Atrial Fibrillation/Atrial flutter: Pharmacologic and Catheter Ablation to Maintain Sinus Rhythm

I. Atrial Fibrillation/Atrial Flutter: What every physician needs to know.

Atrial fibrillation (AF) is the most common arrhythmia requiring therapy and is associated with significant morbidity and mortality. Atrial flutter (AFL) is less common than AF but more difficult to control with drugs and is also associated with an increased risk of stroke. In some patients these arrhythmias may be asymptomatic but still result in heart failure or stroke.

The therapeutic strategies for treating AF and AFL include rate control, maintenance of sinus rhythm, and prevention of embolic events. Treatment of AF and AFL should also improve quality of life and survival. Treatment needs to be individualized to each patient and a given patient may require different therapies over time.

When AF results in symptoms or in deterioration of left ventricular function, restoration and maintenance of sinus rhythm is required. This can be achieved with drugs, cardioversion, or catheter ablation.

Antiarrhythmic drugs have a low to moderate success rate and may result in pro-arrhythmia, heart failure, or extra cardiac adverse effects. Catheter ablation is emerging as a superior alternative to drugs. Several studies have shown that catheter ablation is associated with better sinus rhythm maintenance than currently available antiarrhythmic drugs. However, it is an invasive procedure that can result in serious complications.

Catheter ablation is only performed by a limited number of electrophysiologists who are not able to cope with the growing population of AF patients. Pharmacologic and ablative therapies should not be considered competing approaches but rather staged or complementary treatments in patients with AF.

Ablation is usually considered when antiarrhythmic drugs fail to maintain sinus rhythm. However, antiarrhythmic drugs are still required before and following ablation. New antiarrhythmic drug strategies include more atrial selective agents, drugs similar to amiodarone but with a less toxic profile, or drugs with novel mechanisms of action, such as gap junction facilitation of conduction.

II. Diagnostic Confirmation: Are you sure your patient has Atrial Fibrillation?

An irregular pulse should always raise the suspicion of AF, but an electrocardiogram (ECG) recording is required to diagnose AF. In the electrocardiogram, AF is easily recognized due the absence of a P wave, which is replaced by a fast and irregular atrial activity that results in waves of variable voltage, duration, and frequency. It is frequently associated with an irregular ventricular response (completely irregular), unless the patient has advanced atrioventricular (AV) block or digitalis toxicity.

However, the atrial signals may be too small to discern and in other cases quite large, simulating AFL (coarse atrial fibrillation). Atrial tachycardias and reentrant arrhythmias can sometimes result in an irregular ventricular response mimicking atrial fibrillation.

A careful interpretation of the electrocardiogram and rhythm recording is a prerequisite for proper diagnosis and management of patients with AF. Any episode of suspected AF should be observed in a prolonged ECG recording to evaluate atrial activity. Occasionally, when the ventricular rate is fast, atrioventricular nodal blockade induced by carotid massage or intravenous adenosine administration will facilitate observation of underlying electrical activity.

A. History Part I: Pattern Recognition:

Patients with AF or AFL may be completely asymptomatic or manifest with palpitations, shortness of breath, chest pain, or embolic complications. In some patients, transient ischemic attack (TIA) or stroke may be the initial presentation of AF.

Most patients initially experience asymptomatic, often self-limited episodes of AF. AF progresses from short and infrequent episodes, to more frequent and sustained episodes. Only a small proportion of patients will remain in paroxysmal AF over several decades. Asymptomatic AF is common even in symptomatic patients, irrespective of whether the initial presentation was persistent or paroxysmal.

B. History Part 2: Prevalence:

The prevalence of AF is estimated at 0.4% of the general population, increasing with age. AF prevalence in the general population is increasing steadily and will more than double in the next 50 years. Although the reasons for this increased occurrence are not well known, the aging of the population and the increasing prevalence of hypertension, obesity, metabolic syndrome, and sleep apnea may explain this phenomenon.

AF is uncommon in children except after cardiac surgery. It occurs in less than 1% of those under 60 years of age but in 7% to 8% of those over 80 years of age. It is more frequent in men than in women, and more prevalent in whites that in blacks. The prevalence of AF increases in patients with congestive heart failure or valvular heart disease.

C. History Part 3: Competing diagnoses that can mimic Atrial Fibrillation.

Atrial tachycardias, atrial flutter, and rarely, reentrant tachycardias may mimic AF due to a fast and irregular ventricular response. Careful review of the ECG tracings facilitates the correct diagnosis.

D. Physical Examination Findings.

Physical examination is paramount in determining the presence and hemodynamic effect of AF. Blood pressure, heart rate determined with an stethoscope, jugular venous pressure, presence of third heart sound, murmurs, intensity of the heart sounds, and lung rales need to be identified.

E. What diagnostic tests should be performed?

AF can occur in the absence of an obvious heart abnormality (idiopathic or lone AF) or secondary to heart failure, valvular, or congenital heart disease. Therefore, in addition to a careful clinical evaluation, patients should get an electrocardiogram and an echocardiogram to evaluate for additional abnormalities.

