arrhythmia therapy in the elderly

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As with most diseases in the elderly, an ar-rhythmia has to be placed in the context of

all the other medical conditions that the pa-tient may have. When prescribing drugs, thephysician should consider the changes in ab-sorption and decrease in metabolism and/or ex-cretion that are present in the elderly. Druginteractions may differ in magnitude fromthose in the young. Compliance suffers formultiple reasons, and the risk-benefit ratio fortreatment may change. All of these factorsapply to arrhythmias. When treating arrhyth-mias, it would be optimal to apply “evidencebased” medicine, however the elderly haveoften been excluded from clinical trials. For ex-ample, in the early trials evaluating stroke pre-vention in atrial fibrillation, patients >75 yearswere excluded. Yet, >50% of patients with atrialfibrillation in the U.S. are >75 years of age.1The study policies were eventually changed, butthis is an example of how clinicians may be re-quired to extrapolate information gatheredfrom younger patients to treat the elderly.

This discussion will focus on treatment ofdifferent arrhythmias in the elderly. A contin-ual theme will be to emphasize “should it bedone” not “can it be done.” Editorials seemto emphasize the tendency to withhold valu-able treatment from the elderly. The implica-tion is that this is not fair. Perhaps that is truein many situations, but when observing howdifficult even simple therapies may be for theelderly, and when the comfort of the patientand their family as well as societal resources

are at issue, it is understandable why treat-ment decisions are so much more difficult inthis patient population.

My personal approach to arrhythmia treat-ment is to ask two questions before initiatingtherapy. The first question is: “What is therhythm trying to tell us (i.e., what is thecause)?” Consideration of three broad cate-gories of causes is helpful:• “Outside the body” causes. These are almost

always due to adverse reactions to drugs. Inaddition to prescription drugs, over-the-counter preparations, “health food” sup-plements, and even illicit drug use shouldbe considered. If a drug cause seems likely,stopping it and assessing the effect is a rea-sonable approach.

• “Inside the body” causes. Metabolic abnormalitiesshould be corrected before treating a rhythmby specific means. Both hyperthyroidism andhypothyroidism can cause arrhythmias, andthyroid disease is particularly difficult to diag-nose in the elderly. An acute systemic illnessmay result in severe rhythms, such as atrial fib-rillation, that will resolve once the acuteprocess is no longer present.

• Cardiac causes. It may not be the rhythmthat requires treatment, but rather the as-sociated heart disease. If ischemia or heartfailure can be treated or corrected, the ar-rhythmias may no longer be present.The second question is: “Is treatment

for the arrhythmia needed?” The only tworeasons for treatment are symptom relief

Arrhythmia Therapy in the Elderly

John H. McAnulty, MDFrom the Oregon Health Sciences University, Portland, ORAddress for correspondence/reprint requests: John H. McAnulty, MD, Chief, Division of Cardiology, Oregon HealthSciences University, Cardiology UHN-62, 3181 Southwest Sam Jackson Park Road, Portland, OR 97201Manuscript received August 9, 1999; accepted September 5, 1999

As with other illnesses, the risks and benefits of diagnostic studies and treatments for arrhythmias are altered by age. In the elderly, the risks of treatment are often greater;drug metabolism varies and mechanical approaches (ablation procedures and insertionof electrical devices) are associated with greater complication rates. This paper reviewsrecommendations for diagnosis and treatment of arrhythmias in the elderly. (AJGC. 2000;9:151–158) © 2000 by Cardiovascular Reviews & Reports, Inc.

ARRHYTHMIA THERAPY 152 AMERICAN JOURNAL OF GERIATRIC CARDIOLOGY 2000 VOL. 9 NO. 3

and safety. In many elderly patients, treat-ment of the rhythm may be of no benefitand, in fact, may be harmful. Availabletreatments for arrhythmias are shown in Table I.

BRADYARRHYTHMIASBradyarrhythmias are much more common inthe elderly, and if the symptoms are clearlydue to the bradycardia or if the patient is atrisk of death or injury due to a slow heart rate,

Table I. Antiarrhythmic Therapy in the Elderly

COMMENTS

• Correct the cause If identifiable, reasonable, possible: this is optimal.

• Drugs It is necessary to consider changes in absorption, metabolism, excretion of drugs due to age, and comorbidity.

