Update on Heart Fai lure ManagementLt Col Marla De Jong, USAF, NC; Lynn Doering, RN, DNSC, Sect ion Editors

Atrial Fibrillation (AF) and Heart Failure (HF): ToTreat the AF, be Sure to Treat the HFLiza A. Prudente, RN, MSN, ACNP-BC

Atrial fibrillation (AF) and heartfailure (HF) are on the rise. AF is

the most common sustained cardiacarrhythmia, affecting more than 2million Americans and nearly 15% ofthose over age 85.1 Over 5 millionAmerican have HF, including 12% ofthose over age 80.2,3 HF is the mostcommon reason for hospital admissionof people on Medicare,2 and ac-counted for about 1 million hospitaldischarges in 2005.2,3 Experts predictthat the prevalence of AF will morethan double by 2050 as the popula-tion ages. Likewise, the incidence ofHF will increase with an aging pop-ulation as it shares many of the samepredisposing factors as AF, such ashypertension and fibrotic changes inheart muscle tissue. One-third to one-half of patients with HF develop AF.As shown in Table 1, HF is associatedwith AF especially those with NewYork Heart Association class III or IVHF.11 Importantly, patients with HFwho later develop AF have increasedmortality—a relative risk of 1.6 formen and 2.7 for women.12 Becausethese 2 diseases are often linked orcoexisting, it is increasingly commonfor clinicians to manage patients withboth HF and AF. This article will ex-plore the link between these 2 dis-eases, and available therapies fortreating AF in the HF population.

AF is a manifestation of multiplesimultaneous waves of electrical acti-vation in atria resulting in irregularrapid atrial depolarizations of 300 to600 beats/min. Unlike HF, which isclassified by the severity of symptoms,AF is classified by its duration. Parox-ysmal AF is characterized by intermit-

tent episodes that typically last fewerthan 24 hours and convert spontane-ously within 7 days. Persistent AF ep-isodes last more than 7 days andrequire cardioversion with drugs, elec-trical shock, or both. Permanent AFrefers to a longstanding episode inwhich cardioversion fails or no effort ismade to convert to sinus rhythm.

Two factors are required for AF—triggers that induce it and substratesthat sustain it. Triggers include acuteatrial stretch, bradycardia, and prema-

ture atrial contractions often arisingfrom the pulmonary veins. Substratesrefers to both the structural and elec-trical remodeling of the atrium, par-ticularly the left atrium, that can occurwith longstanding hypertension andwith HF. In this way, HF begets AF.The left atrial hypertension thatarises from left ventricular dysfunctioncontributes to structural and func-tional changes that lead to AF. Leftatrial enlargement that is associatedwith HF is characterized structurally

From the University of Virginia, Charlottesville, VAAddress for correspondence:Liza A. Prudente, RN, MSN, ACNP-BC, University of Virginia, Charlottesville, VAE-mail: lap4n@virginia.eduManuscript received July 13, 2008; accepted July 13, 2008

Table 1. AF Prevalence by NYHA HF Class

STUDY NYHA CLASS AF PREVALENCE (%)

SOLVD Prevention4 I 4.2

SOLVD Treatment5 I 10.1

V-HeFT6 II–III 14.4

CHF-STAT7 II–III 15.4

DIAMOND-CHF8 III–IV 25.8

GESICA9 III–IV 28.9

CONSENSUS10 IV 49.8

Abbreviations: AF, atrial fibrillation; CHF-STAT, congestive heart failure:

survival trial of antiarrhythmic therapy; CONSENSUS, Cooperative North

Scandinavian Enalapril Survival Study; DIAMOND-CHF, Danish

investigators of arrhythmia and mortality on dofetilide-CHF; GESICA,

Groupo de Estudio de la Sobrevida en la Insufiencia Cardiaca en Argentina;

NYHA, New York Heart Association; SOLVD, study of left ventricular

dysfunction; V-HeFT, vasodilator-heart failure trial.

Progress in Cardiovascular Nursing Summer 2008146

by fibrosis between muscle bundlesand functionally by ectopy and short-ened refractory periods. Simply put,the effect is frequent impulses firedinto multiple, rapidly conducting elec-trical pathways, triggering AF in apermissive substrate.

Likewise, AF begets HF.13 Rapidheart rates associated with AF, varia-tions in cardiac output that arise fromirregular intervals between heartbeats,and loss of atrial contribution to car-diac output exacerbate HF symptoms.In addition, AF may worsen mitraland tricuspid regurgitation, further re-ducing forward cardiac output. Fi-nally, prolonged rapid rates associatedwith AF can directly reduce left ven-tricular function, an often reversiblecondition known as tachycardia-in-duced cardiomyopathy.

