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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\u003E\u201cWe need to be cautious about \u2018cookbook\u2019 approaches that do not account for individual patient variations,\u201d said James DeLemos, MD, Associate Professor, University of Texas Southwestern Medical Center, Dallas, acknowledging that patient variations can be difficult to appreciate on clinical grounds alone (e.g., history, PE, ECG); which makes biomarkers all the more important.\u003C\/p\u003E\n         \u003C\/div\u003E\u003Cul class=\u0022kwd-group\u0022\u003E\u003Cli class=\u0022kwd\u0022\u003Ecoronary artery disease\u003C\/li\u003E\u003Cli class=\u0022kwd\u0022\u003Emyocardial infarction\u003C\/li\u003E\u003C\/ul\u003E\u003Cdiv class=\u0022section\u0022 id=\u0022sec-1\u0022\u003E\n         \u003Ch2 class=\u0022\u0022\u003EBiomarkers and Diagnosis\u003C\/h2\u003E\n         \u003Cp id=\u0022p-2\u0022\u003E\u201cWe need to be cautious about \u2018cookbook\u2019 approaches that do not account for individual patient variations,\u201d said James DeLemos, MD, Associate Professor, University of Texas Southwestern Medical Center, Dallas, acknowledging that patient variations can be difficult to appreciate on clinical grounds alone (e.g., history, PE, ECG); which makes biomarkers all the more important.\u003C\/p\u003E\n         \u003Cp id=\u0022p-3\u0022\u003E\u201cThe prototype cardiac biomarkers are the troponins (cTnT, CTnI). These are powerful prognostic markers that can help confirm MI\u2014but they\u0027re also associated with pulmonary embolus (PE), heart failure, and sepsis.\u201d\u003C\/p\u003E\n         \u003Cp id=\u0022p-4\u0022\u003EIn addition to identifying patients in the midst of an event and\/or at high risk, troponins are associated with active thrombotic processes. Dr. DeLemos identified troponins as \u201coptimum biomarkers\u201d and went on to present results from several studies demonstrating that treatment with enoxaparin, and the GP IIb\/IIIa inhibitors, and an invasive approach to revascularization significantly reduce event rates in troponin-positive patients.\u003C\/p\u003E\n         \u003Cp id=\u0022p-5\u0022\u003EDr. DeLemos discussed emerging cardiac biomarkers, including myeloperoxidase and brain natriuetic peptide (BNP). Myeloperoxidase, however, is also a marker for autoimmune diseases and cancer. And BNP elevations are also seen in right ventricular overload states.\u003C\/p\u003E\n         \u003Cp id=\u0022p-6\u0022\u003E\u201cThe new biomarkers are promising,\u201d Dr. DeLemos said, \u201cbut there remains a tremendous need for even more specific cardiac biomarkers.\u201d\u003C\/p\u003E\n      \u003C\/div\u003E\u003Cdiv class=\u0022section\u0022 id=\u0022sec-2\u0022\u003E\n         \u003Ch2 class=\u0022\u0022\u003EModifying Thrombosis\u003C\/h2\u003E\n         \u003Cp id=\u0022p-7\u0022\u003EDeepak Bhatt, MD, Department of Cardiovascular Medicine, Cleveland Clinic, echoed the importance of troponin links to thrombosis. Dr. Bhatt discussed the implications of several key studies, notably the SYNERGY trial (\u003Cem\u003EJAMA\u003C\/em\u003E 2004; 292: 45\u201354) which supported the use of the low molecular weight heparin enoxaparin over unfractionated heparin. In this study, enoxaparin was not found to be absolutely superior.\u003C\/p\u003E\n         \u003Cp id=\u0022p-8\u0022\u003EDr. Bhatt noted that enoxaparin was an adequate \u201cnoninferior\u201d alternative for the treatment of high-risk patients with NSTEMI ACS. \u201cThe endorsement is there, but it is not resounding,\u201d he said.\u003C\/p\u003E\n         \u003Cp id=\u0022p-9\u0022\u003EOverall, most of the recent research consistently supports antithrombotic therapies as a cornerstone of early treatment in ACS\u2014along with moving quickly to invasive strategies. \u201cEarly invasive intervention in NSTEMI ACS is preferred,\u201d Dr. Bhatt said. \u201cThe data supports that this is where we reduce mortality and improve outcomes.\u201d\u003C\/p\u003E\n         \u003Cp id=\u0022p-10\u0022\u003EDr. Bhatt called for additional research to develop more and better antithrombotic agents. \u201cThe optimal drug timing and combination is yet to be determined in managing thrombotic complications in ACS,\u201d he said.