AV node blocking agentsAdenosine Standard useß-blockers Standard use of IV agents

For oral use, a once daily, inexpensive drug is optimal; atenololseems most often to be appropriate.*

Digoxin Still useful because of its low cost, once daily dosing, and fair AVnode blocking effect. For rate control in atrial fibrillation or flutter,may best be used with atenolol. If patient has CHF, digoxin may reduce rehospitalization rate.25

Calcium blockers Standard use of verapamil, diltiazem.Antiarrhythmic agents All have 1%–3% chance of being proarrhythmic. While all may

deserve some discussion, an argument can be made for using eitherflecainide or amiodarone when a drug from this group is selected.*The proarrhythmic effect of flecainide may be worse if a patient iswithin three months of myocardial infarction or has CHF and reduced ejection fraction.26 Still, for all of the tachyarrhythmias,flecainide has been shown to be as effective as any other drug, hasfewer side effects, and requires only twice daily dosing.Amiodarone is equally (or more) effective, may be less proarrhyth-mic, and has to be taken only once daily. Sotalol’s significant ß-blocker effect makes it a consideration on occasion and on morerare occasions, selection of one of the other antiarrhythmic drugsmay be reasonable. Hospitalization for drug initiation is arguable; if the heart is not normal, hospitalization for 24–48 hours for drug initiation is appropriate for the antiarrhythmic drugs except for amiodarone.*

• Catheter ablation Expensive ($10,000–$12,000). Highly effective for PSVT (90% success).Reasonably effective for atrial flutter (75% success).Effective for AV node disruption for atrial fibrillation or flutter (pacemaker required). Role for preventing atrial fibrillation is evolving. Role for treatment of ventricular tachycardia is evolving.

• DevicesPacemakers Expensive (~$5–10,000) but effective for symptomatic bradycardias.Implantable defibrillator (ICD)27 Expensive (~$30,000).

Generally local surgery; usually with deep sedation (an 8–12 hourhospitalization).All now with three tiers of therapy: bradycardia pacing, antitachycardia pacing, and defibrillation. Dual chamber pacing devices available and dual chamber defibrillating capabilities evolving.

*There are strong arguments for alternatives to these recommendations. Despite listening to and knowing them,in balance, the author, in general, uses the drugs suggested in these comments. AV=atrioventricular; CHF=congestive heart failure; PSVT=paroxysmal supraventricular tachycardia.

ARRHYTHMIA THERAPY AMERICAN JOURNAL OF GERIATRIC CARDIOLOGY 2000 VOL. 9 NO. 3

pacemaker implantation is a reliable and safetherapy. Retrospective studies have shown thatthe very elderly receiving pacemakers havesignificant comorbidity, which may diminishthe value of the pacemaker.2 An evaluation ofpatients who received pacemakers in the lastyear of their life emphasized that patients whoneeded the device only briefly or who did notbenefit from a pacemaker, were not clearlyidentifiable by characterization of related dis-eases.3 Thus, if symptoms from a bradycardiaare unacceptable, pacemaker insertion shouldbe considered.

Sinoatrial Dysfunction. Approximately 50% ofbradyarrhythmias in the elderly are due to thismechanism (often called sick sinus syndrome).While it has not been documented that perma-nent pacemakers prolong life in the elderlywith sinoatrial node dysfunction, a prospectiveassessment of this therapy in patients withsinoatrial dysfunction has demonstrated a sig-nificant improvement in health related qualityof life.4 If a patient has well documented symp-tomatic bradycardia or has a remarkably slowrhythm (e.g., in the low 30s), a pacemaker isgenerally required. If an individual has inter-mittent symptoms suggesting a bradycardia,such as dizziness, syncope, poor exercise toler-ance, or fatigue, and is shown to have asympto-matic heart rates in the 40s, it is difficult toknow if a pacemaker will be of benefit. In thesecases, it is usually best to document the rhythmas the cause of symptoms rather than empiri-cally treating with a permanent pacemaker. If adecision is made to insert a pacemaker in a pa-tient with sinoatrial dysfunction, atrial pacingis preferable to ventricular pacing.5 It is stillnot clear whether dual chamber pacing will re-sult in improvement of symptoms, preventionof atrial fibrillation, prevention of strokes, orimproved survival as compared to single cham-ber pacing.6 These issues are being addressedin ongoing prospective trials.7 The prospectiveevaluation of health related quality of lifeshowed no benefits for dual as compared tosingle chamber pacing.4

