A comparison of prasugrel and clopidogrel loading doses on platelet function: magnitude of platelet inhibition is related to active metabolite formation
Background The aim of this study was to compare rate of onset, magnitude, and consistency of platelet inhibition after administration of prasugrel or clopidogrel and to relate platelet inhibition to systemic exposure to each active metabolite. Thienopyridines are prodrugs, metabolized in vivo to act...
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| Veröffentlicht in: | The American heart journal 2007, Vol.153 (1), p.66.e9-66.e16 |
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| creator | Brandt, John T., MD Payne, Christopher D., MS Wiviott, Stephen D., MD Weerakkody, Govinda, PhD Farid, Nagy A., PhD Small, David S., PhD Jakubowski, Joseph A., PhD Naganuma, Hideo, PhD Winters, Kenneth J., MD |
| description | Background The aim of this study was to compare rate of onset, magnitude, and consistency of platelet inhibition after administration of prasugrel or clopidogrel and to relate platelet inhibition to systemic exposure to each active metabolite. Thienopyridines are prodrugs, metabolized in vivo to active metabolites that inhibit the platelet P2Y12 adenosine diphosphate (ADP) receptor. Methods This was an open-label, 2-way, crossover study that randomized healthy subjects (n = 68) to an oral loading dose (LD) of prasugrel 60 mg or clopidogrel 300 mg. Platelet aggregation response to 5 and 20 μmol/L of ADP was measured by turbidometric aggregometry. Plasma concentrations of the active metabolites of prasugrel and clopidogrel were quantified by liquid chromatography with tandem mass spectrometry detection methods. Results Inhibition of platelet aggregation (IPA) after prasugrel was significantly higher ( P < .01) than that after clopidogrel from 15 minutes through 24 hours (5 μmol/L ADP) and from 30 minutes through 24 hours (20 μmol/L ADP). For 20 μmol/L ADP, the median time to reach ≥20% IPA was 30 minutes for prasugrel and 1.5 hours for clopidogrel ( P < .001). The maximum IPA was 84.1% ± 9.5% with prasugrel versus 48.9% ± 27.0% with clopidogrel for 5 μmol/L ADP and 78.8% ± 9.2% versus 35.0% ± 24.5%, respectively, for 20 μmol/L ADP ( P < .001). Response to prasugrel was more consistent compared to clopidogrel ( P < .01). The lower IPA response to clopidogrel was associated with lower plasma concentrations of its active metabolite ( P < .001). Conclusions Prasugrel 60 mg LD results in more rapid, potent, and consistent inhibition of platelet function than clopidogrel 300 mg LD. Lower IPA responses to clopidogrel were associated with lower concentrations of its active metabolite. |
| doi_str_mv | 10.1016/j.ahj.2006.10.010 |
| format | Article |
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Thienopyridines are prodrugs, metabolized in vivo to active metabolites that inhibit the platelet P2Y12 adenosine diphosphate (ADP) receptor. Methods This was an open-label, 2-way, crossover study that randomized healthy subjects (n = 68) to an oral loading dose (LD) of prasugrel 60 mg or clopidogrel 300 mg. Platelet aggregation response to 5 and 20 μmol/L of ADP was measured by turbidometric aggregometry. Plasma concentrations of the active metabolites of prasugrel and clopidogrel were quantified by liquid chromatography with tandem mass spectrometry detection methods. Results Inhibition of platelet aggregation (IPA) after prasugrel was significantly higher ( P < .01) than that after clopidogrel from 15 minutes through 24 hours (5 μmol/L ADP) and from 30 minutes through 24 hours (20 μmol/L ADP). For 20 μmol/L ADP, the median time to reach ≥20% IPA was 30 minutes for prasugrel and 1.5 hours for clopidogrel ( P < .001). The maximum IPA was 84.1% ± 9.5% with prasugrel versus 48.9% ± 27.0% with clopidogrel for 5 μmol/L ADP and 78.8% ± 9.2% versus 35.0% ± 24.5%, respectively, for 20 μmol/L ADP ( P < .001). Response to prasugrel was more consistent compared to clopidogrel ( P < .01). The lower IPA response to clopidogrel was associated with lower plasma concentrations of its active metabolite ( P < .001). Conclusions Prasugrel 60 mg LD results in more rapid, potent, and consistent inhibition of platelet function than clopidogrel 300 mg LD. Lower IPA responses to clopidogrel were associated with lower concentrations of its active metabolite.