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IntheClinic page ITC6-2 Treatmentpage ITC6-6 Practice Improvementpage ITC6-14 Tool Kitpage ITC6-14 page ITC6-15 page ITC6-16 Deborah Cotton, MD, MPHDarren Taichman, MDSankey Williams, MDPhysician WriterThe content of is drawn from the clinical information and education resources of the American College of Physicians(ACP), including (Medical KnowledgeAnnals of Internal Medicinefrom these primary sources in collaboration with the ACP’s Medical Educationand Publishing Division and with the assistance of science writers and physician writ-ers. Editorial consultants from provide expert review of the content.Readers who are interested in these primary resources for more detail can consulthttp://pier.acponline.org, http://www.acponline.org/products_services/mksap/15/?pr31,and other resources referenced in each issue of CME Objective: To review current evidence for the diagnosis and treatment of atrialThe information contained herein should never be used as a substitute for clinical© 2010 American College of Physicians Who is at risk for atrial Atrial fibrillation occurs in lessthan 1% of individuals aged 60 to65 years, but in 8% to 10% of thoseolder than 80 years. Prevalence ishigher in men than in women andhigher in whites than in blacks (1).The risk for AF increases with thepresence and severity of underlyingheart failure and valvular disease. What symptoms and signs shouldcause clinicians to suspect atrial Some patients have prominentsymptoms, including palpitations,shortness of breath, exercise intol-erance, chest pain, and malaise.However, many patients, particular-ly the elderly, have asymptomatic(silent) AF, including some patientswho have severe symptoms duringother AF episodes (4). Symptomsare generally greatest at disease on-set—when episodes are typicallyparoxysmal—and tend to diminishover time, especially when the arrhythmia becomes persistent.Symptoms result from elevation of ventricular rate (either at rest orexaggerated by exercise), irregularventricular rate, and loss of atrialcontribution to cardiac output.On physical examination, signs ofAF include a faster-than-expectedheart rate, which varies greatlyfrom patient to patient, an “irregu-larly irregular” time between heartsounds on auscultation, and periph-eral pulses that vary irregularly in Is a single electrocardiogramsufficient to diagnose or exclude Figure 1 is an electrocardiogram(ECG) showing AF, and it indi-cates that a single ECG is sufficientto diagnose AF provided it isrecorded during the arrhythmia.However, AF is often paroxysmal,so a single ECG showing normalrhythm does not exclude the diag-nosis. Monitoring for a longer timecan be helpful when AF is suspect-ed and the initial ECG is normal.In patients with daily symptoms,24- or 48-hour continuous Holtermonitoring is usually sufficient tomake the diagnosis. In patients withless-frequent symptoms, monitoringduring longer periods with electro-cardiographic loop recorders may benecessary. However, even monitor-ing for periods as long as a monthcan be nondiagnostic in patientswith very infrequent episodes. Inaddition, because patients must turnloop recorders on after symptomsbegin, these recorders are not help-ful in detecting asymptomatic ar-rhythmias or arrhythmia-associatednonspecific symptoms that the pa-tient may not recognize as being re-lated to AF. It may take years tosome patients because they havenonspecific symptoms and long pe-riods between episodes.Some newer devices avoid theseproblems. New types of event mon-itors detect irregular ventricularrhythms and automatically startrecording regardless of symptoms. © 2010 American College of Physicians ITC6-2 In the Clinic Annals of Internal Medicine 7 December2010 1. Kannel WB, BenjaminEJ. Current percep-ology of atrial fibrilla-tion. Cardiol Clin.[PMID:19111760]2. Hart RG, Benavente O,M

cBride R, Pearce LA.Antithrombotic ther-apy to prevent strokein patients with atrialfibrillation: a meta-analysis. Ann InternMed. 1999;131:492-501. [PMID: trial fibrillation (AF) is the most common, clinically significant car-diac arrhythmia. It occurs when a diffuse and chaotic pattern of elec-trical activity in the atria suppresses or replaces the normal sinusmechanism, leading to deterioration of mechanical function. Atrial fibrilla-tion is a major cause of morbidity, mortality, and health care expenditures;prevalence in the United States is 2.3 million cases and is estimated to in-crease to 5.6 million by the year 2050 (1). Atrial fibrillation is associatedwith a 5-fold increased risk for stroke and is estimated to cause 15% of allstrokes (2). Independent of coexisting diseases, the presence of AF confers a2-fold increased risk for all-cause mortality (3). Diagnosis © 2010 American College of Physicians ITC6-3 In the Clinic Annals of Internal Medicine 7 December2010 In addition, implanted pacemakersand implantable defibrillator–cardioverters with atrial leads iden-tify and record both symptomaticand asymptomatic AF. Other new devices continuously record heartrhythms for as long as a month andwirelessly transmit data to a centralmonitoring station, where automat-ed systems interpret cardiacrhythms and report diagnoses inreal time (4a). What is the role of history andphysical examination in patients History and physical examinationhelp determine the duration ofsymptoms and identify potentialunderlying causes. Cliniciansshould seek historical and physicalevidence of hypertension, heartfailure, cardiac surgery, murmursindicative of stenotic or regurgitantvalvular disease, and other indica-tions of structural heart disease. Inaddition, clinicians should look forsigns and symptoms of noncardiaccauses of AF, including pulmonarydisease, hyperthyroidism, use ofadrenergic drugs (such as thoseused to treat pulmonary disease) orother stimulants, and use of alco-hol. A family history might identifyfirst-degree relatives with AF, tic implications. What other electrocardiographicarrhythmias can be confused with Other arrhythmias that are com-monly confused with AF include si-nus rhythm with frequent prematureatrial contractions, atrial flutter, andatrial tachycardia. The key electro-cardiographic findings of AF are theabsence of P waves and the presenceof an irregular ventricular rhythmwithout a recurring pattern. Whenan irregular rhythm is present butthe diagnosis of AF is uncertain, cli-nicians should examine long record-ings from multiple leads looking forpartially obscured P waves in de-formed T waves and ST segments.Figure 2 is an ECG of an irregularrhythm that might be attributed toAF, but the presence of P wavesand other features identify sinusrhythm with frequent prematureatrial contractions. Figure 3 is anECG of another irregular rhythmthat might be attributed to AF, butthe presence of “saw-tooth” P wavesand a ventricular response thatvaries from 2:1 atrioventricularconduction to 4:1 atrioventricularconduction identifies atrial flutter. 3. Benjamin EJ, Wolf PA,DAgostino RB, et al.Impact of atrial fibril-lation on the risk ofdeath: the Framing-ham Heart Study. Cir-52. [PMID:9737513]4. Page RL, WilkinsonWE, Clair WK, et al.Asymptomatic ar-rhythmias in patientswith symptomaticparoxysmal atrial fib-rillation and paroxys-mal supraventriculartachycardia. Circula-[PMID:8281651]4a. Zimetbaum P, Gold-man A. Ambulatoryarrhythmia monitor-ing: choosing theright device. Circula- Figure 1. Electrocardiogram showing atrial fibrillation with rapid ventricular rate. 5. American College ofCardiology/AmericanHeart AssociationTask Force on Prac-tice Guidelines.ACC/AHA/ESC 2006Guidelines for theManagement of Pa-tients with Atrial Fib-rillation: a report ofthe American Collegeof Ca