It is useful and important to ask pa-tients in an acute HF exacerbation abouttheir perceived cardiac rhythm over re-cent days. Simply asking ‘‘Has yourheart felt out of rhythm?’’ or ‘‘Has yourheart been beating faster than usual?’’ aregood ways to start. If the patient’s his-tory or physical examination suggests arhythm disturbance, a Holter monitoror longer term event monitor can aidthe practitioner in arrhythmia diagnosisas the cause for the exacerbation.

In treating HF patients with AF,the aims are to prevent thromboem-bolic complications, reduce detrimen-tal effects on cardiac performance andsymptoms by maximizing HF thera-pies, and, when appropriate, use AF-specific therapies.

PREVENT THROMBOEMBOLICCOMPLICATIONSAF is an independent risk factor forstroke; therefore, antithrombotic ther-apy is a critically important in AF re-gardless of HF status. Clinical practiceis informed by the ACC/AHA/ESCGuidelines for the Management ofPatients With Atrial Fibrillation,14

which bases recommendations on theCHADS2 score,15 shown in Table 2.No antithrombotic therapy is requiredfor a CHADS2 score of 0. For a scoreof 1, therapy with aspirin or warfarin

is recommended. For higher scores,warfarin alone is recommended. Pa-tients with HF score 1 point andtherefore should receive at least aspi-rin, unless other risk factors are pres-ent. Note that prior TIA or strokeequals 2 points and mandates warfarin.

MAXIMIZE HF THERAPIESThere are important common ele-ments in medical therapy for bothHF and AF, and a sensible approach isto first maximize therapy for HF. Themost important common element isblockade of b-adrenergic receptors.b-blockers are prescribed to improvesurvival for patients with HF and tocontrol rapid heart rates for patientswith AF. In fact, for AF patients whosesymptoms only occur with rapid ven-tricular rates, treatment with b-blockersalone may suffice, as there is no mor-tality benefit to antiarrhythmic druguse in this minimally symptomaticpopulation. Rate control may be espe-cially therapeutic for patients withtachycardia-induced cardiomyopathy.

Angiotensin converting enzyme(ACE) inhibitors and angiotensin re-ceptor blockers (ARBs) also improvesurvival in HF, and have been shownto decrease incidence of AF in the HFpopulation, especially in combinationwith amiodarone.16–18 The reasoningis that these agents block the effect ofangiotensin to adversely remodel theatrium structurally (by increased fi-brosis) and electrically (by modulationof calcium and potassium currents).The evidence has arisen from post hoc

analyses of large HF trials; however,the hypothesis that these agents de-crease AF incidence on their own hasnot been tested directly.

Finally, digoxin has been used forcenturies as HF therapy. While its usedoes not decrease mortality, it doesreduce symptoms and the number ofhospitalizations.19 In AF patients, dig-oxin is used as an adjunct in control-ling rapid ventricular rates. It isimportant to know that digitalis tox-icity can occur, though, so the patientwith both AF and HF should not re-ceive larger doses than the patient withHF alone.

USE AF-SPECIFIC THERAPIESThere are additional treatment optionsfor patients in whom AF is the pre-dominant clinical problem. Rhythmcontrol using antiarrhythmic drugscan reduce the AF burden, however,their use must be highly individual-ized. While there appears to be nomortality benefit either in the ab-sence20 or presence of HF,21 antiar-rhythmics may be used to try tomaintain sinus rhythm in HF patientswhose symptoms are worse in AFwhether due to greater dependence onatrial kick (HF with preserved systolicfunction), an irregular heart rhythm,or other factors. Antiarrhythmic druguse, moreover, is complicated by HF.At this time, amiodarone and dofeti-lide are thought reasonably safe inHF,14 though each brings its own ca-veats. For example, amiodarone canlead to systemic side effects, so we

Table 2. The CHADS2 Score for Anticoagulation in Atrial Fibrillation

RISK FACTOR POINTS

C History of CHF 1

H History of HTN 1

A Age � 75 1

D History of DM 1

S Previous CVA or TIA 2

Abbreviations: CHF, congestive heart failure; CVA, cerebrovascular

accident; DM, diabetes mellitus; HTN, hypertension; TIA, transient ischemic

attack.

