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type=\u0022text\/css\u0022 rel=\u0022stylesheet\u0022 href=\u0022\/\/d282kpwvnogo5m.cloudfront.net\/sites\/default\/files\/advagg_css\/css__ce2QY63WIanKyr8eSq7eavr1XQRRmFD6ZSmwpyJi8lM__zXwFqpqmxrZOXXcd_TpBQpjuELbmIP9wBR5UuTDWAO4__YJWWMMdfCJuAFm5cUEp88OsodhO3ZA-2lzRfoBsSlk4.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\u003EDuring a joint session of the American Heart Association and European Society of Cardiology, the biology and genetics of atrial fibrillation as the basis for understanding and managing the condition were discussed.\u003C\/p\u003E\n         \u003C\/div\u003E\u003Cul class=\u0022kwd-group\u0022\u003E\u003Cli class=\u0022kwd\u0022\u003EArrhythmias Genomics\u003C\/li\u003E\u003C\/ul\u003E\u003Cdiv class=\u0022section\u0022 id=\u0022sec-1\u0022\u003E\n         \u003Ch2 class=\u0022\u0022\u003EBiology, Genetics, and Management of AF\u003C\/h2\u003E\n         \u003Cp id=\u0022p-2\u0022\u003EAt a joint session of the AHA and ESC, Stanley Nattel, MD, Montreal Heart Institute, Montreal, Canada, discussed the biology and genetics of atrial fibrillation (AF) as the basis for understanding and managing the condition.\u003C\/p\u003E\n         \u003Cp id=\u0022p-3\u0022\u003EAF can occur due to multiple underlying factors, including heart disease, disturbances in extrinsic regulation, and genetic abnormalities. Development of AF requires an ectopic trigger activity and reentrant substrates to permit the maintenance of the arrhythmia. In many (probably most) cases, the occurrence and manifestations of AF are determined by multiple contributors that act in concert.\u003C\/p\u003E\n         \u003Cp id=\u0022p-4\u0022\u003EChronic coronary artery disease (CAD) is a significant risk factor for AF, increasing the risk 3-fold postmyocardial infarction [Krahn AD et al. \u003Cem\u003EAm J Med\u003C\/em\u003E 1995]. Nishida et al. recently determined the effects of chronic ischemia\/infarction on AF-related substrates in an animal model, providing novel insights into potential underlying mechanisms of AF in patients with CAD [Nishida K et al. \u003Cem\u003ECirculation\u003C\/em\u003E 2011].\u003C\/p\u003E\n         \u003Cp id=\u0022p-5\u0022\u003EWang et al. identified the Pitx2 homeobox gene (a gene that contains a short DNA sequence), which is involved in the development of the myocardial sleeve around pulmonary veins, as a key player in many forms of AF [Wang J et al. \u003Cem\u003EProc Natl Acad Sci USA\u003C\/em\u003E 2010]. In another study, Body et al. found that noncoding single-nucleotide polymorphisms (SNPs) within the chromosome 4q25 region are independently associated with postoperative AF after coronary artery bypass grafting [Body SC et al. \u003Cem\u003ECirc Cardiovasc Genet\u003C\/em\u003E 2009].\u003C\/p\u003E\n         \u003Cp id=\u0022p-6\u0022\u003EWhether these new clinical and genetic discoveries will translate into meaningful changes in clinicians\u0027 ability to predict which patients will develop AF or which patients will respond to prevention or active therapies remains unknown but is actively being pursued.\u003C\/p\u003E\n      \u003C\/div\u003E\u003Cdiv class=\u0022section\u0022 id=\u0022sec-2\u0022\u003E\n         \u003Ch2 class=\u0022\u0022\u003EAblation of AF \u2013 How, When, and What Else?\u003C\/h2\u003E\n         \u003Cp id=\u0022p-7\u0022\u003EAblation is the only proven treatment that is capable of eliminating AF in a substantial proportion of patients. Hakan Oral, MD, University of Michigan, Ann Arbor, Michigan, USA, discussed how and when catheter ablation should be initiated for the treatment of AF.\u003C\/p\u003E\n         \u003Cp id=\u0022p-8\u0022\u003ETargeting the underlying mechanisms is imperative for successful treatment with catheter ablation. These include addressing the arrhythmogenicity of pulmonary and other thoracic veins; autonomic dysregulation; fixed and\/or functional reentry with fibrillatory conduction, including multiple wavelets and high frequency sources (eg, rotors); and electroanatomical remodeling [HRS\/EHRA\/ECAS Expert Consensus Statement. \u003Cem\u003EHeart Rhythm\u003C\/em\u003E 2007].\u003C\/p\u003E\n         \u003Cp id=\u0022p-9\u0022\u003EPulmonary veins have a dominant role in AF [Haissaguerre M et al. \u003Cem\u003EN Engl J Med\u003C\/em\u003E 1998]. Therefore, ablation strategies that target the pulmonary veins and\/or the antrum with the goal of complete electrical isolation are the cornerstone for most AF procedures. For surgical pulmonary vein isolation, entrance and\/or exit blocks should be demonstrated [Heart Rhythm Society Guidelines. \u003Cem\u003EHeart Rhythm\u003C\/em\u003E 2007].