</description><identifier>ISSN: 0002-8703</identifier><identifier>EISSN: 1097-6744</identifier><identifier>DOI: 10.1016/j.ahj.2006.10.010</identifier><identifier>PMID: 17174640</identifier><identifier>CODEN: AHJOA2</identifier><language>eng</language><publisher>United States: Mosby, Inc</publisher><subject>Acute coronary syndromes ; Adult ; Area Under Curve ; Blood Platelets - drug effects ; Cardiovascular ; Cross-Over Studies ; Drug dosages ; Drug therapy ; Female ; Heart attacks ; Humans ; Male ; Metabolites ; Middle Aged ; Piperazines - administration & dosage ; Piperazines - metabolism ; Platelet Aggregation Inhibitors - administration & dosage ; Platelet Aggregation Inhibitors - metabolism ; Prasugrel Hydrochloride ; Purinergic P2 Receptor Antagonists ; Studies ; Thiophenes - administration & dosage ; Thiophenes - metabolism ; Thrombosis ; Ticlopidine - administration & dosage ; Ticlopidine - analogs & derivatives ; Ticlopidine - metabolism</subject><ispartof>The American heart journal, 2007, Vol.153 (1), p.66.e9-66.e16</ispartof><rights>2007</rights><rights>Copyright Elsevier Limited Jan 2007</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c500t-2069f61354d81aa72c945f147733910b89d84f19cabd6a6f6f1c5aacc6142e7f3</citedby><cites>FETCH-LOGICAL-c500t-2069f61354d81aa72c945f147733910b89d84f19cabd6a6f6f1c5aacc6142e7f3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0002870306009021$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,4010,27900,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17174640$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Brandt, John T., MD</creatorcontrib><creatorcontrib>Payne, Christopher D., MS</creatorcontrib><creatorcontrib>Wiviott, Stephen D., MD</creatorcontrib><creatorcontrib>Weerakkody, Govinda, PhD</creatorcontrib><creatorcontrib>Farid, Nagy A., PhD</creatorcontrib><creatorcontrib>Small, David S., PhD</creatorcontrib><creatorcontrib>Jakubowski, Joseph A., PhD</creatorcontrib><creatorcontrib>Naganuma, Hideo, PhD</creatorcontrib><creatorcontrib>Winters, Kenneth J., MD</creatorcontrib><title>A comparison of prasugrel and clopidogrel loading doses on platelet function: magnitude of platelet inhibition is related to active metabolite formation</title><title>The American heart journal</title><addtitle>Am Heart J</addtitle><description>Background The aim of this study was to compare rate of onset, magnitude, and consistency of platelet inhibition after administration of prasugrel or clopidogrel and to relate platelet inhibition to systemic exposure to each active metabolite. Thienopyridines are prodrugs, metabolized in vivo to active metabolites that inhibit the platelet P2Y12 adenosine diphosphate (ADP) receptor. Methods This was an open-label, 2-way, crossover study that randomized healthy subjects (n = 68) to an oral loading dose (LD) of prasugrel 60 mg or clopidogrel 300 mg. Platelet aggregation response to 5 and 20 μmol/L of ADP was measured by turbidometric aggregometry. Plasma concentrations of the active metabolites of prasugrel and clopidogrel were quantified by liquid chromatography with tandem mass spectrometry detection methods. Results Inhibition of platelet aggregation (IPA) after prasugrel was significantly higher ( P < .01) than that after clopidogrel from 15 minutes through 24 hours (5 μmol/L ADP) and from 30 minutes through 24 hours (20 μmol/L ADP). For 20 μmol/L ADP, the median time to reach ≥20% IPA was 30 minutes for prasugrel and 1.5 hours for clopidogrel ( P < .001). The maximum IPA was 84.1% ± 9.5% with prasugrel versus 48.9% ± 27.0% with clopidogrel for 5 μmol/L ADP and 78.8% ± 9.2% versus 35.0% ± 24.5%, respectively, for 20 μmol/L ADP ( P < .001). Response to prasugrel was more consistent compared to clopidogrel ( P < .01). The lower IPA response to clopidogrel was associated with lower plasma concentrations of its active metabolite ( P < .001). Conclusions Prasugrel 60 mg LD results in more rapid, potent, and consistent inhibition of platelet function than clopidogrel 300 mg LD. Lower IPA responses to clopidogrel were associated with lower concentrations of its active metabolite.