Summer 2008 Progress in Cardiovascular Nursing 147

measure thyroid and liver function ev-ery 3 to 6 months, and a chest X-rayyearly. Dofetilide therapy requires ad-equate renal function and must beinitiated in the hospital. Table 3 sum-marizes commonly used drugs, dos-ages, and considerations.

For patients in chronic AF for whomrate control is not possible medically, adefinitive treatment is a cardiac pace-maker and ablation of the AV junctionto induce complete heart block. Thistherapy may be very helpful for patientswhose HF is due to tachycardia-inducedcardiomyopathy, but for others it mayinduce or worsen HF symptoms due tothe obligatory dyssynchronous contrac-tion that results from right ventricularpacing (equivalent to LBBB). Biventric-ular pacing, however, improves func-

tional status in AF patients after AVjunction ablation, especially those withreduced ejection fraction (EF) or HFsymptoms.23

A promising therapy is the left atrialcatheter ablation procedure to isolatethe pulmonary veins, the origin ofmuch AF, and to alter the left atrialsubstrate so that AF is more difficult tosustain. A provocative study by Hais-saguerre and colleagues found a dra-matic increase in EF after thisprocedure in AF patients with preexist-ing LV dysfunction.24 A possible mech-anism is an underappreciated role oftachycardia-induced cardiomyopathy inAF patients. Another goal with thistreatment is to obviate the need for ar-rhythmic drugs to maintain sinusrhythm.

In summary, the rising incidence ofboth HF and AF means that clinicianswill assess, treat, and manage more pa-tients who have both disorders.Clinicians seek to prevent thromboem-bolic complications, reduce detrimen-tal cardiac performance and symptoms,and use AF-specific modalities. Man-agement of patients with both HF andAF begins with maximizing HF ther-apy with b-blockers, and ACE inhib-itors, or ARBs, as these agents will alsohelp to reduce AF incidence and man-age AF symptoms. Use of antithrom-botic therapy should be based on theCHADS2 score. Additional therapyfor AF in the setting of HF can be acomplex management problem involv-ing antiarrhythmic drugs, ablation pro-cedures, and devices.

REFERENCES1 Go AS, Hylek EM, Phillips KA, et al. Prevalence of

diagnosed atrial fibrillation in adults: national implica-tions for rhythm management and stroke prevention:the AnTicoagulation and Risk Factors in Atrial Fibril-lation (ATRIA) Study. JAMA. 2001;285:2370–2375.

2 Division for heart disease and stroke prevention. CDCCenters for Disease Control and Prevention. http://www.cdc.gov/dhdsp/library/fs_heart_failure.htm. Ac-cessed January 7, 2008.

3 Heart disease and stroke statistics:2008 updateat-a-glance. American Heart Association.http://www.americanheart.org/downloadable/heart/1200078608862HS_Stats%202008.final.pdf. AccessedJanuary 7, 2008.

4 Effect of enalapril on mortality and the develop-ment of heart failure in asymptomatic patients withreduced left ventricular ejection fractions. TheSOLVD Investigators. N Engl J Med. 1992;327:685–691.

5 Yusuf S. Effect of enalapril on survival in patients withreduced left-ventricular ejection fractions and conges-tive-heart-failure. New Eng J Med. 1991;325:293–302.

6 Cohn JN, Archibald DG, Ziesche S, et al. Effect ofvasodilator therapy on mortality in chronic con-gestive-heart-failure—results of a veterans-admin-istration cooperative study. New Eng J Med. 1986;314:1547–1552.

7 Massie BM, Fisher SG, Deedwania PC, et al.Effect of amiodarone on clinical status and leftventricular function in patients with congestiveheart failure. Circulation. 1996;93:2128–2134.

8 Torp-Pedersen C, Moller M, Bloch-Thomsen PE, etal. Dofetilide in patients with congestive heart failureand left ventricular dysfunction. Danish investigationsof arrhythmia and mortality on dofetilide study group.N Engl J Med. 1999;341:857–865.

9 Doval HC, Nul DR, Grancelli HO, et al. Ran-domized trial of low-dose amiodarone in severecongestive-heart-failure. Lancet. 1994;344:493–498.

