Atrial fibrillation affects  more than 3 million in the US with projected incidence of 7.56 million by 2050. It is an indipendent predictor for mortality, increases risk for thromboembolic events and reduces quality of life. Atrial fibrillation is caused by atrial electrophysical abnormalities, structural abnormalities and/or systemic processes. Atrial fibrillation is classified as paroxysmal, persistent, long-standing persistant and permanent atrial fibrillation. Atrial fibrillation managment is categorized into rate control, rhythm control and stroke prevention.

Rate control

Beta blockers (metoprolol, carvedilol) and calcium channel blockers (diltiazem, verapamil) preferred over other rate control agents. Avoid beta blockers in patients with severe COPD or astma and calcium channel blockers in patients with HFrEF.

Digoxin can be used in patient with relatively low blood pressure – reduces ventricular rate and improves contractility.

Amiodarone mildly reduces ventricular rate in addition to antiarrythmic properties.

Heart rate goal is <110 in acute settings and <85 for long term.

Rhythm Control

Rhythm control strategy has not shown to reduce mortality compared to rate control strategy. However, it has been shown to reduce atrial fibrillation burden and improve quality of life.

Electrical cardioversion: Optimize elecrolytes, light sedation, syncronized 100-200 J

Pharmacologic cardioversion:

–          Class IC: Flecainide and propafenone. „Pill-in-the-pocket.“ Contraindicated in patient with structural heart disease.

–          Class III: Sotalol, Amiodarone, Dronedarone. Most effective antiarrythmatic class

Catheter ablation:

–          Radiofrequency and cryotherapy ablation to isolate the pulmonary veins

–          Indicated in symptomatic patient that have failed antiarrhytmic therapy

Stroke prevention

Anticoagulation has been shown to lower risk of stroke and mortality. An increased stroke risk has been seen following cardioversion to sinus rhythm due to pre-cardioversion left atrial appendage thrombus formation and post-cardioversion atrial contractile dysfunction/stunning.

Short-term anticoagulation:

–          If less than 24-48 hr -> cardioversion without prior anticoagulation.

–          If more than 48 hr -> anticoagulation for 3 weeks prior vs. TEE

–          All should be on anticoagulation for at least 4 weeks.

Long-term anticoagulation:

–          CHADS-VASc to guide therapy.

–          High age, fragility and fall risk are not contraindications for anticoagulation

–          Consider WATCHMAN in patient that can not be on long-term anticoagulation.