\u003C\/p\u003E\n      \u003C\/div\u003E\u003Cdiv class=\u0022section\u0022 id=\u0022sec-3\u0022\u003E\n         \u003Ch2 class=\u0022\u0022\u003EAssessing and Modifying Inflammation\u003C\/h2\u003E\n         \u003Cp id=\u0022p-11\u0022\u003EMary Cushman, MD, Associate Professor of Medicine (Hematology\/Oncology), University of Vermont School of Medicine, Burlington, stated that elevated levels of C-reactive protein (CRP)\u2014even in asymptomatic individuals\u2014are associated with an up to four-fold increase in CVD risk.\u003C\/p\u003E\n         \u003Cp id=\u0022p-12\u0022\u003E\u201cCRP rises in ACS and is higher in those with cardiovascular disease in general,\u201d said Dr. Cushman, who also highlighted that CPR is produced in smooth muscle cells within human coronary arteries and is expressed preferentially in diseased coronary vessels.\u003C\/p\u003E\n         \u003Cp id=\u0022p-13\u0022\u003EThe data is \u201cvery substantive,\u201d Dr. Cushman said, in support of CRP\u0027s role as an independent predictor of risk. \u201cMany studies demonstrate that CRP is a surprisingly accurate predictor for stroke, MI, and peripheral arterial disease.\u201d\u003C\/p\u003E\n         \u003Cp id=\u0022p-14\u0022\u003EWhile this marker cannot be considered absolutely specific, Dr. Cushman said, \u201cCRP rarely suggests other non-cardiac concerns.\u201d She cited studies in which CRP has been demonstrated to increase predictive value \u201cat all levels of LDL and at all levels of risk scoring.\u201d (However, Dr. Cushman said, CRP levels do not directly correlate with lipid measures, and simultaneous assays of CRP + lipids will add value to risk assessment and stratification.)\u003C\/p\u003E\n         \u003Cp id=\u0022p-15\u0022\u003E\u201cWhat we\u0027re really talking about here, though, is reducing inflammation in our patients at risk,\u201d Dr. Cushman said. \u201cAnd that brings us back to the fundamentals: lifestyle modification, weight loss, exercise. We need to see more and better control of blood pressure and impaired glucose tolerance. It\u0027s great to have biomarkers to guide us, but we have to control the multiple modifiable risks that patients face.\u201d\u003C\/p\u003E\n      \u003C\/div\u003E\u003Cdiv class=\u0022section\u0022 id=\u0022sec-4\u0022\u003E\n         \u003Ch2 class=\u0022\u0022\u003ERevascularization Issues\u003C\/h2\u003E\n         \u003Cp id=\u0022p-16\u0022\u003EControversy has reigned regarding the merits of invasive versus conservative approaches to patients with ACS. Peter B. Berger, MD, Director of Interventional Cardiology, Duke University, Durham, NC, discussed several trials evaluating this question.\u003C\/p\u003E\n         \u003Cp id=\u0022p-17\u0022\u003EThe ISAR-COOL study tested the hypothesis that unstable ACS patients might do equally as well if \u201cbathed in\u201d antithrombotics for a \u201ccooling-off period\u201d prior to revascularization. However, those patients delaying intervention for the antithrombotic pretreatment period did not see improved outcomes compared with \u201cimmediate intervention accompanied by intense anticoagulation,\u201d according to Dr. Berger.\u003C\/p\u003E\n         \u003Cp id=\u0022p-18\u0022\u003EOn the other hand, the ICTUS (Invasive versus Conservative Treatment in Unstable Coronary Syndromes) Trial (deWinter RJ et al, \u003Cem\u003EN Engl J Med\u003C\/em\u003E 2005: 353) found no difference in outcomes between early PCI and conservative approaches. One study arm consisted of troponin-positive patients randomized between early PCI or conservative (medical) treatment. Troponin-normal patients formed the control group. Primary combined endpoint was ACS, MI, or death.\u003C\/p\u003E\n         \u003Cp id=\u0022p-19\u0022\u003EACC\/AHA guidelines recommend that high-risk ACS patients benefit more from an early invasive strategy. Dr. Berger agreed, although conflicting data suggests a need for additional risk stratification guidelines to further identify ACS patients more likely to benefit from early interventions.\u003C\/p\u003E\n      \u003C\/div\u003E\u003Cul class=\u0022copyright-statement\u0022\u003E\u003Cli class=\u0022fn\u0022 id=\u0022copyright-statement-1\u0022\u003E\u00a9 2005 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\/5\/1\/30.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_openurl.js?nzm47q\u0022\u003E\u003C\/script\u003E\n\u003C\/body\u003E\u003C\/html\u003E"}