rdiology/Ameri-can Heart AssociationTask Force on Prac-tice Guidelines andthe European Societyof Cardiology Com-mittee for PracticeGuidelines (WritingCommittee to Revisefor the Managementof Patients With AtrialFibrillation): devel-oped in collaborationwith the EuropeanHeart Rhythm Associ-ation and the HeartRhythm Society. Cir-[PMID:16908781] © 2010 American College of Physicians ITC6-4 In the Clinic Annals of Internal Medicine 7 December2010 How should clinicians classify Although knowledgeable observersdisagree on the answer to this ques-tion, the most accepted conventioncategorizes AF as paroxysmal, persist-ent, or permanent (5) (Box 1).“Paroxysmal” AF means that episodesterminate without intervention infewer than 7 days (often within 24hours). “Persistent” AF means thatepisodes last longer than 7 days or re-quire an intervention, such as car-dioversion, to restore sinus rhythm. “Permanent” AF means that the ar-rhythmia is continuous, and interven-tions to restore sinus rhythm have ei-ther failed or not been attempted.The same patient may be classifiedinto different categories at differenttimes, so clinicians should classify pa-tients according to the current patternor most common pattern.These distinctions are useful because they predict responses to therapy. For example, patientsare less likely to respond to Figure 2. Electrocardiogram showing sinus rhythm with frequent premature atrial contractions. Figure 3. Atrial flutter. Classic “saw-tooth” flutter waves are seen in all 12 leads, and the ventricularresponse is mostly regular. (There is a transient change from 2:1 to 4:1 atrioventricular conduction fol- 6. Furberg CD, Psaty BM,Manolio TA, et al.Prevalence of atrialfibrillation in elderlysubjects (the Cardio-Study). Am J Cardiol.[PMID:8037127]7. Naito M, David D,Michelson EL, et al.consequences of car-diac arrhythmias:evaluation of the rel-ative roles of abnor-mal atrioventricularsequencing, irregular-ity of ventricularrhythm and atrial fib-rillation in a caninemodel. Am Heart J.[PMID:6869209]8. Risk factors for strokeand efficacy of an-tithrombotic therapyin atrial fibrillation.Analysis of pooleddata from five ran-domized controlledtrials. Arch InternMed. 1994;154:1449-57. [PMID:8018000]9. Brand FN, Abbott RD,Kannel WB, Wolf PA.Characteristics andprognosis of loneatrial fibrillation. 30-year follow-up of theFramingham Study.JAMA. 1985:254:3449-53. [PMID:4068186]10. Hart RG, ShermanDG, Easton JD,Cairns JA. Preventionof stroke in patientswith nonvalvularatrial fibrillation.Neurology.[PMID:9748009] © 2010 American College of Physicians ITC6-5 In the Clinic Annals of Internal Medicine 7 December2010 antiarrhythmic drug therapy as thepattern goes from paroxysmal topersistent to permanent. Patients inall 3 categories, however, require What laboratory studies shouldclinicians obtain in patients newlydiagnosed with atrial fibrillation? When patients initially present withAF, clinicians should measure serumelectrolytes and thyroid-stimulatinghormone to identify possible causes.They should measure blood tests forrenal and hepatic function to guidethe selection of drug therapy andcheck a stool Hemoccult test beforestarting anticoagulation. Transtho-racic echocardiography helps deter-mine the patient’s potential respon-siveness to antiarrhythmic therapy bymeasuring left atrial size and assess-ing for valvular heart disease, peri-cardial disease, and left ventricularhypertrophy. A transesophagealechocardiogram to exclude atrial clotis indicated when transthoracic im-ages are inadequate or cardioversionis planned in a patient who has beentherapeutically anticoagulated forless than 3 weeks. In patients withappropriate clinical indications, addi-tional tests may be appropriate toevaluate the patient for pulmonaryembolism, acute myocardial infarc-tion, or acute h

eart failure. What underlying conditionsshould clinicians look for in Eighty percent of patients with AFhave structural heart disease, partic-ularly hypertensive heart disease but also coronary artery disease,valvular heart disease, or cardiomy-opathy. Atrial fibrosis occurs fre-quently with structural heart dis-ease, and many people consideratrial fibrosis central to the ar-rhythmia’s pathogenesis. “Lone” AFrefers to AF in the absence of heartdisease. Some experts believe thatthe diagnosis of lone AF should berestricted to patients younger than60 years of age because it is diffi-cult to exclude structural heart disease in older patients (6).Some acute illnesses are associatedwith AF, including acute myocardialinfarction, pulmonary embolism, andthyrotoxicosis. Atrial fibrillation oc-curs in approximately 40% of pa-tients after cardiac or thoracic sur-gery, but it may also occur after othertypes of major surgery or during asevere illness. Obesity and sleep ap-nea are associated with an increasedincidence of AF.Atrial fibrillation also occurs inpeople who have no predisposingconditions. These patients are typi-cally men 40 to 50 years of age, andsymptoms often occur at night, atrest, following vigorous exercise, orwith alcohol use. The mechanismsare unclear but may involve in-creases in circulating catechola-mines, changes in myocardial conduction times and refractory periods, and increases in vagal tone.Other forms of AF without knownunderlying conditions occur duringwaking hours and are preceded byemotional stress or exercise. Diagnosis... Atrial fibrillation is the most common clinically significant cardiacarrhythmia, and its prevalence increases with advancing age. Typical symptomsinclude palpitations, shortness of breath, and exercise intolerance. However, somepatients report only general malaise, and many patients are asymptomatic. Elec-trocardiogram recordings during episodes are the only way to confirm the diag-nosis. If the diagnosis is suspected and the ECG is normal, longer monitoring witha loop recorder or a Holter monitor can be helpful. The initial assessment shouldinclude laboratory tests for electrolytes, thyroid-stimulating hormone, and renaland hepatic function to rule out underlying disorders or contraindications totherapies. An echocardiogram should be done to look for structural heart disease. CLINICAL BOTTOM LINE Classification of Atrial Fibrillation Paroxysmal: Episodes spontaneously Pe�rsistent: Episodes last 7 days and require intervention to restore sinusPermanent: Interventions to restore sinusrhythm have either failed or have notbeen attempted © 2010 American College of Physicians ITC6-6 In the Clinic Annals of Internal Medicine 7 December2010 What are the complications oftherapy decrease the risk for There are 3 reasons to treat AF: toreduce symptoms, to preventthromboembolism, and to preventcardiomyopathy.Although AF is not always symp-tomatic, the symptoms can be dis-abling. Symptoms are usuallycaused by inappropriately rapidventricular rates or the irregularityof the ventricular response (7). Theloss of atrial contribution to ven-tricular filling (“atrial kick”) is welltolerated by most patients exceptthose with ventricular hypertrophyfrom long-standing hypertension,aortic stenosis, and hypertrophicobstructive cardiomyopathy.Stroke is the most common formof arterial thromboembolism dur-ing AF. In patients with nonvalvu-lar AF, the average annual risk forarterial thromboembolism, includ-ing stroke, is 5%, and the risk ishigher in patients older than age 75years (8). The risk is related to spe-cific features of AF as well as otherrisk factors for thromboembolism(9). Left atrial thrombi cause 75%of strokes in patients with AF (10).It is important to treat the tachycardiaof AF because it can lead to cardiomyopathy if left untreat

