Nonsustained VT or complex VA diagnosed by 24-hour ambulatory ECG^3,11,12 or by 12-lead ECG with 1-minute rhythm strips⁶ in older adults with no clinical evidence of heart disease were not associated with an increased incidence of new coronary events. Exercise-induced nonsustained VT¹³ or complex VA¹⁴ in older adults with no clinical evidence of heart disease also was not associated with an increased incidence of new coronary events. Therefore, asymptomatic nonsustained VA and complex VA in older adults without heart disease should not be treated with antiarrhythmic drugs.

General Therapy

Underlying causes of complex VA should be treated when possible. Treatment of congestive heart failure (CHF), LV dysfunction, digitalis toxicity, hypokalemia, hypomagnesemia, myocardial ischemia (by antiischemic drugs such as β-blockers or by coronary revascularization), hypertension, LV hypertrophy, hypoxia, and other conditions may eliminate or reduce the severity of complex VA. Such patients should not smoke or drink alcohol and should avoid drugs that may cause or increase complex VA.

All older adults with CAD should be treated with aspirin,^15–17 β-blockers,^16–22 angiotensin-converting enzyme (ACE) inhibitors,^{16,17,23–28} and statins^{16,17,29–35} unless there are contraindications to these drugs.

Age-related physiologic changes may affect absorption, distribution, metabolism, and excretion of cardiovascular drugs.³⁶ Numerous physiologic changes that occur with aging affect pharmacodynamics, resulting in changes in end-organ responsiveness to cardiovascular drugs.³⁶ Drug interactions between antiarrhythmic drugs and other cardiovascular drugs are common, especially in older adults.³⁶ Important drug-disease interactions also occur in older adults.³⁶ Class I antiarrhythmic drugs are more proarrhythmic than class III antiarrhythmic drugs. Except for β-blockers, all antiarrhythmic drugs can cause torsade de pointes VT (polymorphous appearance associated with a prolonged QT interval).

Class I Antiarrhythmic Drugs

Class I antiarrhythmic drugs are sodium channel blockers. Class Ia antiarrhythmic drugs have intermediate channel kinetics and prolong repolarization; these drugs include disopyramide, procainamide, and quinidine. Class Ib antiarrhythmic drugs have rapid channel kinetics and shorten repolarization slightly; these drugs include lidocaine, mexiletine, phenytoin, and tocainide. Class Ic antiarrhythmic drugs have slow channel kinetics and have little effect on repolarization; these drugs include encainide, flecainide, lorcainide, moricizine, and propafenone. None of the class I antiarrhythmic drugs have been demonstrated in controlled, clinical trials to decrease sudden cardiac death, total cardiac death, or total mortality.

Table 44-1 shows the effect of class I antiarrhythmic drugs on mortality in patients with heart disease and complex VA.^37–43 A meta-analysis of six double-blind studies of patients with chronic atrial fibrillation who underwent direct-current cardioversion to sinus rhythm showed that the mortality rate at 1 year was higher in patients treated with quinidine (2.9%) than in patients treated with a placebo (0.8%).⁴⁴

Of 1330 patients in the Stroke Prevention in Atrial Fibrillation (SPAF) study, 127 were treated with quinidine, 57 with procainamide, 34 with flecainide, 20 with encainide, and 7 with amiodarone.⁴⁵ The adjusted relative risk of cardiac mortality was increased 1.8 times and the adjusted relative risk of arrhythmic death was increased 2.1 times in patients receiving antiarrhythmic drugs versus no antiarrhythmic drugs.⁴⁵ In patients with a history of CHF, the adjusted relative risk of cardiac death was increased 3.3 times and the adjusted relative risk of arrhythmic death was increased 5.8 times in patients taking antiarrhythmic drugs versus no antiarrhythmic drugs.⁴⁵

An analysis was made of 59 randomized, controlled clinical trials including 23,229 patients that investigated the use of class I antiarrhythmic drugs after myocardial infarction (MI).⁴⁶ The class I antiarrhythmic drugs investigated included aprindine, disopyramide, encainide, flecainide, imipramine, lidocaine, mexiletine, moricizine, phenytoin, procainamide, quinidine, and tocainide. Mortality was increased in patients receiving class I antiarrhythmic drugs versus patients receiving no antiarrhythmic drugs (OR = 1.14).⁴⁶ None of the 59 studies showed that the use of a class I antiarrhythmic drug decreased mortality in patients after MI.⁴⁶

On the basis of the available data, none of the class I antiarrhythmic drugs should be used to treat VT or complex VA in older adult or younger patients with heart disease.