</description><subject>Acute coronary syndromes</subject><subject>Adult</subject><subject>Area Under Curve</subject><subject>Blood Platelets - drug effects</subject><subject>Cardiovascular</subject><subject>Cross-Over Studies</subject><subject>Drug dosages</subject><subject>Drug therapy</subject><subject>Female</subject><subject>Heart attacks</subject><subject>Humans</subject><subject>Male</subject><subject>Metabolites</subject><subject>Middle Aged</subject><subject>Piperazines - administration & dosage</subject><subject>Piperazines - metabolism</subject><subject>Platelet Aggregation Inhibitors - administration & dosage</subject><subject>Platelet Aggregation Inhibitors - metabolism</subject><subject>Prasugrel Hydrochloride</subject><subject>Purinergic P2 Receptor Antagonists</subject><subject>Studies</subject><subject>Thiophenes - administration & dosage</subject><subject>Thiophenes - metabolism</subject><subject>Thrombosis</subject><subject>Ticlopidine - administration & dosage</subject><subject>Ticlopidine - analogs & derivatives</subject><subject>Ticlopidine - metabolism</subject><issn>0002-8703</issn><issn>1097-6744</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNp9ks2KFTEQhYMoznX0AdxIQHDX10r_pLsVhGHwDwZcqOuQTip30qaTNukemDfxcU3PvTIwC1ehKt85JHWKkJcM9gwYfzvu5fW4LwF4rvfA4BHZMejbgrd1_ZjsAKAsuhaqM_IspTGXvOz4U3LGWtbWvIYd-XNBVZhmGW0KngZD5yjTeojoqPSaKhdmq8Nd7YLU1h-oDgkTzfTs5IIOF2pWrxYb_Ds6yYO3y6rxzurfvfXXdrAbQW2i2Sv3NV0ClVl2g3TCRQ7B2QWpCXGSG_mcPDHSJXxxOs_Jz08ff1x-Ka6-ff56eXFVqAZgKUrgveGsamrdMSnbUvV1Y1jdtlXVMxi6Xne1Yb2Sg-aSG26YaqRUirO6xNZU5-TN0XeO4feKaRGTTQqdkx7DmgTvqrbpesjg6wfgGNbo89sEa6DmVR5olyl2pFQMKUU0Yo52kvFWMBBbaGIUOTSxhba1cmhZ8-rkvA4T6nvFKaUMvD8CmAdxYzGKpCx6hdpGVIvQwf7X_sMDtXLWWyXdL7zFdP8LkUoB4vu2NdvSAAfooWTVX8StvpY</recordid><startdate>2007</startdate><enddate>2007</enddate><creator>Brandt, John T., MD</creator><creator>Payne, Christopher D., MS</creator><creator>Wiviott, Stephen D., MD</creator><creator>Weerakkody, Govinda, PhD</creator><creator>Farid, Nagy A., PhD</creator><creator>Small, David S., PhD</creator><creator>Jakubowski, Joseph A., PhD</creator><creator>Naganuma, Hideo, PhD</creator><creator>Winters, Kenneth J., MD</creator><general>Mosby, Inc</general><general>Elsevier Limited</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>3V.</scope><scope>7QO</scope><scope>7RV</scope><scope>7TS</scope><scope>7X7</scope><scope>7XB</scope><scope>88C</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AN0</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>K9.</scope><scope>KB0</scope><scope>M0S</scope><scope>M0T</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>NAPCQ</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope></search><sort><creationdate>2007</creationdate><title>A comparison of prasugrel and clopidogrel loading doses on platelet function: magnitude of platelet inhibition is related to active metabolite formation</title><author>Brandt, John T., MD ; Payne, Christopher D., MS ; Wiviott, Stephen D., MD ; Weerakkody, Govinda, PhD ; Farid, Nagy A., PhD ; Small, David S., PhD ; Jakubowski, Joseph A., PhD ; Naganuma, Hideo, PhD ; Winters, Kenneth J., MD</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c500t-2069f61354d81aa72c945f147733910b89d84f19cabd6a6f6f1c5aacc6142e7f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Acute coronary syndromes</topic><topic>Adult</topic><topic>Area Under Curve</topic><topic>Blood Platelets - drug effects</topic><topic>Cardiovascular</topic><topic>Cross-Over Studies</topic><topic>Drug dosages</topic><topic>Drug therapy</topic><topic>Female</topic><topic>Heart attacks</topic><topic>Humans</topic><topic>Male</topic><topic>Metabolites</topic><topic>Middle Aged</topic><topic>Piperazines - administration & dosage</topic><topic>Piperazines - metabolism</topic><topic>Platelet Aggregation Inhibitors - administration & dosage</topic><topic>Platelet Aggregation Inhibitors - metabolism</topic><topic>Prasugrel Hydrochloride</topic><topic>Purinergic P2 Receptor Antagonists</topic><topic>Studies</topic><topic>Thiophenes - administration & dosage</topic><topic>Thiophenes - metabolism</topic><topic>Thrombosis</topic><topic>Ticlopidine - administration & dosage</topic><topic>Ticlopidine - analogs & derivatives</topic><topic>Ticlopidine - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Brandt, John T., MD</creatorcontrib><creatorcontrib>Payne, Christopher D., MS</creatorcontrib><creatorcontrib>Wiviott, Stephen D., MD</creatorcontrib><creatorcontrib>Weerakkody, Govinda, PhD</creatorcontrib><creatorcontrib>Farid, Nagy A., PhD</creatorcontrib><creatorcontrib>Small, David S., PhD</creatorcontrib><creatorcontrib>Jakubowski, Joseph A., PhD</creatorcontrib><creatorcontrib>Naganuma, Hideo, PhD</creatorcontrib><creatorcontrib>Winters, Kenneth