ed (11). When should clinicians consider Prompt cardioversion should beconsidered for new-onset AFwhen the duration of the arrhyth-mia is less than 48 hours. One ex-ample is a hospitalized patient oncardiac monitoring. Most patientswith AF do not require immediatecardioversion, but it can obviatethe need for anticoagulation andmay be appropriate in selected pa-tients with decompensated heartfailure, severe angina or acute infarction, hypotension, or highrisk for acute stroke. Patients withAF and the Wolff-Parkinson-White syndrome can have ex-tremely rapid atrioventricular con-duction mediated by the accessorypathway, which can be a poten-tially life-threatening conditionand require urgent cardioversion. fibrillation should cliniciansconsider hospitalizing? Although AF is usually managed inan outpatient setting, cliniciansshould consider hospitalizing pa-tients with AF when managementrequires close monitoring for safety(12) (Box 2). Should clinicians attempt ratecontrol or rhythm control? Traditionally, most clinicians havepreferred rhythm control to ratecontrol, but recent, high-qualityclinical trials have shown thatrhythm control generally does notimprove mortality, stroke, hospital-ization, or quality of life comparedwith rate control (13, 14). Ratecontrol is easier to accomplish andprevents exposure to the potentialadverse effects of antiarrhythmicagents. On the other hand, rhythmcontrol may be useful in selectedpatients with severe symptoms (be-fore or after failure of rate control)or in younger patients withoutstructural heart disease.The AFFIRM (Atrial Fibrillation Follow-upInvestigation of Rhythm Management) tri-al included 4060 patients with AF who hadat least 1 risk factor for stroke. The meanage was 69 years, and structural heart dis-ease, aside from hypertension, was unusu-al. All-cause mortality at 5 years was 25.9%in the rate-control group and 26.7% in therhythm-control group (= 0.080). Patientswith apparently successful rhythm controlstill needed anticoagulation because ofpersistent stroke risk, and patients whowere able to maintain sinus rhythm had asurvival advantage that was almost bal-anced by the disadvantage imposed byantiarrhythmic drug therapy (15). 11. Redfield MM, KayGN, Jenkins LS, et al.Tachycardia-relatedcardiomyopathy: aventricular dysfunc-tion in patients withatrial fibrillation re-ferred for atrioven-tricular ablation.Mayo Clin Proc.[PMID:10943231]12. Chung MK. Schweik-ert RA. Wilkoff BL, etal. Is hospital admis-sion for initiation ofantiarrhythmic ther-apy with sotalol foratrial arrhythmias re-quired? Yield of in-hospital monitoringand prediction ofrisk for significant ar-rhythmia complica-tions. JACC.[PMID:9669266]13. Atrial Fibrillation Fol-low-up Investigationof Rhythm Manage-ment (AFFIRM) In-vestigators. A com-parison of ratecontrol and rhythmcontrol in patientswith atrial fibrillation.N Engl J Med.[PMID:12466506]14. Hohnloser SH, KuckKH, Lilienthal J.Rhythm or rate con-trol in atrial fibrilla-tion„Pharmacolog-ical Intervention inAtrial Fibrillation(PIAF): a randomisedtrial. Lancet.[PMID:11117910] Treatment Situations in Which Patientswith Atrial Fibrillation MayRequire Hospitalization Uncertain or unstable underly-Acute myocardial infarction, al-tered mental status, decompen-sated heart failure, or hypotensionIntolerable symptoms despitehemodynamic stabilityElective cardioversion (if moni-tored outpatient setting is notAcute anticoagulation if very-high risk for strokeTelemetry monitoring duringinitiation of certain drugsProcedures such as cardiaccatheterization, electrophysio-logic studies, pacemakers, im-plantable defibrillators, orcatheter or surgical ablation 15. AFFIRM Investiga-tors. Relationshipsbetween sinusrhythm, treatment,and survival in theAtrial Fibrillation Fol-low-Up Investigationof Rhythm Manage-ment

(AFFIRM)Study. Circulation.[PMID:15007003]16. Atrial Fibrillation andCongestive HeartFailure Investigators.Rhythm control ver-sus rate control foratrial fibrillation andheart failure. N EnglJ Med.[PMID:18565859]17. American College ofCardiology/Ameri-can Heart Associa-tion Task Force onPractice Guidelines.ACC/AHA/ESC 2006Guidelines for theManagement of Pa-tients with Atrial Fib-rillation. Circulation.[PMID:16908781]18. Van Gelder IC,Groenveld HF, CrijnsHJGM, et al. Lenientversus Strict ratecontrol in patientswith atrial fibrillation.N Engl J Med.[PMID:20231232]19. Davy JM, Herold M,Hoglund C, et al.Dronedarone for thecontrol of ventricularrate in permanentatrial fibrillation: theEfficacy and safety ofdRonedArone forthe cOntrol of ven-tricular rate duringatrial fibrillation (ER-ATO) study. AmHeart J.[PMID:18760136]20. Vassallo P. TrohmanRG. Prescribingamiodarone: an evi-dence-based reviewtions. JAMA.[PMID:17878423]21. Maisel WH, Kuntzal. Risk of initiatingantiarrhythmic drugtherapy for atrial fib-rillation in patientsadmitted to a uni-versity hospital. AnnIntern Med.[PMID:9265427] © 2010 American College of Physicians ITC6-7 In the Clinic Annals of Internal Medicine 7 December2010 A more recent trial extended these obser-vations to patients with severe heart fail-ure by randomly assigning 1376 patientswith AF, left ventricular ejection fractionof 35%, and heart failure symptoms torate control versus rhythm control. At 37months, death from cardiovascular dis-ease occurred in 25% of the rate-controlgroup and in 27% of the rhythm-controlgroup (= 0.6). There was no improve-ment in all-cause mortality, stroke, heartfailure, or need for hospitalization in therhythm-control group (16). What strategies should cliniciansconsider for rate control in Clinicians should consider drugtherapy to control ventricular rate inall patients with AF, even if rhythmcontrol is eventually done. Althoughcriteria for rate control vary with pa-tient age, the traditional target hasbeen heart rates of 60 to 80 beats perminute at rest and between 90 to115 beats per minute during moder-ate exercise (17). However, a recentstudy comparing a strategy of lenientrate-control (resting heart rate 110beats per minute) with a strategy ofstrict rate control ( 80 beats perminute), found no advantage to thestricter rate control strategy (18).decrease atrioventricular nodal con-duction includes -blockers andnondihydropyridine calcium-channelantagonists (Table 1). A recently ap-proved antiarrhythmic medication,dronedarone, has also been shown tobe safe and modestly effective forrate control of AF (19).Digitalis and amiodarone block theatrioventricular node but are not rec-ommended as first-line monotherapyfor rate control (17). Digitalis doesnot reduce the tachycardia that oc-curs with exercise, and it is unlikelyto control rate in patients with heartfailure and high sympathetic activity.Amiodarone is occasionally used toreduce ventricular response if otheragents have failed, but this practice isdifficult to justify because of the as-sociated toxicities (20). What strategies should cliniciansconsider for rhythm control in Rhythm control is no longer thepreferred strategy in most patientswith AF. The trials comparingrate control with rhythm control,however, have not includedyounger patients or those withhighly symptomatic AF. There-fore, it is reasonable to considerrhythm control in these patients.Also, experienced clinicians oftenprefer rhythm control for the firstepisode of symptomatic AF inyounger patients because manymaintain sinus rhythm withoutantiarrhythmic drug treatment af-ter cardioversion.Patients can be converted to nor-mal sinus rhythm with direct elec-trical current or with drugs. Elec-trical cardioversion is indicatedwhen the patient is hemodynami-cally unstable. When the patient ishemo