Calcium Channel Blockers

Calcium channel blockers are not useful in the therapy of complex VA. Although verapamil can terminate a left septal VT, hemodynamic collapse can occur if intravenous verapamil is given to patients with the more common forms of VT. An analysis was made of randomized, controlled clinical trials (N = 20,342) that investigated the use of calcium channel blockers after MI.⁴⁶ Mortality was insignificantly increased in patients receiving calcium channel blockers than in patients receiving no antiarrhythmic drugs (odds ratio [OR] = 1.04).⁴⁶

On the basis of the available data, none of the calcium channel blockers should be used to treat VT or complex VA in older adult or younger patients with heart disease.

β-Blockers

An analysis of 55 randomized, controlled clinical trials including 53,268 patients that investigated the use of β-blockers after MI showed that mortality was decreased in patients who received β-blockers versus a placebo (OR = 0.81).⁴⁶ β-Blockers caused a greater decrease in mortality in older patients than in younger patients.^18–21,47 Table 44-2 indicates the effect of β-blockers on mortality in patients with heart disease and complex VA.^43,47–52

The decrease in mortality as a result of the use of β-blockers in older adults with heart disease and complex VA is due more to an antiischemic effect than to an antiarrhythmic effect.⁵³ β-Blockers also abolish the circadian distribution of sudden cardiac death or fatal MI,⁵⁴ markedly decrease the circadian variation of complex VA,⁵⁵ and abolish the circadian variation of myocardial ischemia.⁵⁶ Based on the available data, β-blockers should be used to treat older and younger patients with heart disease and complex VA if there are no contraindications to the use of β-blockers.

Angiotensin-Converting Enzyme Inhibitors

ACE inhibitors have been demonstrated to reduce sudden cardiac death in some studies of patients with CHF.^24,57 ACE inhibitors should be used to reduce total mortality in older and younger patients with CHF,^24,26,57,58 an anterior MI,²⁵ and an LV ejection fraction of 40% after MI.^23,26,59 ACE inhibitors should be administered to treat older adult and younger patients with CHF with abnormal LV ejection fraction^24,26,57,58 or with normal LV ejection fraction.^60,61

On the basis of the available data, ACE inhibitors should be used to treat older and younger patients with VT or complex VA associated with CHF, an anterior MI, or an LV ejection fraction of 40% after MI if there are no contraindications to the use of ACE inhibitors. β-Blockers should be administered in addition to ACE inhibitors in treating these patients.⁵⁹

Class III Antiarrhythmic Drugs

Class III antiarrhythmic drugs are potassium channel blockers, which prolong repolarization manifested by an increase in QT interval on the ECG. These drugs are effective in suppressing complex VA, including nonsustained VT, by increasing the refractory period. However, antiarrhythmic aggravation can occur, especially torsade de pointes.

Table 44-3 shows the effect of class III antiarrhythmic drugs on mortality in patients with heart disease.^62–67 None of the class III antiarrhythmic drugs have been found in a double-blind, randomized, placebo-controlled clinical trial to decrease mortality in patients with heart disease and complex VA.

In 481 patients with VT, D,L-sotalol caused torsade de pointes (12 patients) or an increase in VT episodes (11 patients) in 23 patients (5%).⁶⁸ On the basis of the available data, β-blockers are preferred to the use of D,L-sotalol in treating older adult and younger patients with heart disease and VT or complex VA.

Amiodarone is very effective in suppressing VT and complex VA associated with heart disease.^64,65,67,69 However, the incidence of adverse effects from amiodarone approaches 90% after 5 years of therapy.⁷⁰ In the Cardiac Arrest in Seattle: Conventional Versus Amiodarone Drug Evaluation study, the incidence of pulmonary toxicity was 10% at 2 years in patients receiving 158 mg of amiodarone daily.⁶⁹ Amiodarone can also cause hyperthyroidism, hypothyroidism, and cardiac, dermatologic, gastrointestinal, hepatic, neurologic, and ophthalmologic adverse effects.

