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type=\u0022text\/css\u0022 rel=\u0022stylesheet\u0022 href=\u0022\/\/d282kpwvnogo5m.cloudfront.net\/sites\/default\/files\/cdn\/css\/http\/css_Xg7z6oCTVgud_Q0huYz9x9iiD5H_2YPSJ5z2ZViSWdY.css\u0022 media=\u0022all\u0022 \/\u003E\n\u003Clink rel=\u0027stylesheet\u0027 type=\u0027text\/css\u0027 href=\u0027\/sites\/all\/modules\/contrib\/panels\/plugins\/layouts\/onecol\/onecol.css\u0027 \/\u003E\u003C\/head\u003E\u003Cbody\u003E\u003Cdiv class=\u0022panels-ajax-tab-panel panels-ajax-tab-panel-sageoa-tab-art\u0022\u003E\u003Cdiv class=\u0022panel-display panel-1col clearfix\u0022 \u003E\n  \u003Cdiv class=\u0022panel-panel panel-col\u0022\u003E\n    \u003Cdiv\u003E\u003Cdiv class=\u0022panel-pane pane-highwire-markup\u0022 \u003E\n  \n      \n  \n  \u003Cdiv class=\u0022pane-content\u0022\u003E\n    \u003Cdiv class=\u0022highwire-markup\u0022\u003E\u003Cdiv xmlns=\u0022http:\/\/www.w3.org\/1999\/xhtml\u0022 id=\u0022content-block-markup\u0022 xmlns:xhtml=\u0022http:\/\/www.w3.org\/1999\/xhtml\u0022\u003E\u003Cdiv class=\u0022article fulltext-view \u0022\u003E\u003Cspan class=\u0022highwire-journal-article-marker-start\u0022\u003E\u003C\/span\u003E\u003Cdiv class=\u0022section abstract\u0022 id=\u0022abstract-1\u0022\u003E\u003Ch2\u003ESummary\u003C\/h2\u003E\n\u003Cp id=\u0022p-1\u0022\u003EWith the introduction of several new antiplatelet and anticoagulant agents that have multiple actions and interactions, selection of the optimal antithrombotic has become quite complex. This article discusses direct Xa inhibitors, direct thrombin inhibitors, GP IIb\/IIIa inhibitors, adenosine diphosphate inhibitors, as well as novel targets for antithrombotic therapy.\u003C\/p\u003E\n\u003C\/div\u003E\u003Cul class=\u0022kwd-group\u0022\u003E\u003Cli class=\u0022kwd\u0022\u003EThrombotic Disorders\u003C\/li\u003E\u003C\/ul\u003E\u003Cp id=\u0022p-2\u0022\u003EWith the introduction of several new antiplatelet and anticoagulant agents that have multiple actions and interactions, selection of the optimal antithrombotic has become quite complex (\u003Ca id=\u0022xref-fig-1-1\u0022 class=\u0022xref-fig\u0022 href=\u0022#F1\u0022\u003EFigure 1\u003C\/a\u003E). \u201cWe now think of thrombosis as an assembly line where treatment interventions impact hundreds of pathways simultaneously,\u201d said Robert Califf, MD, of Duke University, Durham, North Carolina.\u003C\/p\u003E\u003Cdiv id=\u0022F1\u0022 class=\u0022fig pos-float  odd\u0022\u003E\u003Cdiv class=\u0022highwire-figure\u0022\u003E\u003Cdiv class=\u0022fig-inline-img-wrapper\u0022\u003E\u003Cdiv class=\u0022fig-inline-img\u0022\u003E\u003Ca href=\u0022http:\/\/d282kpwvnogo5m.cloudfront.net\/content\/spmdc\/7\/1\/31\/F1.large.jpg?width=800\u0026amp;height=600\u0026amp;carousel=1\u0022 title=\u0022Antithrombotics 2000\u0026#x2013;2006.\u0022 class=\u0022fragment-images colorbox-load\u0022 rel=\u0022gallery-fragment-images-2122450440\u0022 data-figure-caption=\u0022Antithrombotics 2000\u0026#x2013;2006.\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003E\u003Cimg class=\u0022fragment-image\u0022 alt=\u0022Figure 1.