dynamically stable, the con-version rate with antiarrhythmicdrugs is lower than that with elec-trical direct current but does notrequire deep sedation or generalchoice of antiarrhythmic drug ther-apy to prevent recurrence.Patients should receive therapy toachieve both rate control and ade-quate anticoagulation before electivedirect current or pharmacologic car-dioversion of AF more than 48hours in duration. In addition, theserum potassium level should begreater than 4.0 mmol/L, serummagnesium level should be greaterthan 1.0 mmol/L, and ionized calci-um levels should be greater than 0.5mmol/L. In most cases, cardiover-sion should be performed in a moni-tored hospital setting to permit ade-quate assessment of the degree ofrate control, bradycardia, proarrhyth-mic affects of antiarrhythmic agents,and other adverse effects (21).Antiarrhythmic drugs other thanamiodarone generally have equal © 2010 American College of Physicians ITC6-8 In the Clinic Annals of Internal Medicine 7 December2010 Table 1. Drug Therapy for Rate and Rhythm Control in Atrial FibrillationAgentMechanism of ActionDosageBenefitsSide EffectsNotes Rate-Controlling AgentsMetoprololSelective ß-adrenergic–5 mg IV every 5 min, Convenient IV Bradycardia, hypotension,receptor blocking agentup to 15 mg 50–100 administration in NPOheart block, mg PO twice dailypatients, rapid onset of bronchospasm (lessaction, dependable AV frequently than nonselectivenodal blockadeß-blockers), worsening of CHFPropranololNonselective ß-adrenergic–1–8 mg IV (1 mg everyInexpensive, commonlyBradycardia, hypotension,receptor blocking agent2 min). 10–120 mg PO availableheart block, bronchospasm,3 times daily; long-worsening of CHF80–320 mg PO once daily.EsmololShort-acting IV ß0.05–0.2 mg/kg per Short-acting, titratableBradycardia, hypotension,Occasionally selective adrenergic min IVon or off with very rapidheart block, bronchospasminconsistent effect inreceptor-blocking agenthalf-life(less frequent)high-catecholamine statesPindololNonselective ß-adrenergic–2.5–20 mg PO 2–3Less bradycardia, lessBradycardia, hypotension,Less propensity for receptor blocking agent times dailybronchospasmheart blockheart block than with intrinsic sympatho-AtenololSelective ß-adrenergic–5 mg IV over 5 min,Does not cross blood–Bradycardia, hypotension,receptor blocking agentrepeat in 10 min. brain barrier, fewer heart block25–100 mg PO once CNS side effectsNadololNonselective ß-adrenergic–20–120 mg once dailyLower incidence of Bradycardia, hypotension, Oral form onlyreceptor blocking agentcrossing blood–brain heart blockbarrier, fewer CNS side VerapamilCalcium-channel blocking 5–20 mg in 5-mgConsistent AV nodal Hypotension, heart block,Do not use in theagentincrements IV every blockadedirect myocardial depressionWolff–Parkinson–30 min, or 0.005 mg/kgWhite syndrome120–360 mg PO daily, in divided doses or in DiltiazemCalcium-channel blocking 0.25–0.35 mg/kg IVConsistent AV nodal Hypotension, heart block, lessDo not use in the agentfollowed by 5–15 mg/h.blockademyocardial depressionWolff–Parkinson–120–360 mg PO daily White syndromeas slow releaseDigoxinNa+/K+ pump inhibitor,0.75–1.5 mg PO or IVParticularly useful for Heart block, digoxin-First-line therapyincreases intracellular in 3–4 divided dosesrate control in CHFassociated arrhythmias;only in patients with calciumover 12–24 h. dosage adjustment requireddecreased left-Maintenance dose: in renal impairmentventricular systolic 0.125 mg PO or IV to function. Not useful0.5 mg dailyfor rate control with exer-version of AF or aflutter toProcainamideProlongs conduction 1–2 g q 12 h (shorter-Convenient IV dosingNot recommended becauseNeed to follow drug and slows repolarization acting oral preparationsavailable with of frequent side effects, levels and QT interval by blocking inward Na+ are no longer avail

able)maintenance infusion, including hypotension, for toxicity, adjust fluxand conversion to PO nausea, vomiting, dose in patients with tablets, very effective lupus-like syndrome, QTrenal insufficiency. at converting AF to prolongation, andNot for use in patients NSRarrhythmiawith severe LVQuinidine Prolongs conduction andgluconateslows repolarization. 324–648 mg PO Relatively effective inProarrhythmia, nausea, Not recommended Blocks fast inward Na+ every 8–12 hconverting AF to NSRvomiting, diarrhea, because of frequent channelbut may take several QT prolongationside effects. Follow days to achieve NSR drug levels and QT inter-because of PO dosingval for toxicity. Adjust dosein patients with renal insuf-ficiency. Oral agent only. 22. The Cardiac Arrhyth-mia Suppression Tri-al (CAST) Investiga-tors. Preliminaryreport: effect of en-cainide on mortalityin a randomized trialof arrhythmia sup-pression after my-ocardial infarction. NEngl J Med.[PMID:2473403] © 2010 American College of Physicians ITC6-9 In the Clinic Annals of Internal Medicine 7 December2010 efficacy, so susceptibility to side ef-fects should guide the choice amongthem (Table 1). Drugs that blockcardiac sodium channels (class I ef-fect), such as flecainide andpropafenone, are useful in patientswithout coronary heart disease oradvanced left ventricular dysfunc-tion. They should not be used in pa-tients with significant structural heart disease because they have beenassociated with increased mortalityin these patients (22). Their side ef-fects are due to unwanted sodium-channel blockade in other organ sys-tems, such as the gastrointestinaltract (resulting in anorexia oresophageal reflux) and the centralnervous system. Other class I drugs,such as quinidine and procainamide, Table 1 (continued). Drug Therapy for Rate and Rhythm Control in Atrial FibrillationAgentMechanism of ActionDosageBenefitsSide EffectsNotes DisopyramideSimilar electrophysiologic 150 mg PO every Can be useful in QT prolongation (not PR Rarely used in current era properties to procainamide6–8 h, or 150–300 mgpatients with or QRS), torsades de of antiarrhythmic therapy. and quinidinetwice a dayhypertension and pointes, heart blockOral agent only, negative normal LV functioninotropic properties.FlecainideBlocks Na+ channels 2 mg/kg, IV. 50–150Efficacy in paroxysmalAflutter or atrial tachycardia Not for use in (and fast Na+ current)mg PO every 12 h. AF with structurally with rapid ventricular patients withAlso, single loading normal heartsresponse but not with acutestructurally abnormal doses of 300 mg are single loading doses. VT heartsefficacious in conversion and VF in diseased heartsof recent onset AF.PropafenoneBlocks myocardial 2 mg/kg, IV. 150–300Efficacy in paroxysmal Aflutter or atrial tachycardia Antiarrhythmic and Na+ channelsmg PO every 8 h. Also, and sustained AFwith rapid ventricular response,weak calcium channel single loading doses of but not with acute single and ß-blocking 600 mg are efficacious loading dosesproperties. Not for in conversion of recent use with structuralonset AF.heart disease.IbutilideProlongs action potential 1 mg IV over 10 min. Efficacy in acute and Polymorphic VT (torsades de In some centers, only used duration (and atrial and May be repeated oncerapid conversion of AFpointes) occurred in 8.3% in the electrophysiology ventricular refractoriness) if necessary.to NSRof patients in a clinical trial laboratory. May also be by blocking rapid (most with LV dysfunction), used to facilitate component of delayed QT prolongationunsuccessful direct-rectifier potassium currentcurrent rectifier potassiumAmiodaroneBlocks Na+ channels 5–7 mg/kg IV up to Safest agent for use Bradycardia, QT prolongation, Can be used in the (affinity for inactivated 1500 mg per 24 h. in patients with hyperthyroidism, lung toxicity,