Because amiodarone has not been demonstrated to reduce mortality in older adult or younger patients with VT or complex VA associated with prior MI or CHF and has a very high incidence of toxicity, β-blockers are preferred to the use of amiodarone in treating these patients. Some data suggest that patients receiving amiodarone plus β-blockers have a better survival time than patients receiving amiodarone.⁷¹

Invasive Intervention

If patients have life-threatening VT or VF resistant to antiarrhythmic drugs, invasive intervention should be conducted. Patients with critical CAD and severe myocardial ischemia should undergo coronary artery bypass graft surgery to reduce mortality.⁷²

Surgical ablation of the arrhythmogenic focus in patients with life-threatening VT can be curative. This treatment includes aneurysmectomy or infarctectomy and endocardial resection with or without adjunctive cryoablation based on activation mapping in the operating room.^73–75 However, the perioperative mortality rate is high. Endoaneurysmorrhaphy with a pericardial patch combined with mapping-guided subendocardial resection frequently cures recurrent VT with a low operative mortality and improvement of LV systolic function.⁷⁶ Radiofrequency catheter ablation of VT has also been beneficial in the management of selected patients with arrhythmogenic foci of monomorphic VT.^77–79

Automatic Implantable Cardioverter-Defibrillator

The automatic implantable cardioverter-defibrillator (AICD) is the most effective treatment for patients with life-threatening VT or VF. Table 44-4 indicates the effect of the AICD on mortality in patients with ventricular tachyarrhythmias.^80–86 Tresch and colleagues^74,75 showed in retrospective studies that the AICD was very effective in treating life-threatening VT in older adult and younger patients. The Canadian Implantable Defibrillator study found that patients most likely to benefit from an AICD were those with two of the following factors: age (70 years), LV ejection fraction (35%), and New York Heart Association (NYHA) function class III or IV.⁸⁷

In MADIT-II, the reduction in sudden cardiac death in patients treated with an AICD was significantly reduced: by 68% in 574 patients younger than 65 years, by 65% in 455 patients aged 65 to 74 years, and by 68% in 204 patients aged 75 years.⁸⁸ The median survival in 348 octogenarians treated with AICD therapy was greater than 4 years.⁸⁹

At 26-month follow-up, survival was 91% for patients treated with metoprolol plus an AICD versus 83% for patients treated with D,L-sotalol plus an AICD.⁹⁰ An observational study in 78 patients with CAD and life-threatening VA treated with an AICD showed at the 490-day follow-up that the use of lipid-lowering drugs reduced recurrences of life-threatening VA.⁹¹ At the 33-month follow-up of 1038 patients (mean age, 70 years) who had AICDs, use of β-blockers significantly reduced the frequency of appropriate AICD shocks.⁹² At the 32-month follow-up of 965 of these patients, all-cause mortality was significantly reduced: 46% by use of β-blockers, 42% by use of statins, and 29% by use of ACE inhibitors or angiotensin receptor blockers.⁹³ These data support the use of β-blockers, statins, and ACE inhibitors or angiotensin receptor blockers in the treatment of patients with AICDs.

The American College of Cardiology/American Heart Association (ACC/AHA) guidelines recommend that class I indications for treatment with an AICD are (1) cardiac arrest due to VT or VF not caused by a transient or reversible cause; (2) spontaneous sustained VT; (3) syncope of undetermined origin with clinically relevant, hemodynamically significant sustained VT or VF induced at electrophysiologic study when drug therapy is ineffective, not tolerated, or not preferred; (4) nonsustained VT with CAD, prior MI, LV systolic dysfunction, and inducible VF or sustained VT at electrophysiologic study that is not suppressed by a class I antiarrhythmic drug; (5) patients with prior MI (at least 40 days previously) with an LV ejection fraction less than or equal to 35% who are in NYHA class II or III; (6) patients with prior MI (at least 40 days previously) with an LV ejection fraction less than 30% who are in NYHA class I; and (7) patients with nonischemic dilated cardiomyopathy with an LV ejection fraction less than or equal to 35% who are in NYHA class II or III.⁹⁴