\u0022 src=\u0022http:\/\/d282kpwvnogo5m.cloudfront.net\/content\/spmdc\/7\/1\/31\/F1.medium.gif\u0022\/\u003E\u003C\/a\u003E\u003C\/div\u003E\u003C\/div\u003E\u003Cul class=\u0022highwire-figure-links inline\u0022\u003E\u003Cli class=\u00220 first\u0022\u003E\u003Ca href=\u0022http:\/\/d282kpwvnogo5m.cloudfront.net\/content\/spmdc\/7\/1\/31\/F1.large.jpg?download=true\u0022 class=\u0022highwire-figure-link highwire-figure-link-download\u0022 title=\u0022Download Figure 1.\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003EDownload figure\u003C\/a\u003E\u003C\/li\u003E\u003Cli class=\u00221\u0022\u003E\u003Ca href=\u0022http:\/\/d282kpwvnogo5m.cloudfront.net\/content\/spmdc\/7\/1\/31\/F1.large.jpg\u0022 class=\u0022highwire-figure-link highwire-figure-link-newtab\u0022 target=\u0022_blank\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003EOpen in new tab\u003C\/a\u003E\u003C\/li\u003E\u003Cli class=\u00222 last\u0022\u003E\u003Ca href=\u0022\/highwire\/powerpoint\/11012\u0022 class=\u0022highwire-figure-link highwire-figure-link-ppt\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003EDownload powerpoint\u003C\/a\u003E\u003C\/li\u003E\u003C\/ul\u003E\u003C\/div\u003E\u003Cdiv class=\u0022fig-caption\u0022 xmlns:xhtml=\u0022http:\/\/www.w3.org\/1999\/xhtml\u0022\u003E\u003Cspan class=\u0022fig-label\u0022\u003EFigure 1.\u003C\/span\u003E \u003Cp id=\u0022p-3\u0022 class=\u0022first-child\u0022\u003EAntithrombotics 2000\u20132006.\u003C\/p\u003E\u003Cdiv class=\u0022sb-div caption-clear\u0022\u003E\u003C\/div\u003E\u003C\/div\u003E\u003C\/div\u003E\u003Cp id=\u0022p-4\u0022\u003EJames J. Ferguson, MD, Baylor College of Medicine, Houston, described how he integrates low-molecular-weight heparin (LMWH) into his practice. He noted that for medical management, enoxaparin is superior to unfractionated heparin (UFH) because it is more reliable, easier to use, and safe and effective in transitioning to the catheterization laboratory. Concerns remain, however, about bleeding risks, use in patients with renal dysfunction, and lack of reversibility. In invasive management, the lack of monitoring and uncertainty about prior dosing is problematic, intravenous use is off-label, and the addition of UFH may increase bleeding risk.\u003C\/p\u003E\u003Cp id=\u0022p-5\u0022\u003EFor procedural anticoagulation during percutaneous intervention (PCI) in the absence of a recent subcutaneous dose, the recommended dose of enoxaparin is 0.75 to 1.0 mg\/kg IV in the absence of concomittant GPIIb\/IIIa inhibitors. When GPIIb\/IIIa inhibitors are being used the recommended dose is 0.5 to 0.75 mg\/kg IV. In patients with acute myocardial infarction (MI) treated with fibrinolytic therapy, enoxaparin is clinically superior to UFH although the risk of bleeding is slightly increased. A critical feature in this setting is dose adjustment in the elderly and in patients with renal failure.