatorcontrib>Scott, William A.</creatorcontrib><creatorcontrib>Zellers, Thomas M.</creatorcontrib><creatorcontrib>Fixler, David E.</creatorcontrib><creatorcontrib>Ramaciotti, Claudio</creatorcontrib><creatorcontrib>Journeycake, Janna M.</creatorcontrib><creatorcontrib>Lemler, Matthew S.</creatorcontrib><title>Aspirin Resistance in Children with Heart Disease at Risk for Thromboembolism: Prevalence and Possible Mechanisms</title><title>Pediatric cardiology</title><addtitle>Pediatr Cardiol</addtitle><addtitle>Pediatr Cardiol</addtitle><description>Aspirin is used to prevent thromboembolism in children with heart disease without evidence supporting its efficacy. Studies in adults report a 5%–51% prevalence of aspirin resistance, yet the mechanisms involved are poorly understood. Our aims were to determine its prevalence in these children and to explore its possible mechanisms. One hundred twenty-three cardiac patients routinely receiving aspirin were prospectively enrolled. Platelet function was measured by Platelet Function Analyzer (PFA)-100 using epinephrine and adenosine diphosphate (ADP) agonists. Aspirin resistance was defined as failure to prolong the epinephrine closure time following aspirin administration. Urine levels of 11-dehydro-thromboxane B
2
(11-dTXB
2
) were measured to determine inhibition of the cyclo-oxygenase pathway. The prevalence of aspirin resistance was 26%. Median ADP closure time was shorter for aspirin-resistant (79.60–115 s) than for aspirin-sensitive (100.60–240 s) patients (
p
< 0.01). 11-dTXB
2
levels did not correlate with aspirin resistance. Aspirin-resistant patients had higher 11-dTXB
2
levels before (7297 vs. 4160 pg/mg creatinine;
p
< 0.01) and after (2153 vs. 1412 pg/mg;
p
= 0.03) aspirin, with a similar percentage decrease in thromboxane (70.5% vs. 66.1%;
p
= 0.43). Our findings suggest that resistance is not entirely due to lack of inhibition of platelet thromboxane production. Alternative sources of thromboxane and thromboxane-independent mechanisms, such as ADP-induced platelet activation, may contribute to aspirin resistance.</description><subject>Adolescent</subject><subject>Aspirin - administration & dosage</subject><subject>Aspirin - therapeutic use</subject><subject>Blood Platelets - drug effects</subject><subject>Blood Platelets - physiology</subject><subject>Cardiac Surgery</subject><subject>Cardiology</subject><subject>Child</subject><subject>Child, Preschool</subject><subject>Dose-Response Relationship, Drug</subject><subject>Drug Resistance - physiology</subject><subject>Female</subject><subject>Follow-Up Studies</subject><subject>Heart Defects, Congenital - complications</subject><subject>Heart Defects, Congenital - metabolism</subject><subject>Humans</subject><subject>Infant</subject><subject>Male</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Original</subject><subject>Platelet Aggregation Inhibitors - administration & dosage</subject><subject>Platelet Aggregation Inhibitors - therapeutic use</subject><subject>Prevalence</subject><subject>Prognosis</subject><subject>Retrospective Studies</subject><subject>Risk Factors</subject><subject>Texas - epidemiology</subject><subject>Thromboembolism - epidemiology</subject><subject>Thromboembolism - etiology</subject><subject>Thromboembolism - prevention & control</subject><subject>Thromboxane B2 - analogs & derivatives</subject><subject>Thromboxane B2 - urine</subject><subject>Vascular Surgery</subject><issn>0172-0643</issn><issn>1432-1971</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kE1v2zAMhoVhxZq2-wG7DDrt5k2UPyTtVqTtUqBFgyB3QZbpRZ0_UtFZ0X9fGQmw2w4ESfDhC_Jl7AuI7yCE-kFCyKLKUpkZYXSmPrAFFLnMwCj4yBYClMxEVeTn7ILoWQihhS4_sXNQ2lQg1YK9XNM-xDDwDVKgyQ0eeeqWu9A1EQf-GqYdX6GLE78JhI6Qu4lvAv3h7Rj5dhfHvh4xRReo_8nXEf-6DmcZNzR8PRKFukP-iH7nhoTQFTtrXUf4-ZQv2fbudrtcZQ9Pv-6X1w-Zzws5Zb4xEhonvSzKWjtZysJ4b7wu2kqCLgsD2KYvKtQC8qaCqskVmLoGaH1p8kv27Si7j-PLAWmyfSCPXecGHA9klciNFmoG4Qj6mI6N2Np9DL2LbxaEnW22R5vtXM42W5V2vp7ED3WPzb-Nk68JkEeA0mj4jdE-j4c4pH__o_oOWnyIkw</recordid><startdate>20080301</startdate><enddate>20080301</enddate><creator>Heistein, Lisa C.</creator><creator>Scott, William A.</creator><creator>Zellers, Thomas M.</creator><creator>Fixler, David E.</creator><creator>Ramaciotti, Claudio</creator><creator>Journeycake, Janna M.</creator><creator>Lemler, Matthew S.</creator><general>Springer-Verlag</general><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>20080301</creationdate><title>Aspirin Resistance in Children with Heart Disease at Risk for Thromboembolism: Prevalence and Possible Mechanisms</title><author>Heistein, Lisa C. ; Scott, William A. ; Zellers, Thomas M. ; Fixler, David E. ; Ramaciotti, Claudio ; Journeycake, Janna M. ; Lemler, Matthew S.