\u003C\/p\u003E\n         \u003Cp id=\u0022p-10\u0022\u003EPatients with AF of longer duration, such as those with persistent or permanent AF, may require targeting of additional sites (eg, left atrium, coronary sinus, superior vena cava, ganglionated plexi, and complex fractionated atrial electrograms). Data show that use of this tailored approach eliminated paroxysmal AF in approximately 80% of patients [Oral H et al. \u003Cem\u003ECirculation\u003C\/em\u003E 2006]. Despite these advances, the long-term efficacy of catheter ablation to prevent recurrent AF requires further study. The totality of data suggests that AF ablation achieves \u22651 year of freedom from recurrent AF in many patients who are carefully selected to undergo the procedure. However, patients can have recurrent asymptomatic or symptomatic and unrecognized AF at any time after an ablation procedure. Therefore, adherence to anticoagulation is strictly required\u2014in particular, in those with multiple CHADS\u003Csub\u003E2\u003C\/sub\u003E risk factors for stroke that is associated with AF. Ongoing research in patients may reveal more about the long-term success of AF ablation with heart failure and other advanced structural heart disease.\u003C\/p\u003E\n      \u003C\/div\u003E\u003Cdiv class=\u0022section\u0022 id=\u0022sec-3\u0022\u003E\n         \u003Ch2 class=\u0022\u0022\u003EBottom Line for Referring Clinicians to their EP Colleagues\u003C\/h2\u003E\n         \u003Cp id=\u0022p-11\u0022\u003EIndications for catheter AF ablation include symptomatic AF that is refractory or intolerant to at least one class I or III antiarrhythmic medication. AF ablation may be performed in selected symptomatic patients with heart failure and\/or reduced EF. In rare clinical situations, it may be appropriate as first-line therapy. However, even after a successful AF ablation, it is important to recognize that the ACC\/AHA\/ESC 2011 guideline recommendations for anticoagulation at the time of cardioversion apply to patients who are in AF at the time of AF ablation (as AF termination is the goal of the procedure), including recommendations for the duration of therapeutic anticoagulation before and after the procedure. The presence of an LA thrombus, even if a patient is on a therapeutic anticoagulant, is a contraindication for catheter ablation of AF [HRS\/EHRA\/ECAS Consensus Statement. \u003Cem\u003EHeart Rhythm\u003C\/em\u003E 2007]. The efficacy of the novel oral direct IIa and Xa anticoagulants that are rapidly being approved for use in routine clinical practice in terms of use around the time of AF ablation and cardioversion procedures is actively being explored but not definitively known. In patients with a CHADS\u003Csub\u003E2\u003C\/sub\u003E risk score of 2 or higher, anticoagulation should be continued indefinitely, even after successful ablation.\u003C\/p\u003E\n         \u003Cp id=\u0022p-12\u0022\u003EACCF\/AHA\/HRS Guideline Recommendation for Duration of Anticoagulation after AF Ablation (2011 ACCF\/AHA\/HRS Focused Update on the Management of Patients with AF [Updating the 2006 Guideline])\u003C\/p\u003E\n         \u003Col class=\u0022list-ord \u0022 id=\u0022list-1\u0022\u003E\u003Cli id=\u0022list-item-1\u0022\u003E\n               \u003Cp id=\u0022p-13\u0022\u003ETherapeutic warfarin (INR goal: 2\u20133) is recommended for all patients for at least 2 months following an AF ablation.\u003C\/p\u003E\n            \u003C\/li\u003E\u003Cli id=\u0022list-item-2\u0022\u003E\n               \u003Cp id=\u0022p-14\u0022\u003ELow-molecular-weight heparin or IV heparin should be used as a bridge to resumption of systemic anticoagulation following AF ablation.\u003C\/p\u003E\n            \u003C\/li\u003E\u003Cli id=\u0022list-item-3\u0022\u003E\n               \u003Cp id=\u0022p-15\u0022\u003EDecisions regarding the use of warfarin more than 2 months following ablation should be based on the patient\u0027s risk factors for stroke that is associated with AF and not on the presence or type of AF. Risk determination can be aided by the CHADS\u003Csub\u003E2\u003C\/sub\u003E and CHA\u003Csub\u003E2\u003C\/sub\u003EDS\u003Csub\u003E2\u003C\/sub\u003E-Vasc scores.