Atrioventricular Conduction Abnormalities.The other 50% of elderly patients with brady-cardias have impaired atrioventricular (AV)conduction as the mechanism. In this group,the slow heart rate is usually due to completeheart block. While the role of dual chamber

pacing to prolong life has not been clearlydemonstrated, it is as logical to insert a pace-maker in the elderly patient with AV block asit is in a younger person. However, in the pre-viously mentioned prospective evaluation, thehealth related quality of life was not improvedby dual chamber as compared with singlechamber pacing in these patients.4 If dualchamber pacing is considered, it should berecognized that two leads may be more diffi-cult to insert or position. One approach toachieving both atrial sensing and ventricularpacing with a single lead is to use a lead withatrial and ventricular electrodes with the de-vice programmed to sense and track the atri-um and to pace the ventricle (the VDD mode).

TACHYCARDIASThe diagnosis and features of the commontachycardias in the elderly are similar tothose in younger individuals with the possi-ble exception that the rate of the arrhythmiamight be toward the lower end of the “usual”ranges. Table II provides “rules” for diagno-sis of the regular tachycardias.

Atrial and Ventricular Premature Beats.Although common at all ages, ectopic beatsare found in about 80% of the elderly.8,9

Ventricular ectopy is associated with an in-creased mortality in individuals with structur-al heart disease.8 Ectopic beats should be areason to consider an underlying cause thatmay deserve treatment. There is no definiteevidence that treatment of ectopic beats, nomatter how frequent, enhances survival. If ec-topic beats result in intolerable symptoms, aninitial trial of treatment with ß-blockers is thesafest approach. If this is not effective, therisks of antiarrhythmic drugs as compared toseverity of the symptoms due to the arrhyth-mia has to be balanced. Flecainide is an effec-tive suppressor of ventricular ectopy.

Sinus Tachycardia. This rhythm should notusually be treated directly; rather one shouldlook for the underlying cause. An elderly per-son with sinus tachycardia and angina maybenefit from treatment with a ß-blocker.

Paroxysmal Supraventricular Tachycardia.While more common in healthy young peo-ple, paroxysmal supraventricular tachycardia(PSVT) occurs in the elderly. While the mech-

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anism may more often be AV node reentry inolder people, this rhythm can also occur as aresult of an apparent or concealed accessorypathway with AV reentry. The presentation ofthis arrhythmia is similar to that in youngerpatients (Table II), and the initial treatmentshould be to try to stop the tachycardia withvagal maneuvers. If there is no response to aValsalva maneuver and if there is no carotidbruit, carotid massage (5–10 seconds of firmpressure with massage) may convert therhythm. If this is not successful, adenosine (3 mg or 6 mg in the fragile or small elderlypatient, or up to 12 mg in the average or largeindividual) should be administered rapidlythrough a large vein followed immediately bya saline flush. If there is no clear pharmaco-logic response, including unpleasant sensa-tions caused by the drug, the patency of the IVaccess should be reexamined. If a drug effectis present and the rhythm persists, verapamil5 mg IV followed by 10 mg if needed, or car-dioversion, should be considered.

After an initial episode of PSVT or if thisarrhythmia occurs infrequently, it may not beadvisable to recommend daily medication orto intervene with catheter ablation. On occa-sion, the “as needed” approach should beconsidered. A patient can be taught to try touse vagal maneuvers, including carotid mas-sage to resolve the PSVT. If these are not suc-cessful, the patient can be instructed to use ashort acting drug that blocks the AV node,such as 25–100 mg of metoprolol or 80–160mg of verapamil, and wait for 60–90 min-

utes. Vagal maneuvers may then be per-formed again to see if the combination ofdrug and vagal stimulation will convert therhythm, thus avoiding emergency room vis-its. For some elderly patients, this approachis too complex; for others, associated dis-eases, such as coronary ischemic heart dis-ease, will not allow the arrhythmia to betolerated for any length of time. If the deci-sion is made to use chronic drug therapy, ini-tiation of either a ß-blocker, such as aatenolol 50–100 mg a day or sustained re-lease verapamil 120–240 mg/day, is a reason-able approach. If this therapy does notprevent recurrences, an antiarrhythmic agentalone or in combination with a ß-blocker or acalcium channel blocker can be used (TableII). If the patient has not had a recent is-chemic event and does not have severe con-gestive heart failure, flecainide 50–100 mgbid is often effective and generally well toler-ated. Although the proarrhythmic effect ofamiodarone may be less than with the otherantiarrhythmic drugs, its value in the treat-ment of the PSVT is not clear, and its manypotential adverse effects prevent advocatingthe use of this therapy as a first line drug.Because of the hazards and adverse effects ofantiarrhythmic drugs, catheter ablationshould be considered since it is effective in90% of cases and is safe (Table I).