The electrocardiogram for example can detect the presence of ventricular preexcitation due to an accessory AV pathway that can result in atrial fibrillation. The echocardiogram can identify structural abnormalities (e.g. mitral valve disease, left atrial enlargement, pulmonary hypertension). It is important to rule out treatable conditions that can result in AF including hyperthyroidism, pericarditis, anemia, and congestive heart failure.

During follow-up, patients with AF and AFL should be monitored to detect changes in their condition and risk factors. This is important because the patient may have developed hypertension or diabetes, which may now be an indication for anticoagulation. Similarly, patients that were on anticoagulation due to cardioversion in the first episode of AF may not require long-term anticoagulation due to a low-embolic risk.

Patients may have limited response to the initial antiarrhythmic therapy or poor control of heart rate. In this case, other pharmacologic agents should be tried or catheter ablation should be considered. Patients should be monitored periodically for signs of pro-arrhythmia or ischemia, which may require a change in antiarrhythmic therapy. An ECG should be obtained to determine rate, P–R, QRS, and Q–T intervals.

1. What laboratory studies (if any) should be ordered to help establish the diagnosis? How should the results be interpreted?

In patients with suspected AF, a 12-lead ECG is usually enough to make the correct diagnosis of AF when the arrhythmia is present at the time of the recording. Unexplained palpitations or dyspnea require prolonged monitoring to demonstrate AF and correlate symptoms with the underlying rhythm.

Holter recordings for 24 hours is required in symptomatic patients without a clear diagnosis, especially those with recurrent syncope or unexplained stroke. Transtelephonic recordings, and patient-activated, and automatic devices are sometimes required to establish the diagnosis. Dual-chamber pacemakers and defibrillators can detect AF. Implantable loop recorders provide continuous AF monitoring over a 2-year period with automatic AF detection based on R–R interval analysis.

2. What imaging studies (if any) should be ordered to help establish the diagnosis? How should the results be interpreted?

Although not required for diagnosis, a transthoracic echocardiogram is performed to determine the presence and severity of atrial or ventricular dysfunction, valvular abnormalities, pericardial disease, congenital abnormalities, and to search for pulmonary hypertension.

III. Management.

A detailed medical history should be obtained from each patient with AF. The acute management should be directed to the control of symptoms and prevention of complications.

The initial evaluation should include determination of the stroke risk, and search for conditions that predispose or are frequently associated with AF (alcohol, hyperthyroidism, hypertension, diabetes mellitus, family history of AF, peripheral vascular disease, chronic pulmonary disease, stroke, heart failure, congenital heart disease, Wolff-Parkinson-White syndrome). The 12-lead ECG should be inspected for signs of structural heart disease (myocardial infarction, ischemia, hypertrophy, bundle branch block, ventricular preexcitation, cardiomyopathy).

Patients with AF and hemodynamic instability require urgent rate control and cardioversion in most cases to stabilize the patient. This is frequently the case after heart surgery or in patients with hypertrophic cardiomyopathy that do not tolerate the lack of atrial systole.

After the initial management of symptoms and complications, conditions that cause or exacerbate AF should be identified. In addition to a careful physical examination, an echocardiogram is useful to detect ventricular dysfunction, valvular heart disease, pericarditis, pulmonary hypertension, and congenital anomalies.

Hypertension, diabetes, hyperthyroidism, renal insufficiency, and proteinuria should be identified. An exercise stress test is recommended in patients with risk factors for coronary artery disease. Cardiac catheterization should be performed in patients with evidence of myocardial ischemia or unexplained myocardial dysfunction or with possible pulmonary hypertension.

Despite our incomplete understating of the pathophysiology of AF, treatment has improved over the last decade due to recent advances in catheter ablation, new antiarrhythmic drugs, pacing, and anticoagulation. All therapies have limitations regarding efficacy and safety, and frequently more than one therapeutic modality is used simultaneously or sequentially to treat patients with AF.

Antiarrhythmic drugs are limited by frequent recurrences, adverse effects, and pro-arrhythmia. Catheter ablation has moderate success and the procedure has to be repeated in approximately 25% of patients due to recurrence of conduction between the pulmonary veins and the left atrium, the presence of extrapulmonary foci, and/or abnormal atrial substrate.

Repeat procedures are required more often in patients with persistent atrial fibrillation due to more extensive electrical abnormalities. Catheter ablation may be considered curative in patients in whom the substrate or the source of the arrhythmia is relatively localized, while in most patients the procedure should be considered palliative since the abnormal substrate is modified but not normalized.

Hence, some patients, especially those with persistent AF, will require antiarrhythmic drugs to maintain sinus rhythm even after ablation has been performed. This should not be considered a failure of the ablation procedure since drugs are usually effective only after catheter ablation has previously been performed.

Treatment of patients with AF and AFL should improve the quality of life and reduce complications associated with these arrhythmias. Prevention of complications requires anticoagulant therapy in many patients, control of the ventricular rate, and therapy of concomitant cardiac diseases. Cardioversion, antiarrhythmic drug therapy, and or catheter ablation are frequently required in a staged therapy.