The 2009 updated ACC/AHA guidelines for treatment of CHF with class I indications recommend use of an AICD in (1) patients with current or prior symptoms of CHF and reduced LV ejection fraction with a history of cardiac arrest, VF, or hemodynamically destabilizing VT; (2) patients with CAD at least 40 days after MI, an LV ejection fraction equal to or less than 35%, NYHA class II or III symptoms on optimal medical therapy, and an expected survival greater than 1 year; and (3) patients with nonischemic cardiomyopathy, an LV ejection fraction equal to or less than 35%, NYHA class II or III symptoms on optimal medical therapy, and an expected survival greater than 1 year; and (4) may be used in patients receiving cardiac resynchronization therapy for NYHA class II or ambulatory class IV symptoms despite recommended optimal medical therapy.^95,96

ACC/AHA class IIa indications for treatment with an AICD are (1) unexplained syncope, significant LV dysfunction, and nonischemic cardiomyopathy; (2) sustained VT and normal or near normal LV function; (3) hypertrophic cardiomyopathy with one or more major risk factors for sudden cardiac death; (4) prevention of sudden cardiac death in patients with arrhythmogenic right ventricular dysplasia/cardiomyopathy who have one or more risk factors for sudden cardiac death; (5) reduction of sudden cardiac death in patients with long-QT syndrome who have syncope and/or VT while using β-blockers; (6) nonhospitalized patients awaiting cardiac transplantation; (7) Brugada syndrome with syncope; (8) Brugada syndrome with documented VT that has not resulted in cardiac arrest; (9) patients with catechol­aminergic polymorphic VT with syncope and/or documented sustained VT on β-blockers; and (10) cardiac sarcoidosis, giant cell myocarditis, or Chagas disease.⁹⁴

During 1243 days mean follow-up of 549 patients, mean age 74 years, who had an AICD for CHF, 163 (30%) had appropriate AICD shocks, 71 (13%) had inappropriate AICD shocks, and 63 (12%) died. ⁹⁷ Stepwise logistic regression analysis showed that significant independent prognostic factors for appropriate AICD shocks were smoking (OR = 3.7) and statins (OR = 0.54) , for inappropriate AICD shocks were atrial fibrillation (OR = 6.2) and statins (OR = 0.52), and for time to mortality were age (hazard ratio [HR] = 1.08 per 1-year increase), ACE inhibitors or angiotensin receptor blockers (HR = 0.25), AF (HR = 4.1), right ventricular pacing (HR = 3.6), digoxin (HR = 2.9), hypertension (HR = 5.3), and statins (HR = 0.32).⁹⁷

During implantation and during the 38-month follow-up observation of 1,060 patients (mean age, 70 years) who had AICDs, complications occurred in 60 patients (5.7%).⁹⁸ In a registry of 5,399 AICD recipients for primary or secondary prevention, rates of appropriate AICD shocks were similar among patients aged 18 to 49, 50 to 59, 60 to 69, 70 to 79, and 80 years and older.⁹⁹

Predisposing Factors

Factors predisposing to AF include alcohol, atrial myxoma, atrial septal defect, cardiomyopathies, chronic lung disease, conduction system disease, CHF, CAD, diabetes mellitus, drugs, emotional stress, excessive coffee, hypertension, hyperthyroidism, hypoglycemia, hypokalemia, hypovolemia, hypoxia, myocarditis, neoplastic disease, pericarditis, pneumonia, postoperative state, pulmonary embolism, systemic infection, and valvular heart disease. Table 44-5 lists the increased prevalence of echocardiographic findings in 254 older adult patients with chronic AF compared with 1445 older adult patients with sinus rhythm (mean age, 81 years).¹⁰⁵ In the Framingham Heart Study, low serum thyrotropin levels were independently associated with a 3.1 times increase in the development of new AF in older adults.¹⁰⁶