Atrial Fibrillation. This is a difficult arrhyth-mia to treat. It is a disease primarily confinedto the elderly. The unique aspect of atrial fib-


Table II. Tachyarrhythmias: The “Important” Four Regular Tachycardias

RATE (BPM)*

TACHYCARDIA ONSET AND TERMINATION P WAVE QRS COMPLEX QRS WIDTH

Sinus tachycardia Gradual 100–150 100–150 Narrow or wide

(PSVT) Abrupt 150–250 150–250 Narrow or wide

Atrial flutter Abrupt 250–350 <P wave rate: Narrow or wideoften one-halfthe P wave rate

Ventricular tachycardia Abrupt ≤QRS rate 100–300 Wide

*These values apply about 95% of the time. Sinus tachycardia will occasionally be >150, but the farther itstrays above this value, the more other rhythms should be considered. Likewise, paroxysmal supraventriculartachycardia (PSVT) may be <150, but the same thought process applies. Wide QRS ≥0.12 seconds.


rillation is its association with embolicstrokes, particularly in the elderly. Thrombusformation in the atrium is the presumedmechanism in most patients, although ahigh association of strokes with aorticatheromas in patients with atrial fibrillationmakes the pathophysiology less clear.10 Thestroke risk in untreated atrial fibrillation averages patients who are 60–75 years of ageis 3%–8% per year. By age 80, it may be≥ 10% per year.11–14 This high incidence, aswell as the obvious consequences of a stroke,emphasize the need to address the issue of stroke prevention in every patient withatrial fibrillation.

“Once a patient with atrial fibrillation, al-ways a patient with atrial fibrillation.” Thisconcept is important when considering strokeprevention. Although it is logical to assumethat the stroke risk is less if atrial fibrillationdoes not recur, there is no evidence that strokerisk is any less when a patient who has hadatrial fibrillation is in sinus rhythm. Patientsare often converted from atrial fibrillation tosinus rhythm with the thought that therapy toprevent strokes will be unnecessary. There isno available information to indicate that this isappropriate.13–16 Stroke prevention measuresare still required, particularly in patients whomay not realize when they are in atrial fibrilla-tion. The risk of stroke can be reduced by approximately 70% with warfarin.11–14 Un-fortunately, warfarin is particularly difficult toadminister to elderly patients. The risk ofbleeding increases with age. The risk of cen-tral nervous system bleeding has been as highas 1.8% per year in patients >75 years; therate of major bleeding exceeds 5% per year.Warfarin has to be stopped in >10% of thosepatients taking the drug. Recent largeprospective trials have resulted in the follow-ing treatment recommendations.11–14

In patients with atrial fibrillation, whetherintermittent or persistent, the use of an-tithrombotic therapy should be considered.Risk factors that increase the chance of throm-boembolism include a previous thromboem-bolic event, left ventricular dysfunction,systolic blood pressure >160 mm Hg that per-sists, and “older age.” (“Older age” is not welldefined; in one trial this included women butnot men >75 years.11 Metaanalysis has sug-gested age >65 is an independent risk factor.)The international normalized ratio (INR)

should be maintained between 2–3. If an el-derly individual does not have one of theserisk factors or is considered to be at high riskof bleeding with warfarin, aspirin 325 mg/dayhas been shown to be somewhat effective instroke prevention.11,14 Lower dose aspirin hasnot been shown to be beneficial.