Clear risk factors for peripheral embolism include congestive heart failure, low ejection fraction (EF), prior TIA, stroke or peripheral embolism, age, hypertension, diabetes, and structural heart disease. Age is a risk for stroke in patients older than 65 and even more clear in those older than 75. Mitral stenosis and mechanical heart valves are indications for anticoagulation. The presence of vascular disease, female sex, renal insufficiency, and proteinuria are also risk factors for stroke.

Patients with paroxysmal AF have similar risk factors for stroke as those with persistent or permanent AF in the presence of similar risk factors. In contrast, patients younger than 60, with no clinical risk factors or echocardiographic evidence of cardiovascular disease (lone AF) have a very low stroke risk. For those that require anticoagulation, vitamin K antagonists or the new oral anticoagulant drugs that do not require monitoring should be prescribed.

A. Immediate management.

AF with rapid ventricular response can result in hemodynamic instability. This is more common in patients with an accessory AV pathway or after heart surgery. Under these conditions, external direct current cardioversion is required to stabilize the patient. In other patients with more stable circulatory status, control of the ventricular response and anticoagulation therapy should be initiated.

If cardioversion is contemplated and the patient has not previously been anticoagulated and the onset of the AF is more than 48 hours, a transesophageal echocardiogram can be performed to rule out a left atrial thrombus before cardioversion. Transthoracic echocardiogram can provide useful information to guide clinical decision making, but cannot exclude thrombus in the left atrial appendage (LAA).

B. Physical Examination Tips to Guide Management.

Physical examination is paramount in determining the presence and hemodynamic effect of AF. Blood pressure, heart rate determined with an stethoscope, jugular venous pressure, presence of a third heart sound, murmurs, intensity of the heart sounds, and lung rales need to be identified.

C. Long-term management.

Antiarrhythmic drugs reduce the recurrence of AF. Most patients with AF should receive a beta-blocker initially for rate control. Amiodarone is reserved for those who have failed treatment with other antiarrhythmic drugs or have significant structural heart disease.

The drugs more frequently used or studied include sodium channel blockers (disopyramide, quinidine, flecainide, propafenone), potassium channel blockade (dofetilide, sotalol), and multichannel blockers (amiodarone, dronedarone). Amiodarone remains the most effective drug to prevent recurrence of AF.

All drugs are associated with the potential for proarrhythmia, although it is rare with amiodarone. Antiarrhythmic agents have been associated with increased mortality in several studies.

Flecainide and propafenone can be administered in patients without significant structural heart disease, but should not be used in patients with coronary artery disease or in those with reduced ejection fraction. Precautions should be observed when using these drugs in the presence of intraventricular conduction delay because of the risk of inducing advanced AV block.

Upon initiation of these drugs, regular ECG monitoring is required because a prolongation of the QRS duration of more than 25% may result in ventricular arrhythmias. Concomitant atrioventricular node blockade is recommended because of the potential to convert AF to AFL with 1:1 AV conduction. Quinidine although effective, is associated with increased mortality due to torsades de pointes.

Amiodarone is a good therapeutic option in patients with frequent, symptomatic AF recurrences despite therapy with other antiarrhythmic drugs. Unlike most other agents, amiodarone can be safely administered in patients with structural heart disease, including patients with heart failure.

Sotalol is less effective than amiodarone but can be administered to patients with ischemic heart disease. Because it prolongs the Q–T interval and induced bradycardia, it can result in torsades de pointes. Sotalol is renally eliminated and therefore the dose should be adjusted accordingly.

Dronedarone is a multichannel blocker similar to, but less effective than, amiodarone. It has a low potential for proarrhythmia. This drug increases mortality in patients with advanced heart failure and should not be used in New York Hospital Association (NYHA class IV or class III with recent exacerbation. Dronedarone should not be used in patients with persistent atrial fibrillation in whom sinus rhythm has not been restored.

Catheter ablation has been developed to cure AF and AFL. Although extremely effective in eliminating AFL, long-term follow-up of patients with AF indicates that while sinus rhythm is better preserved with catheter ablation than with antiarrhythmic drugs, recurrences are common.In general, catheter ablation should be reserved for patients with AF, which remains symptomatic despite optimal medical therapy, including rate and rhythm control.

For patients with either persistent AF or long-standing persistent AF, more extensive and frequently repeated procedures may be necessary. Since amiodarone treatment may be associated with serious and frequent adverse effects, especially during long-term treatment, it is reasonable to consider catheter ablation as an alternative to amiodarone treatment in younger patients.

Patients with heart failure that is exacerbated or induced by AF can benefit significantly from catheter ablation. Restoration of sinus rhythm can improve the ejection fraction.

IV. Management with Co-Morbidities

Diabetes mellitus, hypertension, hyperthyroidism, obesity, sleep apnea, and chronic pulmonary disease should be treated concomitantly with these arrhythmias.

V. Patient Safety and Quality Measures

What's the Evidence for specific management and treatment recommendations?

"For specific managements and treatment recommendations please consult: 2011 ACCF/AHA/HRS focus update of the ACC/AHA/ESC 2006 guidelines". Circulation. vol. 123. 2011. pp. e269-367.

DRG Codes and Expected Length of Stay.

DRG code for AF is: 427.31.

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