Associated Risks

The Framingham study showed that the incidence of death from cardiovascular causes was 2.0 times higher in men and 2.7 times higher in women with chronic AF than in men and women with sinus rhythm.¹⁰⁷ The Framingham study also demonstrated that after adjustment for preexisting cardiovascular conditions, the odds ratio for mortality in patients with AF was 1.5 in men and 1.9 in women.¹⁰⁸ At the 42-month follow-up of 1359 patients (mean age, 81 years) with heart disease, patients with AF had a 2.2 times higher probability of developing new coronary events than those with sinus rhythm after controlling for other prognostic variables.¹⁰⁹ In 106,780 Medicare beneficiaries (65 years of age) from the Cooperative Cardiovascular Project treated for acute MI, AF was present in 22%.¹¹⁰ Compared with sinus rhythm, older adults with AF had a higher in-hospital mortality (25% vs. 16%), 30-day mortality (29% vs. 19%), and 1-year mortality (48% vs. 33%).¹¹⁰ AF was an independent predictor of in-hospital mortality (OR = 1.2), 30-day mortality (OR = 1.2), and 1-year mortality (OR = 1.3).¹¹⁰ Older adults who developed AF while they were hospitalized had a worse prognosis than older adults who already had AF.¹¹⁰

AF is an independent risk factor for thromboembolic (TE) stroke, especially in older patients.^100,101 In the Framingham study, the relative risk of stroke in patients with nonrheumatic AF compared with patients in sinus rhythm was 2.6 times higher in patients aged 60 to 69 years, 3.3 times higher in patients aged 70 to 79 years, and 4.5 times higher in patients aged 80 to 89 years.¹⁰⁰ AF was an independent risk factor for TE stroke in 2101 patients, mean age 81 years, with a relative risk of 3.3.¹⁰¹ The 3-year incidence of TE stroke was 38% in patients with AF and 11% in patients with sinus rhythm.¹⁰¹ The 5-year incidence of TE stroke was 72% in patients with AF and 24% in patients with sinus rhythm.¹⁰¹

AF was present in 313 of 2384 patients (13%), mean age 81 years.¹¹¹ AF was present in 201 of 1024 patients (17%) with LV hypertrophy and in 112 of 1360 patients (8%) without LV hypertrophy.¹¹¹ At the 44-month follow-up, both AF (risk ratio [RR] = 3.2) and LV hypertrophy (RR = 2.8) were independent risk factors for new TE stroke. The higher prevalence of LV hypertrophy in older adults with chronic AF contributes to the higher incidence of TE stroke in older adults with AF.

At the 45-month follow-up of 1846 patients, mean age 81 years, both AF (RR = 3.3) and 40% to 100% extracranial carotid arterial disease (ECAD) (RR = 2.5) were independent risk factors for new TE stroke.¹¹² Older adults with both chronic AF and 40% to 100% ECAD had a 6.9 times higher probability of developing new TE stroke than those with sinus rhythm and no significant ECAD.¹¹²

Symptomatic cerebral infarctions were present in 22% of 54 autopsied patients aged 70 years or older with paroxysmal AF.¹¹³ Symptomatic cerebral infarction was 2.4 times more common in older patients with paroxysmal AF than in older patients with sinus rhythm.¹¹³ AF also causes silent cerebral infarction.¹¹⁴

AF is a predisposing factor for CHF in older patients. As much as 30% to 40% of LV end-diastolic volume may be attributable to left atrial contraction in older patients. Absence of a coordinated left atrial contraction decreases late diastolic filling of the left ventricle because of loss of the atrial kick. A rapid ventricular rate associated with AF also shortens the diastolic filling period, which further decreases LV filling.

A retrospective analysis of the Studies of Left Ventricular Dysfunction Prevention and Treatment Trials found that AF was an independent risk factor for all-cause mortality (RR = 1.3), progressive pump failure death (RR = 1.4), and death or hospitalization for CHF (RR = 1.3).¹¹⁵

AF was present in 132 of 355 patients (37%), mean age 80 years, with prior MI, CHF, and an abnormal LV ejection fraction.¹¹⁶ AF was present in 98 of 296 patients (33%), mean age 82 years, with prior MI, CHF, and a normal LV ejection fraction.¹¹⁶ In this study, AF was an independent risk factor for mortality with a risk ratio of 1.5.¹¹⁶