J., MD</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Biotechnology Research Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Physical Education Index</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Healthcare Administration Database (Alumni)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research Database</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>British Nursing Database</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Healthcare Administration Database</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Research Library (Corporate)</collection><collection>Nursing & Allied Health Premium</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><jtitle>The American heart journal</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Brandt, John T., MD</au><au>Payne, Christopher D., MS</au><au>Wiviott, Stephen D., MD</au><au>Weerakkody, Govinda, PhD</au><au>Farid, Nagy A., PhD</au><au>Small, David S., PhD</au><au>Jakubowski, Joseph A., PhD</au><au>Naganuma, Hideo, PhD</au><au>Winters, Kenneth J., MD</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>A comparison of prasugrel and clopidogrel loading doses on platelet function: magnitude of platelet inhibition is related to active metabolite formation</atitle><jtitle>The American heart journal</jtitle><addtitle>Am Heart J</addtitle><date>2007</date><risdate>2007</risdate><volume>153</volume><issue>1</issue><spage>66.e9</spage><epage>66.e16</epage><pages>66.e9-66.e16</pages><issn>0002-8703</issn><eissn>1097-6744</eissn><coden>AHJOA2</coden><abstract>Background The aim of this study was to compare rate of onset, magnitude, and consistency of platelet inhibition after administration of prasugrel or clopidogrel and to relate platelet inhibition to systemic exposure to each active metabolite. Thienopyridines are prodrugs, metabolized in vivo to active metabolites that inhibit the platelet P2Y12 adenosine diphosphate (ADP) receptor. Methods This was an open-label, 2-way, crossover study that randomized healthy subjects (n = 68) to an oral loading dose (LD) of prasugrel 60 mg or clopidogrel 300 mg. Platelet aggregation response to 5 and 20 μmol/L of ADP was measured by turbidometric aggregometry. Plasma concentrations of the active metabolites of prasugrel and clopidogrel were quantified by liquid chromatography with tandem mass spectrometry detection methods. Results Inhibition of platelet aggregation (IPA) after prasugrel was significantly higher ( P < .01) than that after clopidogrel from 15 minutes through 24 hours (5 μmol/L ADP) and from 30 minutes through 24 hours (20 μmol/L ADP). For 20 μmol/L ADP, the median time to reach ≥20% IPA was 30 minutes for prasugrel and 1.5 hours for clopidogrel ( P < .001). The maximum IPA was 84.1% ± 9.5% with prasugrel versus 48.9% ± 27.0% with clopidogrel for 5 μmol/L ADP and 78.8% ± 9.2% versus 35.0% ± 24.5%, respectively, for 20 μmol/L ADP ( P < .001). Response to prasugrel was more consistent compared to clopidogrel ( P < .01). The lower IPA response to clopidogrel was associated with lower plasma concentrations of its active metabolite ( P < .001). Conclusions Prasugrel 60 mg LD results in more rapid, potent, and consistent inhibition of platelet function than clopidogrel 300 mg LD. Lower IPA responses to clopidogrel were associated with lower concentrations of its active metabolite.</abstract><cop>United States</cop><pub>Mosby, Inc</pub><pmid>17174640</pmid><doi>10.1016/j.ahj.2006.10.010</doi></addata></record> |
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| subjects | Acute coronary syndromes Adult Area Under Curve Blood Platelets - drug effects Cardiovascular Cross-Over Studies Drug dosages Drug therapy Female Heart attacks Humans Male Metabolites Middle Aged Piperazines - administration & dosage Piperazines - metabolism Platelet Aggregation Inhibitors - administration & dosage Platelet Aggregation Inhibitors - metabolism Prasugrel Hydrochloride Purinergic P2 Receptor Antagonists Studies Thiophenes - administration & dosage Thiophenes - metabolism Thrombosis Ticlopidine - administration & dosage Ticlopidine - analogs & derivatives Ticlopidine - metabolism |
| title | A comparison of prasugrel and clopidogrel loading doses on platelet function: magnitude of platelet inhibition is related to active metabolite formation |
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