Atrial fibrillation (AF) is a common supraventricular tachyarrhythmia.  It is the result of disorganized atrial depolarizations which leads to extremely rapid atrial contraction rates.  Atrial rates become so rapid as to result in a lack of effective atrial contraction.  On electrocardiogram there is a lack of p waves with atrial electrical activity being represented by small irregular undulations at baseline (f waves) with a rate of 350-600 beats/min.  Ventricular contractions are “irregularly irregular” with a rate between 100-160 beats/min.  AF with a slow ventricular response (<70 beats/min) may be seen in patients with digitalis toxicity or sick sinus syndrome, or in patients receiving chronic beta blocker or calcium channel blocker therapy.  Patients are generally greater than 60 years of age at initial presentation unless there is an underlying condition which predisposes them to this arrythmia (hyperthyroidism, Wolf-Parkinson-White syndrome, etc.).  The prevalence of this arrhythmia increases with advancing age.  Most patients also have underlying heart disease (coronary artery disease, hypertension, rheumatic heart disease, nonrheumatic valvular disease, cardiomyopathy, or congestive heart failure), diabetes mellitus, or abuse alcohol.  When AF occurs in patients who lack underlying cardiac disease or a history of hypertension, this is referred to as lone AF.  AF is commonly seen in the post operative period following cardiac surgery, and this group of patients is not considered at risk for chronic AF as this arrhythmia often abates after the first couple of weeks post operatively.

     When patients present initially it is important to rule out acute myocardial infarction if associated with appropriate symptoms, underlying heart disease, and thyrotoxicosis.  It is imperative to try to determine the onset of symptoms although this is often difficult unless the patient has recently had a normal ECG prior to the acute event.  If the onset cannot accurately be determined, consideration for anticoagulation is the next step.  Current recommendations are for all patients with AF, both paroxysmal or chronic, to be evaluated for the need for long term anticoagulation. Patient’s whose AF is secondary to thyrotoxicosis without any underlying heart disease do not require anticoagulation. The CHADS (congestive heart failure, hypertension, age, diabetes mellitus, stroke/TIA history) score can be used to decide which patients require anticoagulation. Patients are assigned one point for congestive heart failure, hypertension, age greater than 75 years old, and diabetes mellitus. Patients are assigned two points for a history of stroke or TIA. If the CHADS score is greater than or equal to two, anticoagulation is indicated. If the CHADS score is zero, then aspirin therapy is adequate. When the CHADS score is one, either aspirin versus anticoagulation may be used depending on the situation. Anticoagulation is accomplished via coumadin, direct thrombin inhibitors (dabigatran or ximelagatran), or direct factor Xa inhibitors (apixaban or rivaroxaban).

     If the patient is unstable (pulmonary edema, myocardial infarction, or unstable angina) at initial presentation, immediate cardioversion is indicated.  Immediate cardioversion should also be considered initially in AF patients with a wide-complex ventricular response as these patients often have a preexcitation syndrome and respond poorly to many medications used for AF. Rate control is considered the treatment of choice in patients with AF who are stable although much debate exists regarding rhythm versus rate control and the optimal rate of control.

Patients should undergo echocardiography to assess the left atrial size and the left ventricular function.  Echocardiography may also demonstrate hypokinetic/akinetic areas of the myocardium which would suggest underlying coronary artery disease (either ongoing ischemia or prior myocardial infarction).  An enlarged left atrial size (greater than 5 cm) is indicative of a poor chance of conversion to normal sinus rhythm (NSR).  Transesophageal echocardiography (TEE) is superior to transthoracic echocardiography (TTE) in that it allows for adequate evaluation of the left atrial appendage for the presence of thrombi.  If no thrombus is present, cardioversion may proceed.  Even if the TEE shows no evidence of thrombi, anticoagulation should be instituted if there are no contraindications secondary to the potential for post conversion atrial dysfunction which results in stasis and the potential for coagulation.

     If the patient is stable and cardioversion is going to be attempted, the patient should be placed on an agent for rate control (beta-blocker, digoxin, or nondihydropyridine calcium channel blocker) and should be adequately anticoagulated (target INR of 2-3) with coumadin for three weeks prior to conversion.  Post conversion, anticoagulation should be continued for at least four weeks.  Patients who continue to have paroxysms of AF should continue anticoagulation indefinitely as they are at high risk for stroke and for eventually developing chronic AF.  Continuation of a rate-controlling agent such as a beta blocker is also advisable post conversion if there are no contraindications.    

     Chemical or electrical cardioversion (synchronized, direct-current or transvenous internal cardioversion) may be used to attempt to convert AF to NSR.  Intravenous ibutilide prior to electrical cardioversion may be effective for refractory cases.  Amiodarone, dronedarone, procainamide and ibutilide are options for chemical cardioversion.  Procainamide is the drug of choice when there is underlying WPW.  If NSR can not be restored, chronic anticoagulation when appropriate with rate control are recommended.  When AF is refractory to the above mentioned medications and symptoms of systolic dysfunction are present, atrioventricular node ablation with pacemaker implantation should be considered.

When cardioversion fails or is deemed unnecessary, then rate control may be attempted with dronedarone, amiodarone, beta-blockers, nondihyropyridine calcium channel blockers or digoxin). The optimal rate of control is not known, but titration against the patients symptoms may drive therapy. Concomitant hypertension should be aggressively controlled and evidence suggests a benefit in using ACE inhibitors or ARB's as these agents can reverse atrial fibrosis and structural remodeling of the atria.

     AF secondary to hyperthyroidism should be rate controlled with beta blocker therapy (calcium channel blockers may also be used) and the patient should be placed on antithyroid medication (tapazole or PTU) to make the patient euthyroid.  Digitalis therapy should be avoided in patients with underlying hyperthyroidism.  After the patient has been euthyroid for approximately six weeks, they should undergo radioablation therapy with radioactive iodine.  If the arrhythmia persists several months after effective thyroid management, consider that the arrhythmia was not secondary to the hyperfunctioning thyroid and manage the arrhythmia as above.