Wolff–Parkinson–channels). Noncompetitive 400–800 mg PO daily, structural heart disease,argyria (blue discoloration White syndrome. ß- and ß-receptor for 3–4 wk, followed good efficacy in of skin) with chronic useinhibitor.by 100–400 mg PO maintaining NSR dailychronicallySotalolNonselective ß- and 80–240 mg PO everySimilar efficacy to Fatigue, depression, ß-blocking properties, but-blocking agent, 12 hquinidine, but fewer bradycardia, torsades de some positive inotropic prolongs action adverse effects. Better pointes, CHFactivity. Lethal arrhythmias potential durationrate control because of possible. Adjust dose in ß-blocking properties.patients with renal insuffi-ciency. Initiate on telemetry.DofetilideBlocks rapid component 500 µg twice dailyMore effective than QT prolongation, torsades Must be strictly dosed of the delayed rectifier quinidine in conversionde pointes (2%–4% risk). according to renal potassium current (I),to and maintenance of function, body size, prolonging refractoriness NSR.and age. Contra-without slowing conductionindicated in patients with creatinine clearance mL/min. Initiate on telemetry.DronedaroneSimilar to amiodarone—400 mg twice dailyWell-tolerated and safeGastrointestinal intoleranceblocks sodium, potassium, AF = atrial fibrillation; AV = atrioventricular; CHF = congestive heart failure; CNS = central nervous system; IV = intraventricular; LV = left ventricular; NPO =nil per os; NSR = normal sinus rhythm; PO = orally; VF = ventricular fibrillation; VT = ventricular tachycardia. 23. Zimetbaum P. Amio-darone for atrial fib-rillation. N Engl JMed 2007;356;935-[PMID:17329700]24. Hohnloser SH, CrijnsHJ, van Eickels M, etal; ATHENA Investi-gators. Effect ofdronedarone on car-diovascular events inatrial fibrillation. NEngl J Med.Epub 2009 Aug 30.PMID:1921368025. Lafuente-Lafuente C,Mouly S, Longas-Tejero MA, BergmanJF. Antiarrhythmicsfor maintaining sinusrhythm after car-dioversion of atrialfibrillation. CochraneDatabase Syst Rev26. Roy D, Talajic M, Do-rian P, et al. Amio-darone to preventrecurrence of atrialfibrillation. CanadianTrial of Atrial Fibrilla-tion Investigators. NEngl J Med.[PMID:10738049]27. CHARM Investiga-tors. Prevention ofatrial fibrillation inpatients with symp-tomatic chronicheart failure by can-desartan in the Can-desartan in Heartfailure: Assessmentof Reduction in Mor-tality and morbidity(CHARM) program.Am Heart J.[PMID:16838426]28. Stroke Prevention inAtrial Fibrillation In-vestigators. Lessonsfrom the Stroke Pre-vention in Atrial Fib-rillation trials. AnnIntern Med.[PMID:12755555]29. Jung F, DiMarco JP.Treatment strategiesfor atrial fibrillation.Am J Med.[PMID:9552091]30. Zabalgoitia M,Halperin JL, PearceLA, et al. Trans-diographic corre-lates of clinical riskof thromboem-bolism in nonvalvu-lar atrial fibrillation.Stroke Prevention inAtrial Fibrillation IIIInvestigators. J AmColl Cardiol.[PMID:9626843] © 2010 American College of Physicians ITC6-10 In the Clinic Annals of Internal Medicine 7 December2010 are used infrequently because ofnoncardiac side effects and a concernfor proarrhythmia. Drugs that blockpotassium channels and thus haveclass III effects, such as sotalol anddofetilide, can prolong the QT inter-val and cause torsades de pointes.Amiodarone can be used in patientswith advanced structural heart dis-ease. However, amiodarone can causepermanent liver and lung toxicitythat is dose- and duration-dependent(23). Hepatic toxicity is characterizedby hepatitis that can progress to cir-rhosis. Pulmonary toxicity can devel-op within 6 weeks or after years oftherapy and most often manifests ascough and dyspnea. Pulmonary im-aging can demonstrate a broad rangeof findings, including segmental ordiffuse infiltrates. Other side effectsinclude thyroid dysfunction (hypo-thyroidism, hyperthyroidism), sunsensitivity

, and ocular symptoms.Dronedarone is a multichannelblocking drug similar in structureto amiodarone but without iodine.A study of 4300 patients demon-strated its safety in patients withheart failure (24). As a result,dronedarone is approved by theU.S. Food and Drug Administra-tion (FDA) to reduce hospitaliza-tions in patients with AF but iscontraindicated for decompensatedcongestive heart failure. It is less ef-ficacious but better tolerated thanamiodarone (24). When should clinicians useantiarrhythmic drugs to preventthe recurrence of atrial Antiarrhythmic drugs have onlymodest effects compared withplacebo in prolonging the time torecurrence of AF (25) (Table 1).Therefore, antiarrhythmic drugtherapy is generally considered effective if it reduces the frequency of episodes and symptoms.The Canadian Trial of Atrial Fibrillation ran-domly assigned 403 patients to amiodarone, sotalol, or propafenone and found that af-ter mean follow-up of 16 months, recur-rence of AF was 35% for amiodarone ther-apy compared with 63% for sotalol orpropafenone therapy (26)Some nonantiarrhythmic drugs, suchas angiotensin-converting enzymeinhibitors and statins, reduce the in-cidence of AF in patients with heartfailure, presumably because of theirantifibrotic effects (27). When is anticoagulation indicated Patients with paroxysmal, persist-ent, and permanent AF have thesame indications for anticoagula-tion. Anticoagulation is indicatedwhen the risk for thromboem-bolism exceeds that for anticoagu-lation-associated bleeding (8, 17).For example, a patient older than65 years with AF and no other riskfactors has a risk for thromboem-bolism of about 1%, which approxi-mates the risk for major bleedingon warfarin when the internationalnormalized ratio (INR) is betweenBecause of the delicate balance be-tween risk and benefit, investigatorshave developed guides to indicatewhich patients with AF warrantanticoagulation therapy. The mostpopular of these guides is the(Cardiac Failure, Hyper-tension, Age, Diabetes, and Stroke[Doubled])score (31, 32), which isdiscussed in Table 2, and Table 3presents recommendations for ther-apy based on this score. Cliniciansshould consider long-term anticoagulation in patients who are athigh risk for recurrent AF or haveasymptomatic AF, intracardiacthrombus, or known risk factors forthromboembolism, which include75 years, recent heart failure,left ventricular dysfunction, dia-betes mellitus, hypertension, andprevious thromboembolism. Manyclinicians use a cutoff of 65 ratherthan 75 years to initiate warfarin 31. Gage BF, WatermanAD, Shannon W, etal. Validation of clini-schemes for predict-ing stroke: resultsfrom the NationalRegistry of Atrial Fib-rillation. JAMA.[PMID:11401607]32. van Walraven C, HartRG, Wells GA, et al. Aclinical predictionrule to identify pa-tients with atrial fib-rillation and a lowrisk for stroke whiletaking aspirin. ArchIntern Med.[PMID:12719203] © 2010 American College of Physicians ITC6-11 In the Clinic Annals of Internal Medicine 7 December2010 therapy when the patient also hascoronary artery disease.A 2007 meta-analysis of 28 044 patientswith AF in 29 clinical trials reported that,compared with control patients, patientson adjusted-dose warfarin (6 trials, 2900participants) had 64% (95% CI, 49% to74%) fewer strokes and patients on an-tiplatelet agents (8 trials, 4876 partici-pants) had 22% (CI, 6% to 35%) fewerstrokes. Warfarin was superior to an-tiplatelet therapy (relative risk reduction,39% [CI, 22% to 52%]) (12 trials, 12 963 par-ticipants), and both therapies were associ-ated with a beneficial tradeoff betweenstrokes and major extracranial hemor-Some recent data indicate that cur-rent incidences of stroke and bleed-ing are lower because of improvedtherapy for hypertension (34), andother recent data indicate that theincidence of major bl