If atrial fibrillation results in hemodynamicinstability, immediate treatment is required. Ifhemodynamic compromise is severe, urgentcardioversion in the sedated patient is re-quired using 150–200 joules of synchronizeddirect current (DC) energy, preferably usinganterior/posterior paddles. In most patients,rapid rate control with verapamil (5 mg IVwith repeated 5–10 mg boluses if necessary)or diltiazem (10–20 mg IV followed by an IVdrip at 1–2 mg/min) is appropriate alternativefirst line therapy. Esmolol is a rapidly actingß-blocker drug with short duration of actionthat can also be useful for rate control. If thepatient remains in atrial fibrillation and if therhythm has been present for <48 hours, car-dioversion can be considered. When dis-cussing the use of antiarrhythmic drugs, allhave the potential of being proarrhythmic. Ifthe patient has congestive heart failure or car-diomegaly, it is appropriate to initiate therapywith patients in the hospital. Initiation ofamiodarone at low doses may be an exceptionto this rule. While several antiarrhythmicdrugs may be considered, flecainide is a rea-sonable choice because of its low symptomaticside effect profile and its twice daily regimen,but the use of flecainide is of concern becauseof its proarrhythmic effect. It is possible thatthis effect increases with age.16,17 Additionally,flecainide and other IC agents may slow theatrial rate enough to actually allow enhancedAV conduction and a more rapid ventricularrate. It is appropriate to use a ß-blocker orcalcium blocking drug to avoid rapid conduc-tion. Alternative drugs include sotalol andpropafenone—most started on sotalol shouldprobably be hospitalized.18

If the rhythm is presumed to have persist-ed longer, it is advisable to maintain ratecontrol with oral verapamil, ß-blockers, ordigoxin, to initiate warfarin therapy, andhave the patient return in 3–4 weeks for car-dioversion. An alternative approach is toperform a transesophageal echocardiogram(TEE) to determine if the left atrium is freeof thrombus (the standard transthoracic

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echocardiogram will not reliably provide thisinformation) and then proceed immediatelyto cardioversion if the TEE is negative. Thediscomfort, risk, and expense of the use ofthe TEE discourages routine use of this ap-proach. In addition, anticoagulation must beinstituted for at least four weeks after car-dioversion even if the TEE does not show thepresence of an atrial clot, since the atriummay be hypokinetic and a clot may form after cardioversion.

If an individual is in atrial fibrillation and isasymptomatic, an argument can be made forinitiating stroke prevention medication andmaintaining heart rate control at a mean rateof 80–85 bpm with AV nodal blocking agents(a combination of digoxin and low doseatenolol is most effective).15 If an individual issymptomatic with atrial fibrillation despite ratecontrol, initiation of an oral antiarrhythmicdrug is appropriate. Again, all antiarrhythmicdrugs have potential of having a proarrhyth-mic effect and most should probably be startedin the hospital, particularly in patients withcongestive heart failure or cardiomegaly.Amiodarone, at low doses, may be an excep-tion to this rule. While several antiarrhythmicdrugs may be considered, flecainide is a rea-sonable (although controversial) choice be-cause of its low symptomatic side effect profileand its twice daily regimen. If used, flecainidecan slow the atrial rate enough to actually en-hance AV conduction, so it is important that itbe used in combination with either a ß-blockeror calcium channel blocking drug. Alternativedrugs include sotalol and propafenone and these should probably be initiated in thehospital.18 Amiodarone is probably the mosteffective drug to prevent recurrent atrial fib-rillation. Its long list of complications19 makemany physicians hesitate to recommend it asfirst line therapy, but it is well tolerated in lowdoses by the majority of patients and has theadvantage of being less proarrhythmic thanother drugs. Antiarrhythmic drug use by itselfmay convert the rhythm back to normal sinusrhythm. If it does not, cardioversion while thepatient is taking the drug may result in rever-sion and persistence of sinus rhythm.

Alternatives to drug therapy are beingevaluated for treatment of atrial fibrillationin select situations. These include use of theatrial defibrillator, which may be useful in in-dividuals who have a moderate frequency of

poorly tolerated paroxysmal atrial fibrilla-tion. Catheter ablation of atrial fibrillation isstill in its infancy. More commonly, AV nodeablation with insertion of a permanent pace-maker can be performed in the patient whererate control is difficult or drugs are not toler-ated.20 Surgical therapy, termed the Mazeprocedure for atrial fibrillation, would seeminappropriate in the elderly unless they re-quire heart surgery for other reasons.

Atrial Flutter. A clinical rule is that “atrialflutter is atrial fibrillation.” This statementemphasizes that the principles of manage-ment of these arrhythmias are similar. Thereare differences between atrial flutter and fib-rillation. First, less is known about the throm-boembolic risk with atrial flutter, but strokesdo occur. Therefore, it would seem appropri-ate to apply the same rules with regard to an-tithrombotic therapy to patients with atrialflutter. Second, the ventricular response maybe more difficult to control with atrial flutter.This is a reason to consider ablation of theflutter circuit or the AV node if the drugs donot work or are not tolerated. Atrial fluttercan more often be cured by catheter ablationof the arrhythmia circuit (as compared toatrial fibrillation), and this should be consid-ered in the patient who has typical atrial flut-ter and is particularly bothered by thisarrhythmia. In all other regards, the recom-mendations that have been made for atrialfibrillation seem to apply.