\u003C\/p\u003E\u003Cdiv class=\u0022section\u0022 id=\u0022sec-1\u0022\u003E\n\u003Ch2 class=\u0022\u0022\u003EDirect Xa Inhibitors\u003C\/h2\u003E\n\u003Cp id=\u0022p-6\u0022\u003ELars Wallentin, MD, Uppsala University Hospital, Uppsala, Sweden, described recent results with the subcutaneous direct Xa inhibitor fondaparinux in 20,078 patients with non-ST-elevation acute coronary syndromes (nSTE-ACS) enrolled in the OASIS-5 trial. Patients assigned to fondaparinux 2.5 mg\/day had a 13% reduction in death, MI, refractory ischemia, or major bleeding at 6 months (p \u0026lt;.00001) compared with those randomized to enoxaparin 1 mg\/kg BID. Major bleeding was also reduced (approximately 50%). Dr. Wallentin added that because of the reduction in bleeding risk fondaparinux will play a prominent role in the medical management of nSTE-ACS in the new European guidelines. However, in patients undergoing PCI, some distally-acting anticoagulant (eg, unfractionated heparin) appears to be necessary to reduce the risk of procedural thrombosis, based on findings from OASIS-5 that demonstrated an increase in catheter thrombus formation in the fondaparinux arm.\u003C\/p\u003E\n\u003Cp id=\u0022p-7\u0022\u003EOral direct Xa inhibitors will be important antithrombotics of the future, he predicted. Apixiban and rivaroxaban are already in phase 2\u20133 trials for deep-vein thrombosis (DVT) prevention and stroke prevention in AF, and several drugs are in phase 2 and 3 studies in ACS.\u003C\/p\u003E\n\u003C\/div\u003E\u003Cdiv class=\u0022section\u0022 id=\u0022sec-2\u0022\u003E\n\u003Ch2 class=\u0022\u0022\u003EDirect Thrombin Inhibitors\u003C\/h2\u003E\n\u003Cp id=\u0022p-8\u0022\u003EThrombin plays a central role in thrombosis and given the complexity of its role and structure, agents that directly inhibit thrombin appear to have different features. As a group, compared with UFH, the DTIs are \u201cboth encouraging and disappointing,\u201d Dr. Califf observed. In ACS, their effects are confined to reducing non-fatal MI, \u003Cem\u003Enot\u003C\/em\u003E mortality. In the PCI setting, he said, bivalirudin is a \u201creasonable concept,\u201d since it reduces the risk of bleeding compared with standard therapy with heparin + GP IIb\/IIIa inhibitors, but it is not as effective in reducing non-fatal MI.\u003C\/p\u003E\n\u003Cp id=\u0022p-9\u0022\u003EIn patients with low-to-intermediate-risk of ischemic complications, bivalirudin is rational as a \u201cstand alone\u201d anticoagulant, particularly in patients with an elevated bleeding risk. Newer IV and oral DTIs are now entering late-stage clinical trials (\u003Ca id=\u0022xref-table-wrap-1-1\u0022 class=\u0022xref-table\u0022 href=\u0022#T1\u0022\u003ETable 1\u003C\/a\u003E).\u003C\/p\u003E\n\u003Cdiv id=\u0022T1\u0022 class=\u0022table pos-float\u0022\u003E\u003Cdiv class=\u0022table-inline\u0022\u003E\u003Cdiv class=\u0022callout\u0022\u003E\u003Cspan\u003EView this table:\u003C\/span\u003E\u003Cul class=\u0022callout-links\u0022\u003E\u003Cli class=\u00220 first\u0022\u003E\u003Ca href=\u0022\/\u0022 class=\u0022table-expand-inline\u0022 data-table-url=\u0022\/highwire\/markup\/11016\/expansion?postprocessors=highwire_figures%2Chighwire_math%2Chighwire_inline_linked_media%2Chighwire_embed\u0026amp;table-expand-inline=1\u0022 html=\u00221\u0022 fragment=\u0022#\u0022 external=\u00221\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003EView inline\u003C\/a\u003E\u003C\/li\u003E\u003Cli class=\u00221\u0022\u003E\u003Ca href=\u0022\/highwire\/markup\/11016\/expansion?width=1000\u0026amp;height=500\u0026amp;iframe=true\u0026amp;postprocessors=highwire_figures%2Chighwire_math%2Chighwire_inline_linked_media\u0022 class=\u0022colorbox colorbox-load table-expand-popup\u0022 