eeding remainshigh in the elderly (35). As a result,some experts advise alternative ther-apy for anticoagulation (36), butcoagulation in patients with AF havenot changed. Also, although genetictests can identify variants in some ofthe enzymes that control warfarinmetabolism (37), most experts donot recommend using these genetictests until clinical trials determinewhether the information they pro-vide can improve patient outcomesfrom better warfarin dosing. What anticoagulation regimensshould clinicians use in patients Warfarin is the first choice for anti-coagulation in patients with AF, andthe dose should be adjusted to anINR of 2.0 to 3.0. Most patientswith prosthetic valves should havethe warfarin dose adjusted to anINR of 2.5 to 3.5. Aspirin 325 mg/dcan be used as an alternative to war-farin in the following circumstances:contraindication/allergy to warfarin;no previous stroke or transient is-chemic attack; 75 years of age; andno hypertension, diabetes, or heartfailure (38). Aspirin plus clopidogrelprevents more strokes than aspirin alone (39), but this combination isnot as effective as warfarin and has ableeding risk equivalent to that ofwarfarin (40).In patients at lower risk for throm-boembolism, the clinician can startwarfarin without a loading dose orconcurrent heparin, but patients athigher risk for thromboembolismshould be hospitalized and given Table 2. Stroke Risk in Patients with Nonvalvular Atrial Fibrillation Not Treatedwith Anticoagulation According to CHADSRisk CriteriaScore Past stroke or TIA2�Age 75 y1Hypertension1Diabetes mellitus1Heart failure1 Patients (n= 1733)Adjusted Stroke Rate (%/y)(95% CI)CHADS 1201.9 (1.2 to 2.0)04632.8 (2.0 to 3.8)15234.0 (3.1 to 5.1)23375.9 (4.6 to 7.3)32208.5 (6.3 to 11.1)46512.5 (8.2 to 17.5)5518.2 (10.5 to 27.4)6 = Cardiac Failure, Hypertension, Age, Diabetes, and Stroke (Doubled); TIA = transient ischemic attack.* Reproduced from reference 5 with permission from the American Heart Association.The adjusted stroke rate was derived from multivariate analysis assuming no aspirin use. Data from from references 30 and 31. Table 3. Antithrombotic Therapy for Patients with Atrial Fibrillation* Risk CategoryRecommended Therapy No risk factorsAspirin, 81–325 mg daily1 moderate risk factorAspirin, 81–325 mg daily or warfarin (INR, 2.0–3.0, target 2.5)Any high risk factor or Warfarin (INR, 2.0–3.0, target more than 1 moderate2.5)*risk factor Less-Validated or Weaker Moderate Risk FactorsHigh Risk FactorsRisk Factors Female sexAge 75 yPrevious stroke, TIA, or embolismAge 65–74 yHypertensionMitral stenosisCoronary artery diseaseHeart failureProsthetic heart valveThyrotoxicosisLV ejection fraction Diabetes mellitus INR = international normalized ratio; LV = left ventricular; TIA = transient ischemic attack.* Reproduced from reference 5 with permission from the American Heart Association.�If mechanical valve, target INR 2.5. 33. Hart RG, Pearce LA,Aguilar MI. Meta-analysis: antithrom-botic therapy to pre-vent stroke inpatients who havenonvalvular atrial fib-rillation. Ann InternMed. 2007;146:857-67. [PMID:17577005]34. Hart RG, Tonarelli SB,Pearce LA. Avoidingcentral nervous sys-tem bleeding duringantithrombotic ther-apy: recent data andideas. Stroke.[PMID:15947271]35. Hylek EM, Evans-Molina C, Shea C, etal. Major hemor-rhage and tolerabili-ty of warfarin in thefirst year of therapyamong elderly pa-tients with atrial fib-rillation. Circulation.[PMID:17515465]36. Singer DE, Chang Y,Fang MC, et al. Thenet clinical benefitof warfarin anticoag-ulation in atrial fibril-lation. Ann InternMed. 2009;151:297-[PMID:19721017]37. Lenzini P. WadeliusM. Kimmel S, et al.Integration of genet-ic, clinical, and INRdata to refine war-farin dosing. ClinicalPharmacol Ther.[PMID:20375999]38. The SPAF III WritingCommittee for the

Stroke Prevention inAtrial Fibrillation In-vestigators. Patientswith nonvalvularatrial fibrillation atlow risk of strokeduring treatmentwith aspirin: StrokePrevention in AtrialFibrillation III Study.JAMA.[PMID:9565007]39. ACTIVE Investigators.Connolly SJ. Pogue J.Hart RG. HohnloserSH. Pfeffer M.Chrolavicius S. YusufS. Effect of clopido-grel added to aspirinin patients with atri-al fibrillation. N EnglJ Med.[PMID:19336502] © 2010 American College of Physicians ITC6-12 In the Clinic Annals of Internal Medicine 7 December2010 unfractionated heparin while waitingto achieve target levels for oral anti-coagulation. Data on use of low-mo-lecular-weight heparin in this settingare limited.Warfarin should be used to achievean INR of 2.0 to 3.0 for at least 3to 4 consecutive weeks before car-dioversion and at least 4 weeks af-ter cardioversion in patients withAF lasting more than 48 hours. Analternative approach is to performa transesophageal echocardiogram,and if clot is not present, anticoag-ulate with heparin for 48 hours be-fore cardioversion followed by 4weeks of warfarin anticoagulation(40). Patients with thrombus in theleft atrial appendage must be anti-coagulated for 4 weeks before car-dioversion regardless of the dura-tion of AF, and most cliniciansrepeat the transesophagealechocardiogram before cardiover-sion to confirm that the thrombushas resolved.Warfarin has a narrow therapeuticwindow, and its metabolism is af-fected by many drug and dietaryinteractions, requiring frequentINR monitoring and dosage ad-justments. These limitations haveprompted a search for alternativeOne clinical trial of dabigatran, a directthrombin inhibitor, compared 2 doses (110mg and 150 mg twice daily) of dabigatranwith warfarin in patients who had nonvalvu-lar AF. The lower dose of dabigatran was as ef-fective as warfarin in preventing strokes, andit was associated with fewer bleeding compli-cations than warfarin. The higher dose ofdabigatran was more effective than warfarinin preventing strokes and caused an equiva-lent number of bleeding events (41).The FDA has approved dabigatranat 150 mg twice daily for preven-tion of stroke and systemic em-bolism in persons with AF and creatinine clearance greater than 30mL/min. However, the FDA ap-proval does not allow a superiorityclaim over warfarin. When should clinicians considernondrug therapies for patients Clinicians should consider nondrugtherapy only after failure of drugtherapy. Nondrug therapies includeuse of a catheter or surgery to ab-late the atrioventricular node fol-lowed by permanent pacing,catheter or surgical ablation ofparts of the atrium where AF be-gins, and occluding the left atrialappendage for stroke prevention.Atrioventricular nodal catheter ab-lation is used when pharmacologicrate control cannot be achieved,usually because of intolerance tomedications. This situation is mostcommon in elderly patients or pa-tients with advanced heart failureor obstructive pulmonary disease,which limits the use of -blockers.Atrioventricular nodal ablation ishighly effective (42) but requirespacemaker insertion and can leadto progressive left ventricular dys-function. Pacing therapy withoutatrioventricular nodal ablation haslittle effect on the burden of AFbut may be helpful in patients withparoxysmal AF and symptomaticbradycardia, which is often a sideeffect of drug therapy.Ablation of parts of the atriumwhere AF begins has been shownto be effective in preventing recur-rent symptomatic AF in highly se-lected patients (43). The ideal pa-tient is a young, otherwise healthyperson without structural heart dis-ease who has paroxysmal AF. Re-cent guideline statements have ac-knowledged that it may bereasonable to provide this therapyfor highly symptomatic patientswith paroxysmal AF in whom anattempt at antiarrhythmic drugtherapy has failed. This