Ventricular Tachycardias. Sustained rapidventricular tachycardia is generally not welltolerated in the elderly. Immediate sedationfollowed by cardioversion with synchronizedDC energy, 100–200 joules may be required.Patients with this rhythm are likely to haverecurrences (30% incidence at one year), andgenerally chronic therapy is required if there isno correctable underlying cause. Therapeuticoptions include drug therapy with amio-darone or sotalol or an implanted defibrilla-tor (ICD). Two large, long term prospectivetrials, the Antiarrhythmics Vs. ImplantableDefibrillators (AVID) and the CanadianImplantable Defibrillator Study (CIDS)trials,21,22 demonstrated a modest survivalbenefit with the ICD in comparison to drugtherapy. Treatment with an ICD has resultedin a prolongation of a life averaging three



months over a three year period. The devicecan now be inserted without a thoracotomy.Thus, it should be considered in the elderlypatient who does not have significant lifethreatening comorbidity. Drug therapy withamiodarone is a reasonable alternative.

Ventricular Fibrillation. Survivors of ven-tricular fibrillation are at high risk for recur-rence, and the principles of therapy fortreatment of ventricular tachycardia are ap-plicable to this group.21,22

Nonsustained Ventricular Tachycardia. Thisrhythm is very common in the elderly8 and isassociated with an increase in mortality (if theleft ventricular ejection fraction is ≤ 0.40).Optimal treatment has not been fully defined.If the patient has unacceptable symptoms, drugtherapy is required. If ß-blockers are not effec-tive, flecainide or amiodarone could be used.Two recent studies suggest that defibrillatortherapy in highly selected patients who are in-ducible to sustained ventricular tachycardiamay result in better survival than in patientstreated with medical therapy, including amio-darone (Multicenter Automatic DefibrillatorImplantation Trial [MADIT], MulticenterUnsustained Tachycardia Trial [MUSTT]).23,24

This has significant implications because thesize of this population is much greater thanthose who have sustained ventricular tachycar-dia or fibrillation. The degree of survival bene-fit is still not fully defined in the larger group ofpatients with decreased left ventricular functionwho have nonsustained ventricular tachycardia,but who do not undergo electrophysiologicalstudy. This is being addressed in the MADIT IItrial. Thus, therapeutic recommendations inpatients with nonsustained ventricular tachycar-dia need to be individualized until further datais available.

REFERENCES

1 Feinberg WM, Blackshear JL, Laupacis A, et al.Prevalence, age distribution and gender of patientswith atrial fibrillation. Arch Intern Med.1995;155:469–473.

2 Shen WK, Hayes KL, Hammil SC, et al. Survivaland functional independence after implantationof a permanent pacemaker in octogenarians andnonagenarians. A population-based study. AnnIntern Med. 1996;125(6):476–480.

3 Hefflin BJ. Final-year-of life pacemaker recipients.J Am Geriatr Soc. 1998;46(11):1396–1400.

4 Lamas GA, Orav EJ, Stambler BS, et al, for thePacemaker Selection in the Elderly Investigators.Quality of life and clinical outcomes in elderly pa-tients treated with ventricular pacing as comparedwith dual chamber pacing. N Engl J Med.1998;338:1097–1104.

5 Andersen HR, Nielsen JC, Thomsen PE, et al. Longterm follow up of patients from a randomized trialof atrial versus ventricular pacing for sick-sinus syn-drome. Lancet. 997;350(9086):1210–1216.

6 Brady PA, Shen EK, Neubauer SA, et al. Pacingmode and long term survival in elderly patientswith congestive heart failure: 1980–1985. J IntervCard Electrophysiol. 1997;1(3):193–201.

7 MOST Investigators. Mode selection trial spon-sored by NHLBI. In progress.

8 Frishman WH, Heiman M, Karpenos A, et al.Twenty-four hour ambulatory electrocardiographyin elderly subjects: Prevalence of various arrhyth-mias and prognostic implications (report from theBronx Longitudinal Aging Study). Am Heart J.1996;132:297–302.