\u003C\/p\u003E\n            \u003C\/li\u003E\u003Cli id=\u0022list-item-4\u0022\u003E\n               \u003Cp id=\u0022p-16\u0022\u003EDiscontinuation of warfarin therapy postablation is generally not recommended in patients who have a CHADS\u003Csub\u003E2\u003C\/sub\u003E score \u2265 2.\u003C\/p\u003E\n            \u003C\/li\u003E\u003C\/ol\u003E\n      \u003C\/div\u003E\u003Cdiv class=\u0022section\u0022 id=\u0022sec-4\u0022\u003E\n         \u003Ch2 class=\u0022\u0022\u003EAnticoagulation for AF\u003C\/h2\u003E\n         \u003Cp id=\u0022p-17\u0022\u003EElaine M. Hylek, MD, MPH, Boston University Medical Center, Boston, Massachusetts, USA, discussed anticoagulation for AF.\u003C\/p\u003E\n         \u003Cp id=\u0022p-18\u0022\u003EAccording to Dr. Hylek, five randomized trials in nonrheumatic AF (AFASAK, SPAF, BAATAF, CAFA, and SPINAF) found significant efficacy in the use of warfarin\u2014a 66% overall risk reduction for stroke\u2014however, only about half of high-risk patients with AF receive warfarin therapy in routine clinical practice (\u003Ca id=\u0022xref-fig-1-1\u0022 class=\u0022xref-fig\u0022 href=\u0022#F1\u0022\u003EFigure 1\u003C\/a\u003E) [Friberg L et al. \u003Cem\u003EEur Heart J\u003C\/em\u003E 2006; Waldo AL et al. \u003Cem\u003EJ Am Coll Cardiol\u003C\/em\u003E 2005].\u003C\/p\u003E\n         \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\/11\/15\/20\/F1.large.jpg?width=800\u0026amp;height=600\u0026amp;carousel=1\u0022 title=\u0022Underutilization of Anticoagulation Therapy in AF.\u0022 class=\u0022fragment-images colorbox-load\u0022 rel=\u0022gallery-fragment-images-2034022548\u0022 data-figure-caption=\u0022Underutilization of Anticoagulation Therapy in AF.\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\/11\/15\/20\/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\/11\/15\/20\/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\/11\/15\/20\/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\/11685\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 attrib\u0022\u003E\u003Cspan class=\u0022fig-label\u0022\u003EFigure 1.\u003C\/span\u003E \n               \u003Cp id=\u0022p-19\u0022 class=\u0022first-child\u0022\u003EUnderutilization of Anticoagulation Therapy in AF.\u003C\/p\u003E\n            \u003Cq class=\u0022attrib\u0022 id=\u0022attrib-1\u0022\u003EReproduced with permission from E. Hylek, MD.\u003C\/q\u003E\u003Cdiv class=\u0022sb-div caption-clear\u0022\u003E\u003C\/div\u003E\u003C\/div\u003E\u003C\/div\u003E\n         \u003Cp id=\u0022p-20\u0022\u003ENovel anticoagulants for stroke prevention in AF include dabigatran (RE-LY), apixaban (ARISTOTLE), rivaroxaban (ROCKET-AF), and edoxaban (ENGAGE AF-TIMI 48; \u003Ca class=\u0022external-ref external-ref-type-clintrialgov\u0022 href=\u0022\/lookup\/external-ref?link_type=CLINTRIALGOV\u0026amp;access_num=NCT00781391\u0026amp;atom=%2Fspmdc%2F11%2F15%2F20.atom\u0022\u003ENCT00781391\u003C\/a\u003E) [Connolly SJ et al. \u003Cem\u003EN Engl J Med\u003C\/em\u003E 2009; Granger CB et al; \u003Cem\u003EN Engl J Med\u003C\/em\u003E 2011; Patel M et al. \u003Cem\u003EN Engl J Med\u003C\/em\u003E 2011; Ruff CT \u003Cem\u003EAm Heart J\u003C\/em\u003E 2010]. All of these trials have been completed, except ENGAGE (estimated end date in 2012).\u003C\/p\u003E\n         \u003Cp id=\u0022p-21\u0022\u003EBased on research findings from the pivotal Phase 3 studies, the United States Food and Drug Administration (FDA) approved dabigatran and rivaroxaban as having similar efficacy as therapeutic warfarin to reduce the risk of stroke in patients with nonvalvular AF. The FDA granted a priority review to apixaban in March 2012 for the prevention of stroke and systemic embolism in AF patients, given the positive results in ARISTOTLE that demonstrated reduction in stroke, bleeding, and mortality. ENGAGE AF-TIMI 48 is slated to end in 2012 and may provide for more flexible dosing (two doses studied, dose adjustments made before and after randomization). However, further research is needed to understand how to optimize the effectiveness of these novel agents in routine practice.\u003C\/p\u003E\n      \u003C\/div\u003E\u003Cul class=\u0022copyright-statement\u0022\u003E\u003Cli class=\u0022fn\u0022 id=\u0022copyright-statement-1\u0022\u003E\u00a9 2011 MD Conference Express\u00ae\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\/11\/15\/20.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?nzmv41\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?nzmv41\u0022\u003E\u003C\/script\u003E\n\u003C\/body\u003E\u003C\/html\u003E"}