ACC/AHA/ESC 2006 Guidelines for Management of Atrial Fibrillation – ‘Rate Control’

In addition to allowing adequate time for ventricular filling and avoiding rate-related ischemia, enhancement of intraventricular conduction with rate reduction may result in improved hemodynamics in atrial fibrillation. It may be useful to evaluate the heart rate response to submaximal or maximal exercise or to monitor the rate over an extended period (e.g., by 24-h Holter recording).

Criteria for rate control vary with patient age but usually involve achieving ventricular rates between 60 and 80 beats per minute at rest and between 90 and 115 beats per minute during moderate exercise.

Hemodynamic and Clinical Consequences of Rapid rate:
Patients who are symptomatic with rapid ventricular rates during AF require prompt medical management, and cardioversion should be considered if symptomatic hypotension, angina, or HF is present. A sustained, uncontrolled tachycardia may lead to deterioration of ventricular function (tachycardia-related cardiomyopathy) and that improves with adequate rate control.

Tachycardia-induced cardiomyopathy tends to resolve within 6 months of rate or rhythm control; when tachycardia recurs, LV ejection fraction declines and HF develops over a shorter period, and this is associated with a relatively poor prognosis.

Pharmacological Rate Control During Atrial Fibrillation
RECOMMENDATIONS:

Class I :

1. Measurement of the heart rate at rest and control of the rate using pharmacological agents (either a beta blocker or nondihydropyridine calcium channel antagonist, in most cases) are recommended for patients with persistent or permanent AF.
   (Level of Evidence: B)
2. In the absence of preexcitation, intravenous dministration
   of beta blockers (esmolol, metoprolol, or propranolol) or nondihydropyridine calcium channel antagonists (verapamil, diltiazem) is recommended to slow the ventricular response to AF in the acute setting, exercising caution in patients with hypotension or HF. (Level of Evidence: B)
3. Intravenous administration of digoxin or amiodarone is recommended to control the heart rate in patients with AF and HF who do not have an accessory pathway. (Level of Evidence: B)
4. In patients who experience symptoms related to AF during activity, the adequacy of heart rate control should be assessed during exercise, adjusting pharmacological treatment as necessary to keep the rate in the physiological range. (Level of Evidence: C)
5. Digoxin is effective following oral administration to control the heart rate at rest in patients with AF and is indicated for patients with HF, LV dysfunction, or for sedentary individuals. (Level of Evidence: C)

Class IIa:

1. A combination of digoxin and either a beta blocker or nondihydropyridine calcium channel antagonist is reasonable to control the heart rate both at rest and during exercise in patients with AF. The choice of medication should be individualized and the dose modulated to avoid bradycardia. (Level of Evidence:B)
2. It is reasonable to use ablation of the AV node or accessory pathway to control heart rate when pharmacological therapy is insufficient or associated with side effects. (Level of Evidence: B)
3. Intravenous amiodarone can be useful to control the heart rate in patients with AF when other measures are unsuccessful or contraindicated. (Level of Evidence: C)
4. When electrical cardioversion is not necessary in patients with AF and an accessory pathway, intravenous procainamide or ibutilide is a reasonable alternative. (Level of Evidence: C)

Class IIb:

1. When the ventricular rate cannot be adequately controlled both at rest and during exercise in patients with AF using a beta blocker, nondihydropyridine calcium channel antagonist, or digoxin, alone or in combination, oral amiodarone may be administered to control the heart rate. (Level of Evidence: C)
2. Intravenous procainamide, disopyramide, ibutilide, or amiodarone may be considered for hemodynamically stable patients with AF involving conduction over an accessory pathway. (Level of Evidence: B)
3. When the rate cannot be controlled with pharmacological
   agents or tachycardia-mediated cardiomyopathy is suspected, catheter-directed ablation of the AV node may be considered in patients with AF to control the heart rate. (Level of Evidence: C)

Class III:

1. Digitalis should not be used as the sole agent to control the rate of ventricular response in patients with paroxysmal AF. (Level of Evidence: B)
2. Catheter ablation of the AV node should not be attempted without a prior trial of medication to control the ventricular rate in patients with AF. (Level of Evidence: C)
3. In patients with decompensated HF and AF, intravenous administration of a nondihydropyridine calcium channel antagonist may exacerbate hemodynamic compromise and is not recommended. (Level of Evidence: C)
4. Intravenous administration of digitalis glycosides or nondihydropyridine calcium channel antagonists to patients with AF and a preexcitation syndrome may paradoxically accelerate the ventricular response and is not recommended. (Level of Evidence: C)

When rapid control of the ventricular response to AF is required or oral administration of medication is not feasible, medication may be administered intravenously. Otherwise, in hemodynamically stable patients with a rapid ventricular response to AF, negative chronotropic medication may be administered orally. Combinations may be necessary to achieve rate control in both acute and chronic situations, but proper therapy requires careful dose titration. Some patients develop symptomatic bradycardia that requires permanent pacing. Nonpharmacological therapy should be considered when pharmacological measures fail.