9 Lok NS, Lau CP. Prevalence of palpitations, cardiacarrhythmias and their associated risk factors in ambulant elderly. Int J Cardiol. 1996;54(3):231–236.

10 Blackshear JL, Pearce LA, Hart RG, et al, for theCommittee on Echocardiography. Aortic plaque inatrial fibrillation: Prevalence, predictors and throm-boembolic implications. Stroke. 1999;30:834–840.

11 Stroke Prevention in Atrial Fibrillation Investigators.Adjusted-dose warfarin versus low-intensity, fixed-dose warfarin plus aspirin for high-risk patients withatrial fibrillation: The Stroke Prevention in AtrialFibrillation III randomized clinical trial. Lancet. 1996;348:633–638.

12 Boston Area Anticoagulation Trial for AtrialFibrillation Investigators. The effect of low-dose war-farin on the risk of stroke in nonrheumatic atrial fibrillation. N Engl J Med. 1990;323: 1505–1511.

13 Veterans Affairs Stroke Prevention in NonrheumaticAtrial Fibrillation Investigators. Warfarin in the pre-vention of stroke associated with nonrheumatic atrialfibrillation. N Engl J Med. 1992;327:1406–1412.

14 Stroke Prevention in Atrial Fibrillation Investigators.Prospective identification of patients with nonvalvularatrial fibrillation at low-risk of stroke during treat-ment with aspirin. JAMA. 1998;279:1273–1277.

15 Farshi R, Kistner D, Sarma JSM, et al. Ventricularrate control in chronic atrial fibrillation duringdaily activity and programmed exercise: Acrossover open-label study of five drug regimens.J Am Coll Cardiol. 1999;33(2):304–310.

16 Marcus FI. The hazzards of using type IC antiar-rhythmic drugs for the treatment of paroxysmalatrial fibrillation. Am J Cardiol. 1990;66:366–367.

17 Akiyama T, Pawitan Y, Campbell WB, et al. Effectsof advancing age on the efficacy and side effects of antiarrhythmic drugs in post myocardial infarc-tion in patients with ventricular arrhythmias. The CAST investigators. J Am Geriatr Soc.1992:40:666–672.

18 Marcus FI. Risks of initiating therapy with sotalolfor treatment of atrial fibrillation. J Am Coll Cardiol.1998;32:177–180.

157

19 Vorperian VR, Havighwst TC, Miller S. et al.Adverse effects of low dose amiodarone: Meta-analysis. J Am Coll Cardiol. 1997;30:791–798.

20 Wood MA, Brown-Mahoney C, Kay N, et al. Clinicaloutcomes after ablation and pacing therapy for atrialfibrillation: A metaanalysis. Circulation. 2000;101:1138–1144.

21 The AVID Investigators. A comparison of antiar-rhythmic drug therapy with implantable defibrilla-tors in patients resuscitated from near fatalventricular arrhythmias. N Engl J Med.1997;337:1576–1583.

22 Cappato R. Secondary prevention of sudden death:The Dutch Study, the Antiarrhythmics VersusImplantable Defibrillator Trial, the Cardiac ArrestStudy Hamburg, and the Canadian ImplantableDefibrillator Study. Am J Cardiol.1999;83(5B):68D–73D.

23 Moss AJ, Hall WJ, Cannom DS, et al. (MADIT).Improved survival with an implanted defibrillator

in patients with prior myocardial infarction, lowejection fraction and asymptomatic non-sustainedventricular tachycardia. N Engl J Med.1996;335:1933–1940.

24 Buxton AE, Lee KL, Fisher JD, et al. A randomizedstudy of the prevention of sudden death in patientswith coronary artery disease. MulticenterUnsustained Tachycardia Trial Investigators. N Engl J Med. 1999;341(25):1882–1890.

25 DIG Investigators. The effect of digoxin on mortal-ity and morbidity in patients with heart failure. N Engl J Med. 1997;336(8):525–533.

26 The Cardiac Arrhythmia Suppression Trial (CAST)Investigators. Increased mortality due to encainideor flecainide in a randomized trial of arrhythmiasuppression after myocardial infarction. N Engl JMed. 1989;321:406–412.

27 Geelen P, Lorga FA, Primo J, et al. Experience withimplantable cardioverter defibrillator therapy in el-derly patients. Eur Heart J. 1997;18:1339–1342.


arrhythmia therapy in the elderly

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