relativelyaggressive approach may preventprogressive AF-related morbidity(e.g., residual risk for stroke, med-ication side effects), but long-termbenefit on mortality has not beendemonstrated. The effect of 40. ACTIVE WritingGroup of the ACTIVEInvestigators. Clopi-dogrel plus aspirinversus oral anticoag-ulation for atrial fib-rillation in the Atrialfibrillation Clopido-grel Trial with Irbe-sartan for preventionof Vascular Events(ACTIVE W): a ran-domised controlledtrial. Lancet.[PMID:16765759]41. Connolly SJ,Ezekowitz MD, YusufS, et al; RE-LY Steer-ing Committee andInvestigators. Dabi-gatran versus war-farin in patients withatrial fibrillation. NEngl J Med.Epub 2009 Aug 30.[PMID:19717844]42. Wood MA, Brown-Mahoney C, Kay GN,Ellenbogen KA. Clini-cal outcomes afterablation and pacingtherapy for atrial fib-rillation : a meta-analysis. Circulation.[PMID:10715260]43. Packer DL, Asir-vatham S, MungerTM. Progress in non-pharmacologic ther-apy of atrial fibrilla-tion. J CardiovascElectrophysiol.[PMID:15005218]44. Crandall MA. BradleyDJ. Packer DL. Asir-vatham SJ. Contem-porary managementof atrial fibrillation:update on anticoag-ulation and invasivemanagement strate-gies. Mayo ClinicProc. 2009;84:643-62.[PMID:19567719]45. Cruz-Gonzalez I. YanBP. Lam YY. Left atrialappendage exclu-sion: state-of-the-art.Catheter CardiovascInterv. 2010;75:806-13. [PMID:20088009] © 2010 American College of Physicians ITC6-13 In the Clinic Annals of Internal Medicine 7 December2010 ablation on mortality rates, qualityof life, and health care costs willprobably be better established dur-ing the coming years (44). Mini-mally invasive surgical ablation isalso available at specialized centers.Occlusion of the left atrial ap-pendage to prevent strokes may be an acceptable option in selectedhigh-risk patients who are not can-didates for oral anticoagulationtherapy. Additional studies areneeded to verify the safety and ef-fectiveness of these devices beforethey can be recommended (45). How should clinicians monitor Although there are few studies about what type of monitoring is appropriate for patients with AF, mostclinicians agree that patients shouldhave regular follow-up to determinethe effectiveness of therapy. For manypatients, monitoring warfarin antico-agulation drives the frequency of fol-low-up. During these visits cliniciansshould also ask about palpitations,easy fatigability, and dyspnea on exer-tion to determine whether symptomsare adequately controlled. In addition,they should measure resting and exer-cise heart rates to determine the ade-quacy of therapy. Patients who havenot improved on rhythm-controldrugs should be switched to rate-con-trol drugs. Except for amiodarone,which requires liver and thyroid func-tion studies every 6 months and chestradiography every year, routine testsfor drug side effects are not necessary. recommend using these genetictests until clinical trials determinewhether the information they pro-vide improves patient outcomes.Dabigatran is a new anticoagulantthat in early trials appears to be aseffective as warfarin for prevent-ing thromboembolism but hasfewer adverse effects (41). TheFDA has recently approved it forprevention of stroke and systemicembolism in patients with AF.Catheter ablation of parts of theatrium where AF begins has be-come more widely accepted forpreventing recurrent AF in select-ed patients, especially for youngand otherwise healthy personswithout structural heart diseasewho have paroxysmal AF (43, 44). What’s New in This Update? In the Cliniclast considered themanagement of AF in 2008 (46).Since then, several importantchanges have occurred. In therate-control strategy for the drugtreatment of AF, the upper targetfor heart rate at rest has increasedfrom 80 to 110 beats per minute(18). Dronedrone, a new antiar-rhythmic drug similar to

amio-darone in effectiveness but withfewer side effects, has becomeavailable for the management ofpatients with AF, primarily in therhythm-control strategy (19, 24).Although genetic tests can identi-fy variants in some of the en-zymes that control warfarin me-tabolism (37), most experts do not Treatment... Atrial fibrillation treatment goals include reducing the frequency andseverity of symptoms, preventing stroke, and preventing tachycardia-related car-diomyopathy. Selection of patients for anticoagulation with aspirin or warfarinshould be based on the CHADSscore. Focus treatment first on rate control by us-ing beta-blockers or calcium-channel antagonists aiming for a resting rate be-tween 60 and 110 beats per minute. Rhythm control may be reasonable in pa-tients who do not respond to rate control. Atrial ablation and atrioventricularnodal ablation therapy may be appropriate for selected patients with highlysymptomatic AF despite drug therapy. CLINICAL BOTTOM LINE PracticeImprovement 46. Callans DJ. Atrial fibril-lation. Ann InternMed. 2008;149:ITC4-1-15. [PMID: 18981484]47. Snow V, Weiss KB,LeFevre M, et al.Management ofnewly detected atri-al fibrillation: a clini-cal practice guide-line from theAmerican Academyof Family Physiciansand the AmericanCollege of Physi-cians. Ann InternMed. 2003;139:1009-17. [PMID:14678921]48. Camm AJ, KirchhofP, Lip GYH, et al.Guidelines for themanagement of atri-al fibrillation. TheTask Force for theManagement of Atri-al Fibrillation of theEuropean Society ofCardiology (ESC). EurHeart J (2010) doi:10.1093/eurheartj/ehq278. First pub-lished online: August InthTool KitIn the Clinic AtrialFibrillation PIER Modules www.pier.acponline.orgAccess the PIER module on atrial fibrillation for updated, evidence-based information designed for rapid access at the point of care. Quality Measures pier.acponline.org/qualitym/prv.htmlAccess the PIER Quality Measure Tool, which links newly developedquality measures issued by the Ambulatory Quality Alliance and thePhysician Quality Improvement QA Alliance and CMS’s PhysicianQuality Reporting Initiative program to administrative criteria foreach measure and provides clinical guidance to help implement themeasures and improve quality of care. Patient Information www.annals.intheclinic/toolsDownload copies of the Patient Information sheet that appears on thefollowing page for duplication and distribution to your patients. Anticoagulation Flow Sheet www.acponline.org/running_practice/quality_improvement/projects/cfpi/doc_anticoag.pdfDownload a copy of a flow sheet to help manage patients on warfarin. Guidelines www.americanheart.org/downloadable/heart/222_ja20017993p_1.pdfAccess the American Heart Association, American College ofCardiology, and European Society of Cardiology joint 2006 guidelinesfor the management of patients with atrial fibrillation.www.annals.org/cgi/reprint/139/12/1009.pdfAccess the American College of Physicians/American Academy ofFamily Physicians 2003 guidelines for the management of newlydetected atrial fibrillation.www.nice.org.uk/Guidance/CG36Access guidelines for the management of atrial fibrillation from the UnitedKingdom’s National Institute for Health and Clinical Excellence.http://eurheartj.oxfordjournals.org/content/early/2010/08/28/eurheartj.ehq278.full?sid=692900ce-f77f-4a46-9ef7-b2c317bc9413Access 2010 guidelines for the management of atrial fibrillation fromthe Task Force for the Management of Atrial Fibrillation of theEuropean Society of Cardiology 7 December2010 Annals of Internal Medicine In the Clinic ITC6-14 © 2010 American College of Physicians Do U.S. stakeholders considermanagement of patients with atrialfibrillation when evaluating thequality of care physicians deliver? The Centers for Medicare & Medi-caid Services has issued specifica-tions for 74 measures