Specail considerations in patients with the Wolff-Parkinson-White (WPW) Syndrome: Intravenous beta blockers, digitalis, adenosine, lidocaine, and nondihydropyridine calcium channel antagonists, all of which slow conduction across the AV node, are contraindicated in patients with the WPW syndrome and tachycardia associated with ventricular preexcitation, because they can facilitate antegrade conduction along the accessory pathway during AF, resulting in acceleration of the ventricular rate, hypotension, or ventricular fibrillation. When the arrhythmia is associated with hemodynamic compromise, however, early direct-current cardioversion is indicated. In hemodynamically stable patients with preexcitation, type I antiarrhythmic agents or amiodarone may be administered intravenously. Beta blockers and calcium channel blockers are reasonable for oral chronic use.

Patients With Both Atrial Fibrillation and Atrial Flutter:
A patient treated with AV nodal blocking drugs whose ventricular rate is well controlled during AF may experience a rise or fall in rate if he or she develops atrial flutter. This is also true when antiarrhythmic agents such as propafenone or flecainide are used to prevent recurrent AF. These compounds may increase the likelihood of 1:1 AV conduction during atrial
flutter, leading to a very rapid ventricular response. Thus, when
these agents are given for prophylaxis against recurrent paroxysmal AF or atrial flutter, AV nodal blocking drugs should be routinely coadministered. An exception may be patients with
paroxysmal AF who have undergone catheter ablation of the
cavotricuspid isthmus to prevent atrial flutter.

Regulation of Atrioventricular Nodal Conduction by Pacing:
Because ventricular pacing prolongs the AV nodal refractory period as a result of concealed retrograde penetration, it eliminates longer ventricular cycles and may reduce the number of short ventricular cycles related to rapid AV conduction during AF. Pacing at approximately the mean ventricular rate during spontaneous AV conduction can regulate
the ventricular rhythm during AF. This may be useful for patients with marked variability in ventricular rates or for those who develop resting bradycardia during treatment with medication.

AV Nodal Ablation:
AV nodal ablation in conjunction with permanent pacemaker
implantation provides highly effective control of the heart rate
and improves symptoms in selected patients with AF. In general, patients most likely to benefit from this strategy
are those with symptoms or tachycardia-mediated cardiomyopathy related to rapid ventricular rate during AF that cannot be controlled adequately with antiarrhythmic or negative chronotropic medications.

Catheter ablation of inferior atrial inputs to the AV node slows the ventricular rate during AF and improves symptoms without
pacemaker implantation. This technique has several limitations, however, including inadvertent complete AV block
and a tendency of ventricular rate to rise over the 6 months following ablation. Ablation of the AV inputs in the atrium may improve the reliability of the junctional escape mechanism. 

Complications of AV nodal ablation include those associated with pacemaker implantation, ventricular arrhythmias, thromboembolism associated with interruption of anticoagulation, the rare occurrence of LV dysfunction, and progression from paroxysmal to persistent AF. Limitations include the persistent need for anticoagulation, loss of AV synchrony, and lifelong pacemaker dependency. There is also a finite risk of sudden death due to torsades de pointes or  ventricular fibrillation. Patients with abnormalities of diastolic ventricular compliance who depend on AV synchrony to maintain cardiac output, such as those with hypertrophic cardiomyopathy or hypertensive heart disease, may experience persistent symptoms after AV nodal ablation and pacemaker implantation. Hence, patients should be counseled regarding each of these considerations before proceeding with this irreversible measure.

Patients with normal LV function or reversible LV dysfunction
undergoing AV nodal ablation are most likely to benefit from standard AV nodal ablation and pacemaker implantation. For those with impaired LV function not due to tachycardia, a biventricular pacemaker with or without defibrillator capability should be considered. Upgrading to a biventricular device should be considered for patients with heart failure and an RV pacing system who have undergone AV node ablation.

Ref: J. Am. Coll. Cardiol. 2006;48;e149-e246

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