Table 3. Drug Therapy for AF in HF Patients

DRUG DOSE SIDE EFFECT CONSIDERATION

b-blocker Long-acting preferred; dosedriven by heart rate goal:12.5–200 mg daily

Bradycardia, hypotension Goal heart rate for AF is70–80 at rest and o110with activity

ACE Inhibitor,ARB

Usual starting dose Hyperkalemia, hypotension Irbesartan plus amiodaronedecreased recurrenceof AF22

Amiodarone May start with loadingat 800 mg daily for7 d, then 200 mgdaily thereafter

May cause hypo/hyperthyroidism;elevated liver enzymes,pulmonary fibrosis, sunsensitivity

Monitor labs and chest X-rayregularly, encourage useof sun block

Dofetilide Dose based on creatinineclearance—start at500 mcg twice dailyif 60 mL/min

Long QT interval, torsades depointes at start of therapy

FDA—mandated 72-hhospitalization at therapyinitiation to monitor QTinterval

Abbreviations: ACE, angiotensin converting enzyme; ARB, angiotensin l receptor blocker.

Progress in Cardiovascular Nursing Summer 2008148

10 Swedberg K. Effects of enalapril on mortality insevere congestive-heart-failure—results of thecooperative-North-Scandinavian-enalapril-survival-study (consensus). New Eng J Med. 1987;316:1429–1435.

11 Markides V, Prystowsky EN. Mechanisms under-lying the development of atrial arrhythmias in heartfailure. Curr Opin Cardiol. 2003;18:32–38.

12 Wang TJ, Larson MG, Levy D, et al. Temporalrelations of atrial fibrillation and congestive heartfailure and their joint influence on mortality—TheFramingham Heart Study. Circulation. 2003;107:2920–2925.

13 Miyasaka Y, Barnes ME, Gersh BJ, et al. Incidenceand mortality risk of congestive heart failure inatrial fibrillation patients: a community-basedstudy over two decades. Eur Heart J. 2006;27:936–941.

14 Fuster V, Ryden LE, Asinger RW, et al. ACC/AHA/ESC Guidelines for the management of pa-tients with atrial fibrillation: executive summary areport of the American College of Cardiology/American Heart Association Task Force on Prac-tice Guidelines and the European Society ofCardiology Committee for Practice Guidelines

and Policy Conferences (committee to developguidelines for the management of patients withatrial fibrillation) developed in collaborationwith the North American Society of Pacing andElectrophysiology. Circulation. 2001;104:2118–2150.

15 Gage BF, Waterman AD, Shannon W, et al.Validation of clinical classification schemes forpredicting stroke: results from the national reg-istry of atrial fibrillation. JAMA. 2001;285:2864–2870.

16 Vermes E, Tardif JC, Bourassa MG, et al. Enalaprildecreases the incidence of atrial fibrillation in patientswith left ventricular dysfunction—insight from thestudies of left ventricular dysfunction (SOLVD) trials.Circulation. 2003;107:2926–2931.

17 Wachtell K, Lehto M, Gerdts E, et al. AngiotensinII receptor blockade reduces new-onset atrial fi-brillation and subsequent stroke compared to ate-nolol—the losartan intervention for end pointreduction in hypertension (LIFE) study. J Am CollCardiol. 2005;45:712–719.

18 Maggioni AP, Latini R, Carson PE, et al. Valsartanreduces the incidence of atrial fibrillation in pa-tients with heart failure: results from the Valsartan

Heart Failure Trial (Val-HeFT). Am Heart J.2005;149:548–557.

19 The effect of digoxin on mortality and morbidityin patients with heart failure. The digitalis inves-tigation group. N Engl J Med. 1997;336:525–533.

20 Olshansky B, Rosenfeld LE, Warner AL, et al. Theatrial fibrillation follow-up investigation of rhythmmanagement (AFFIRM) study: approaches to con-trol rate in atrial fibrillation. J Am Coll Cardiol.2004;43:1201–1208.

21 Roy D, Talajic M, Nattel S, et al. Rhythm controlversus rate control for atrial fibrillation and heartfailure. New Eng J Med. 2008;358:2667–2677.

22 Madrid AH, Bueno MG, Rebollo JMG, et al. Useof irbesartan to maintain sinus rhythm in patientswith long-lasting persistent atrial fibrillation a pro-spective and randomized study. Circulation.2002;106:331–336.

23 Doshi RN, Daoud EG, Fellows C, et al. Left ven-tricular-based cardiac stimulation post AV nodalablation evaluation (the PAVE study). J CardiovascElectrophysiol. 2005;16:1160–1165.

24 Hsu LF, Jais P, Sanders P, et al. Catheter ablationfor atrial fibrillation in congestive heart failure.New Eng J Med. 2004;351:2373–2383.

Summer 2008 Progress in Cardiovascular Nursing 149