that make upthe 2008 Physician Quality Report-ing Initiative, although none of themdirectly measure the quality of AFtherapy. However, one of the strokemeasures examines the percentage ofpatients 18 years of age or older witha diagnosis of ischemic stroke ortransient ischemic attack and docu-mented paroxysmal, persistent, orpermanent AF who were prescribedan anticoagulant at discharge. What do professionalorganizations recommend withregard to the management of In 2003, the American College ofPhysicians and the AmericanAcademy of Family Physicians re-leased a guideline on AF manage-ment (47). The material presentedin this review has been updated andis consistent with the 2006 guide-lines from the American Heart As-sociation and American College ofCardiology (17) and the 2010guidelines by the European Societyof Cardiology (48). In the ClinicAnnals of Internal Medicine Patient Information THINGS YOU SHOULDKNOW ABOUT ATRIALFIBRILLATION What is atrial fibrillation? Atrial fibrillation is an irregular and sometimes veryfast heart beat. Atrial fibrillation can come and goor be constant. It is more common in people withheart conditions and in older people than in youngerpeople . Atrial fibrillation can lead to 3 bad Symptoms can make a person unable to do theirOver the long term, a very fast heartbeat candamage heart muscle.Atrial fibrillation can cause stroke when blood clotsform in the heart and travel to the brain. How would I know if I have atrial Many people with atrial fibrillation have nosymptoms and don’t know that they have it.When people have symptoms, they includepalpitations (pounding in the chest), shortness of breath, or tiredness.Your doctor may see atrial fibrillation on anelectrocardiogram (ECG) if an episode occurs duringIf you have symptoms that could be atrial fibrillationbut your ECG is normal, your doctor may send youfor a test that records your heartbeat while you goabout your usual activities.If you have atrial fibrillation, your doctor may do anechocardiogram to look for heart problems.Echocardiograms use sound waves to take picturesof the heart. What is the treatment? Many patients with atrial fibrillation need to be ondrugs to prevent stroke. Some people need onlyaspirin. Others need to take the blood thinnerTreatment usually includes drugs to slow the heartdown or make it more regular.Less often, more aggressive treatment withcatheters, surgery, or a pacemaker is needed.Atrial fibrillation treatment can have dangerous sideeffects. It is important to follow instructions and seeyour doctor regularly. For More Information www.nlm.nih.gov/medlineplus/tutorials/atrialfibrillation/htm/_no_50_nowww.hrspatients.org/patients/heart_disorders/atrial_fibrillation/default.aspHeart Rhythm Societycirc.ahajournals.org/cgi/content/full/117/20/e340American Heart Association 4. CME Questions 7 December2010 Annals of Internal Medicine In the Clinic ITC6-16 © 2010 American College of Physicians An 88-year-old man is evaluated forfollow-up of persistent atrial fibrillationwith a rapid ventricular responsediagnosed several months ago. His initialdiagnosis was made during evaluationbefore cataract surgery. He underwenttransesophageal echocardiography–guidedcardioversion after diagnosis, but the atrialhas been managed with warfarin, digoxin,and verapamil. He was initially prescribedatenolol, but discontinued it because ofside effects of fatigue and impairedconcentration and memory. He is entirelyasymptomatic despite an inadequatelycontrolled ventricular rate. He also hashypertension treated with valsartan. Hestates that he generally is averse to takingOn physical examination, his bloodpressure is 140/80 mm Hg, and his pulse is147/min. Cardiac auscultation reveals an2/6 holosystolic murmur. Estimated centralvenous pressure is 6 cm HO. The lungs areclear to

auscultation and there is nohormone level is normal. A 24-hour ambulatory monitordemonstrates a mean heart rate of137/min, with a minimum rate of 70/minand a maximum rate of 170/min. Which of the following is the mostappropriate management for this patient?A.AmiodaroneB.Atrioventricular node ablation byC.Maze surgical procedure to ablateatrial fibrillation origin in the atriumD.Radiofrequency ablation of atrialA 42-year-old man is evaluated forrecurrent, highly symptomatic paroxysmalatrial fibrillation. He was initiallydiagnosed 6 months ago. His evaluationresting electrocardiogram andechocardiogram were normal. Despite treatment with metoprolol, episodes occur3 to 4 times daily and last from a fewminutes to several hours. During events,he feels drained and unable toconcentrate, with a sensation of anbut denies chest discomfort and syncope.Episodes are triggered by activity, caffeine,and alcohol (both of which hediscontinued upon diagnosis). He takes nomedications other than the metoprolol. On physical examination, blood pressureis 130/60 mm Hg and pulse is 70/minand regular. Sare normal, andthere is no murmur or extra heartsounds. Estimated central venouspressure is 5 cm HO, and the lungs areclear. There is no edema. The remainderof the physical examination is normal. Which of the following is the mostappropriate management for this patient?A.Add amiodoroneB.Add digoxinC.24-hour ambulatory monitoringD.Implanted loop recorderA 60-year-old woman is evaluated forfollow-up after hospitalization 2 weeksago for pulmonary edema and volumeoverload that readily resolved withintravenous diuretics. She is currentlyfeeling well without edema or shortnessof breath. A stress echocardiogram donein the hospital was negative for ischemiaand showed an ejection fraction of 60%She has a history of hypertension,hyperlipidemia, and chronic atrialfibrillation. She takes metoprolol (75 mg twice daily), hydrochlorothiazide,warfarin, aspirin, and pravastatin. On physical examination, she is afebrile.Blood pressure is 150/90 mm Hg and pulseis 50/min. Jugular veins are not distended,and the lungs are clear. Cardiacexamination shows an irregularly irregularrhythm with variable intensity of the Swith no murmurs. There is no edema. Which of the following is the mostappropriate adjustment to herA.Add candesartanB.Add digoxinC.Change hydrochlorothiazide toD.Increase metoprolol dosageA 77-year-old woman is admitted to thehospital for intermittent dizziness overthe past few days. She does not havesyncope, orthopnea, or edema. Sheunderwent coronary artery bypass graftsurgery 6 years ago after myocardialinfarction. She has hypertension,fibrillation with a history of rapidventricular response. Over the pastseveral years, she has “slowed down” andhas had problems with memory, whichshe attributes to aging. Medications aremetoprolol, hydrochlorothiazide,pravastatin, lisinopril, aspirin, andOn physical examination, her bloodpressure is 137/88 mm Hg and her pulseis 52/min. Estimated central venouspressure is 7 cm HO. The point ofmaximum impulse is felt in the fifthintercostal space and at the midcostalbradycardia with regular Swell as an Smurmur is heard at the left upper sternalborder. The lungs are clear toauscultation. Edema is not present. On telemetry, she has sinus bradycardiawith rates between 40/min and 50/min,with two symptomatic sinus pauses of 3to 5 seconds each. Which of the following is the mostappropriate management for this patient?A.Add amiodaroneB.Discontinue metoprololC.EchocardiographyD.Pacemaker implantation 1. Questions are largely from the ACP’s Medical Knowledge Self-Assessment Program (MKSAP, accessed at http://www.acponline.org/products_services/mksap/15/?pr31). Go to www.annals.org/intheclinic/ to complete the quiz and earn up to 1.5 CME credits, or to purchase the complete MK