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c342t-cd921da2c245b8a25249cc9c84f62185491ef8966e8013d616d3719bb11fc593</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Adolescent</topic><topic>Aspirin - administration & dosage</topic><topic>Aspirin - therapeutic use</topic><topic>Blood Platelets - drug effects</topic><topic>Blood Platelets - physiology</topic><topic>Cardiac Surgery</topic><topic>Cardiology</topic><topic>Child</topic><topic>Child, Preschool</topic><topic>Dose-Response Relationship, Drug</topic><topic>Drug Resistance - physiology</topic><topic>Female</topic><topic>Follow-Up Studies</topic><topic>Heart Defects, Congenital - complications</topic><topic>Heart Defects, Congenital - metabolism</topic><topic>Humans</topic><topic>Infant</topic><topic>Male</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Original</topic><topic>Platelet Aggregation Inhibitors - administration & dosage</topic><topic>Platelet Aggregation Inhibitors - therapeutic use</topic><topic>Prevalence</topic><topic>Prognosis</topic><topic>Retrospective Studies</topic><topic>Risk Factors</topic><topic>Texas - epidemiology</topic><topic>Thromboembolism - epidemiology</topic><topic>Thromboembolism - etiology</topic><topic>Thromboembolism - prevention & control</topic><topic>Thromboxane B2 - analogs & derivatives</topic><topic>Thromboxane B2 - urine</topic><topic>Vascular Surgery</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Heistein, Lisa C.</creatorcontrib><creatorcontrib>Scott, William A.</creatorcontrib><creatorcontrib>Zellers, Thomas M.</creatorcontrib><creatorcontrib>Fixler, David E.</creatorcontrib><creatorcontrib>Ramaciotti, Claudio</creatorcontrib><creatorcontrib>Journeycake, Janna M.</creatorcontrib><creatorcontrib>Lemler, Matthew S.</creatorcontrib><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>Pediatric cardiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Heistein, Lisa C.</au><au>Scott, William A.</au><au>Zellers, Thomas M.</au><au>Fixler, David E.</au><au>Ramaciotti, Claudio</au><au>Journeycake, Janna M.</au><au>Lemler, Matthew S.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Aspirin Resistance in Children with Heart Disease at Risk for Thromboembolism: Prevalence and Possible Mechanisms</atitle><jtitle>Pediatric cardiology</jtitle><stitle>Pediatr Cardiol</stitle><addtitle>Pediatr Cardiol</addtitle><date>2008-03-01</date><risdate>2008</risdate><volume>29</volume><issue>2</issue><spage>285</spage><epage>291</epage><pages>285-291</pages><issn>0172-0643</issn><eissn>1432-1971</eissn><abstract>Aspirin is used to prevent thromboembolism in children with heart disease without evidence supporting its efficacy. Studies in adults report a 5%–51% prevalence of aspirin resistance, yet the mechanisms involved are poorly understood. Our aims were to determine its prevalence in these children and to explore its possible mechanisms. One hundred twenty-three cardiac patients routinely receiving aspirin were prospectively enrolled. Platelet function was measured by Platelet Function Analyzer (PFA)-100 using epinephrine and adenosine diphosphate (ADP) agonists. Aspirin resistance was defined as failure to prolong the epinephrine closure time following aspirin administration. Urine levels of 11-dehydro-thromboxane B
2
(11-dTXB
2
) were measured to determine inhibition of the cyclo-oxygenase pathway. The prevalence of aspirin resistance was 26%. Median ADP closure time was shorter for aspirin-resistant (79.60–115 s) than for aspirin-sensitive (100.60–240 s) patients (
p
< 0.01). 11-dTXB
2
levels did not correlate with aspirin resistance. Aspirin-resistant patients had higher 11-dTXB
2
levels before (7297 vs. 4160 pg/mg creatinine;
p
< 0.01) and after (2153 vs. 1412 pg/mg;
p
= 0.03) aspirin, with a similar percentage decrease in thromboxane (70.5% vs. 66.1%;
p
= 0.43). Our findings suggest that resistance is not entirely due to lack of inhibition of platelet thromboxane production. Alternative sources of thromboxane and thromboxane-independent mechanisms, such as ADP-induced platelet activation, may contribute to aspirin resistance.</abstract><cop>New York</cop><pub>Springer-Verlag</pub><pmid>17896127</pmid><doi>10.1007/s00246-007-9098-7</doi><tpages>7</tpages></addata></record> |
| fulltext | fulltext |
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| ispartof | Pediatric cardiology, 2008-03, Vol.29 (2), p.285-291 |
| issn | 0172-0643 1432-1971 |
| language | eng |
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| source | MEDLINE; SpringerNature Journals |
| subjects | Adolescent Aspirin - administration & dosage Aspirin - therapeutic use Blood Platelets - drug effects Blood Platelets - physiology Cardiac Surgery Cardiology Child Child, Preschool Dose-Response Relationship, Drug Drug Resistance - physiology Female Follow-Up Studies Heart Defects, Congenital - complications Heart Defects, Congenital - metabolism Humans Infant Male Medicine Medicine & Public Health Original Platelet Aggregation Inhibitors - administration & dosage Platelet Aggregation Inhibitors - therapeutic use Prevalence Prognosis Retrospective Studies Risk Factors Texas - epidemiology Thromboembolism - epidemiology Thromboembolism - etiology Thromboembolism - prevention & control Thromboxane B2 - analogs & derivatives Thromboxane B2 - urine Vascular Surgery |
| title | Aspirin Resistance in Children with Heart Disease at Risk for Thromboembolism: Prevalence and Possible Mechanisms |
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