rel=\u0022gallery-fragment-tables\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003EView popup\u003C\/a\u003E\u003C\/li\u003E\u003Cli class=\u00222 last\u0022\u003E\u003Ca href=\u0022\/highwire\/powerpoint\/11016\u0022 class=\u0022highwire-figure-link highwire-figure-link-ppt\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003EDownload powerpoint\u003C\/a\u003E\u003C\/li\u003E\u003C\/ul\u003E\u003C\/div\u003E\u003C\/div\u003E\u003Cdiv class=\u0022table-caption\u0022\u003E\u003Cspan class=\u0022table-label\u0022\u003ETable 1.\u003C\/span\u003E \u003Cp id=\u0022p-10\u0022 class=\u0022first-child\u0022\u003EDirect Thrombin Inhibitors in Human Trials.\u003C\/p\u003E\u003Cdiv class=\u0022sb-div caption-clear\u0022\u003E\u003C\/div\u003E\u003C\/div\u003E\u003C\/div\u003E\n\u003C\/div\u003E\u003Cdiv class=\u0022section\u0022 id=\u0022sec-3\u0022\u003E\n\u003Ch2 class=\u0022\u0022\u003EGP IIb\/IIIa Inhibitors\u003C\/h2\u003E\n\u003Cp id=\u0022p-11\u0022\u003EGP IIb\/IIIa inhibitors have been used for over a decade and are among the best studied agents in medicine. However, as new antithrombotics emerge, the role of older, established drugs needs to be periodically reevaluated, said Robert P. Giugliano, MD, Brigham \u0026amp; Women\u0027s Hospital, Boston.\u003C\/p\u003E\n\u003Cp id=\u0022p-12\u0022\u003ETheir primary role is in patients planning to undergo PCI. In patients with ST-elevation myocardial infarction (STEMI), prior meta-analyses have shown inconsistent results, but the most recent long-term individual patient data from three European studies demonstrated a durable reduction in death and MI with abciximab compared to placebo. In patients with STEMI, attention has now turned to the question of optimal timing of initiation of therapy (early in the emergency department vs later in the catheterization laboratory).\u003C\/p\u003E\n\u003Cp id=\u0022p-13\u0022\u003EIn patients with nSTE-ACS, current guidelines recommend GP IIb\/IIIa inhibitors for high-risk patients and for those who are planning to undergo an early invasive strategy, since these agents have been demonstrated to reduce ischemic complications prior to and during PCI. However, with newer and potentially safer antithrombotics being developed, the benefits of GP IIb\/IIIa inhibitors in reducing ischemic complications must be balanced with the increased risk of bleeding, especially in women and the elderly, Dr. Giugliano said. Recent studies have suggested that excessive dosing of antithrombotics may increase the rate of bleeding; adjusting for renal dysfunction is important to avoid this complication.\u003C\/p\u003E\n\u003C\/div\u003E\u003Cdiv class=\u0022section\u0022 id=\u0022sec-4\u0022\u003E\n\u003Ch2 class=\u0022\u0022\u003EAdenosine Diphosphate Inhibitors\u003C\/h2\u003E\n\u003Cp id=\u0022p-14\u0022\u003EClopidogrel has become an essential agent in the PCI setting. A loading dose should be used for rapid onset, and doses \u0026gt; 300 mg appear to have a role in overcoming some of the problems with clopidogrel\u2014delay in efficacy, variability of response, and metabolic interferences. For example, a loading dose of 600\u2013900 mg has been shown to have a better effect on platelet aggregation, but whether this translates clinically remains to be