A rapid ventricular rate associated with chronic or paroxysmal AF may cause a tachycardia-related cardiomyopathy, which may be an unrecognized curable cause of CHF.^117,118 Control of a rapid ventricular rate by radiofrequency ablation of the atrioventricular (AV) node with permanent pacing caused an improvement in LV ejection fraction in patients with medically refractory AF.¹¹⁹

Clinical Symptoms

Older adults with AF may be symptomatic or asymptomatic with their arrhythmia detected by physical examination or by an ECG. Examination of a person after a stroke may lead to the diagnosis of AF. Symptoms may include palpitations, skips in heartbeat, fatigue on exertion, exercise intolerance, cough, dizziness, chest pain, and syncope. A rapid ventricular rate associated with loss of atrial contraction reduces cardiac output and may cause hypotension, angina pectoris, CHF, acute pulmonary edema, and syncope, especially in older adults with mitral stenosis, aortic stenosis, or hypertrophic cardiomyopathy.

Diagnostic Tests

When AF is suspected, a 12-lead ECG with a 1-minute rhythm strip should be obtained to confirm the diagnosis. If paroxysmal AF is suspected, a 24-hour ambulatory ECG should be obtained. All patients with AF should have an M-mode, two-dimensional, and Doppler echocardiogram to determine the presence and severity of cardiac abnormalities causing AF and to identify risk factors for stroke. Appropriate tests for noncardiac causes of AF should be performed when clinically indicated. Thyroid function tests should be performed because AF or CHF may be the only clinical manifestations of apathetic hyperthyroidism in older adults.

General Treatment Measures

Along with drug therapy, treatment of AF should include therapy of the underlying disorder (such as hyperthyroidism, pneumonia, or pulmonary embolism) when possible. Surgical candidates for mitral valve replacement should undergo surgery if it is clinically indicated. If mitral valve replacement is not performed in patients with significant mitral valve disease, elective cardioversion should not be performed in patients with AF. Precipitating factors such as CHF, hypoxia, hypokalemia, hypoglycemia, hypovolemia, and infection should be treated immediately. Alcohol, coffee, and drugs (especially sympathomimetics) that precipitate AF should be avoided. Paroxysmal AF associated with the tachycardia-bradycardia (sick sinus) syndrome should be treated with permanent pacing in combination with the use of drugs to slow a rapid ventricular rate associated with AF.¹²⁰

Control of Very Rapid Ventricular Rate

Immediate direct-current cardioversion should be performed in patients who have paroxysmal AF with a very rapid ventricular rate associated with an acute MI, chest pain caused by myocardial ischemia, hypotension, severe CHF, or syncope. Intravenous verapamil,¹²¹ diltiazem,¹²² or β-blockers^123–126 may be used to immediately slow a very rapid ventricular rate associated with AF.

Control of Rapid Ventricular Rate

Digitalis glycosides are ineffective in converting AF to sinus rhythm.¹²⁷ Digoxin is also ineffective in slowing a rapid ventricular rate associated with AF if there is associated hyperthyroidism, fever, hypoxia, acute blood loss, or any condition involving increased sympathetic tone.¹²⁸ However, digoxin should be used for slowing a rapid ventricular rate in AF unassociated with increased sympathetic tone, the Wolff-Parkinson-White syndrome, or hypertrophic obstructive cardiomyopathy, especially if there is LV systolic dysfunction. The usual maintenance oral dose of digoxin administered to patients with AF is 0.25 to 0.5 mg daily, with the dose decreased to 0.125 to 0.25 mg daily for older adults who are more susceptible to digitalis toxicity.¹²⁹

Oral verapamil,¹³⁰ diltiazem,¹³¹ or a β-blocker¹³² should be added to the therapeutic regimen if a rapid ventricular rate associated with AF occurs at rest or during exercise despite digoxin. These drugs act synergistically with digoxin to depress conduction through the AV junction. In a study of digoxin 0.25 mg daily, diltiazem-CD 240 mg daily, atenolol 50 mg daily, digoxin 0.25 mg plus diltiazem-CD 240 mg daily, and digoxin 0.25 mg plus atenolol 50 mg daily, digoxin and diltiazem as single drugs were least effective and digoxin plus atenolol was most effective in controlling ventricular rate in AF during daily activity.¹³³

Amiodarone is the most effective drug for slowing a rapid ventricular rate associated with AF.^134,135 However, its adverse effect profile limits its use in the treatment of AF. Oral doses of 200 to 400 mg of amiodarone daily may be administered to selected patients with symptomatic life-threatening AF refractory to other drug therapy.