proven. Metabolism and drug-drug interactions are other avenues of research, including an examination of polymorphisms that may dictate response to the drug. New ADP receptor antagonists in development, including prasugrel (a more potent oral thienopyridine), AZD 6140 (a reversible PGY\u003Csub\u003E12\u003C\/sub\u003E inhibitor), and cangrelor (a short-acting intravenous thienopyridine), are expected to improve upon the current deficiencies with clopidogrel, said Philippe-Gabriel Steg, MD, of the University of Paris.\u003C\/p\u003E\n\u003C\/div\u003E\u003Cdiv class=\u0022section\u0022 id=\u0022sec-5\u0022\u003E\n\u003Ch2 class=\u0022\u0022\u003ENovel Targets for Antithrombotic Therapy\u003C\/h2\u003E\n\u003Cp id=\u0022p-15\u0022\u003ERobert A. Harrington, MD, Duke University, Durham, North Carolina, looked to the future, observing that novel agents will change the field tremendously. Aptamers are single-stranded nucleic acids that adopt a specific shape, enabling them to bind with high affinity and specificity to target proteins. RNA aptamers are being developed as highly specific anticoagulants with rapid onset\/offset and an available antidote. New platelet surface receptors, such as the thrombin receptor antagonist SCH 530348, can achieve very high platelet blockade with a low risk of bleeding. Also at ACC, Moliterno, et al presented findings from a multinational randomized study of SCH 530348 in PCI, showing very high rates of platelet aggregation, low rates of bleeding (similar to placebo), and a 4.0% rate of 60-day death or MI at the highest dose, compared with 7.3% for placebo (p=0.20). Should randomized controlled trials of these and other novel targets and agents confirm these promising initial findings, clinicians will have more effective, and safer, options for preventing thrombosis.\u003C\/p\u003E\n\u003C\/div\u003E\u003Cul class=\u0022copyright-statement\u0022\u003E\u003Cli class=\u0022fn\u0022 id=\u0022copyright-statement-1\u0022\u003E\u00a9 2007 MD Conference Express\u003C\/li\u003E\u003C\/ul\u003E\u003Cspan class=\u0022highwire-journal-article-marker-end\u0022\u003E\u003C\/span\u003E\u003C\/div\u003E\u003Cspan id=\u0022related-urls\u0022\u003E\u003C\/span\u003E\u003C\/div\u003E\u003Ca href=\u0022http:\/\/mdc.sagepub.com\/content\/7\/1\/31.abstract\u0022 class=\u0022hw-link hw-link-article-abstract\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003EView Summary\u003C\/a\u003E\u003C\/div\u003E  \u003C\/div\u003E\n\n  \n  \u003C\/div\u003E\n\u003C\/div\u003E\n  \u003C\/div\u003E\n\u003C\/div\u003E\n\u003C\/div\u003E\u003Cscript type=\u0022text\/javascript\u0022 src=\u0022http:\/\/mdc.sagepub.com\/sites\/all\/modules\/highwire\/highwire\/plugins\/highwire_markup_process\/js\/highwire_figures.js?nzmbo2\u0022\u003E\u003C\/script\u003E\n\u003Cscript type=\u0022text\/javascript\u0022 src=\u0022http:\/\/mdc.sagepub.com\/sites\/all\/modules\/highwire\/highwire\/plugins\/highwire_markup_process\/js\/highwire_openurl.js?nzmbo2\u0022\u003E\u003C\/script\u003E\n\u003Cscript type=\u0022text\/javascript\u0022 src=\u0022http:\/\/mdc.sagepub.com\/sites\/all\/modules\/highwire\/highwire\/plugins\/highwire_markup_process\/js\/highwire_tables.js?nzmbo2\u0022\u003E\u003C\/script\u003E\n\u003C\/body\u003E\u003C\/html\u003E"}