Therapeutic concentrations of digoxin do not decrease the frequency of episodes of paroxysmal AF or the duration of episodes of paroxysmal AF detected by 24-hour ambulatory ECG.^136,137 In fact, digoxin has been demonstrated to increase the duration of episodes of paroxysmal AF, a result consistent with its action in reducing the atrial refractory period.¹³⁶ Therapeutic concentrations of digoxin also do not prevent a rapid ventricular rate from developing in patients with paroxysmal AF.^136–138 Therefore, digoxin should be avoided in patients with sinus rhythm with a history of paroxysmal AF.

Nondrug Therapies

Radiofrequency catheter modification of AV conduction should be performed in patients with symptomatic AF in whom a rapid ventricular rate cannot be slowed by drug therapy.^139,140 If this procedure does not control the rapid ventricular rate associated with AF, complete AV block produced by radiofrequency catheter ablation followed by permanent pacemaker implantation should be performed.^141,142 In 44 patients, mean age 78 years, radiofrequency catheter ablation followed by pacemaker implantation was successful in ablating the AV junction in 43 of 44 patients (98%) with AF and a rapid ventricular rate not controlled by drug therapy.¹⁴²

In patients with CHF and chronic AF, AV junction ablation with implantation of a VVIR pacemaker was superior to drug therapy in controlling symptoms in a randomized, controlled study of 66 patients.¹⁴³ Surgical techniques have also been developed for use in patients with AF in whom a rapid ventricular rate cannot be slowed by drug treatment.^144–146 Appropriate indications for using an implantable Atrioverter in the treatment of AF need further investigation.¹⁴⁷

Randomized studies have demonstrated that circumferential pulmonary vein radiofrequency ablation was more effective than antiarrhythmic drug therapy in preventing recurrence of AF (93% vs. 35%) in 198 patients at 1 year¹⁴⁸ and (87% vs. 37%) in 67 patients at 1 year.¹⁴⁹ There are no long-term follow-up data showing a reduction in stroke risk in patients apparently cured of AF with radiofrequency catheter ablation. Anticoagulation therapy still needs to be administered to these patients who are at increased risk of developing TE stroke. Left atrial appendage closure with the Watchman device is a reasonable alternative to consider for patients at high risk for TE stroke but with contraindications to oral anticoagulant therapy.¹⁵⁰

Tachycardia-Bradycardia Syndrome

Paroxysmal AF associated with the tachycardia-bradycardia (sick sinus) syndrome should be treated with a permanent pacemaker in combination with drugs to decrease a rapid ventricular rate associated with AF.¹²⁰ Ventricular pacing is an independent risk factor for the development of chronic AF in patients with paroxysmal AF associated with the tachycardia-bradycardia syndrome.¹⁵¹ Patients with paroxysmal AF associated with the tachycardia-bradycardia syndrome and no signs of AV conduction abnormalities should be treated with atrial pacing or dual-chamber pacing rather than with ventricular pacing because atrial pacing is associated with less AF, fewer TE complications, and a lower risk of AV block than is ventricular pacing.¹⁵²

Wolff-Parkinson-White Syndrome

Direct-current cardioversion should be performed if a rapid ventricular rate in paroxysmal AF associated with the Wolff-Parkinson-White syndrome is life-threatening or fails to respond to drug treatment. Drug treatment for paroxysmal AF associated with the Wolff-Parkinson-White syndrome includes propranolol plus procainamide, disopyramide, or quinidine.¹⁵³ Digoxin, verapamil, and diltiazem are contraindicated in patients with AF associated with the Wolff-Parkinson-White syndrome because these drugs shorten the refractory period of the accessory AV pathway, causing faster conduction down the accessory pathway. This results in a marked increase in ventricular rate. Radiofrequency catheter ablation or surgical ablation of the accessory conduction pathway should be considered in patients with AF and fast AV conduction over the accessory pathway.¹⁵⁴