classification of AF into the following 3 patterns

Pathophysiology
Atrial fibrillation (AF) shares strong associations with other cardiovascular diseases, such as heart failure, coronary artery disease (CAD), valvular heart disease, diabetes mellitus, and hypertension. The exact mechanisms by which cardiovascular risk factors predispose to AF are not understood fully but are under intense investigation. Catecholamine excess, hemodynamic stress,

atrial ischemia, atrial inflammation, metabolic stress, and neurohumoral cascade activation are all purported to promote AF.

Pathophysiology
AF appears to require both an initiating event

and a permissive atrial substrate. These mechanisms include multiple wavelets, mother waves, fixed or moving rotors, and macro-reentrant circuits.

Pathophysiology
Automatic focus
A focal origin of AF is supported by several experimental models

showing that AF persists only in isolated regions of atrial myocardium.

The pulmonary veins appear to be the most frequent source of these

automatic foci, but other foci have been demonstrated in several areas throughout the atria. Cardiac muscle in the pulmonary veins appears to have active electrical properties that are similar, but not identical, to those of atrial myocytes. Heterogeneity of electrical conduction around the pulmonary veins is theorized to promote reentry and sustained AF. Thus, pulmonary vein automatic triggers may provide the initiating event, and heterogeneity of conduction may provide the sustaining conditions in many patients with AF.

Pathophysiology
Multiple wavelet
proposes that fractionation of wave fronts propagating through the

atria results in self-perpetuating "daughter wavelets."

The number of wavelets is determined by the refractory period,

conduction velocity, and mass of atrial tissue. Increased atrial mass, shortened atrial refractory period, and delayed intra-atrial conduction increase the number of wavelets and promote sustained AF.

Etiology

Hemodynamic stress Atrial ischemia Inflammation Noncardiovascular respiratory causes Alcohol and drug use Endocrine disorders Neurologic disorders Genetic factors Advancing age

Epidemiology
affecting 4% of individuals older than 60

years and 8% of persons older than 80 years

25% of individuals aged 40 years and older will

develop AF during their lifetime

prevalence
0.1% in persons younger than 55 years
3.8% in persons 60 years or older 10% in persons 80 years or older

Epidemiology
incidence of AF is significantly higher in men than in

women in all age groups more common in whites than in blacks 10-15% of cases : disease occurs in the absence of comorbidities (lone atrial fibrillation) rate of ischemic stroke in patients with nonrheumatic AF averages 5% a year, which is somewhere between 2 and 7 times the rate of stroke in patients without AF
prevalence of stroke in patients younger than 60 years is

less than 0.5%; however, in those older than 70 years, the prevalence doubles with each decade. attributable risk of stroke from AF is estimated to be 1.5% for those aged 50-59 years, and it approaches 30% for those aged 80-89 years.

Prognosis
AF is associated with a 1.5- to 1.9-fold higher

risk of death, which is in part due to the strong association between AF and thromboembolic events, according to data from the Framingham heart study. The risk of stroke from AF that lasts longer than 24 hours is a major concern and is usually addressed by prescribing a blood thinner (Coumadin or dabigatran).

History
90% of AF episodes asymptomatic palpitations, dyspnea, fatigue, dizziness,

angina, and decompensated heart failure

Physical Examination
Vital signs: irregularly irregular pulse,

tachycardic, with heart rates typically in the 110- to 140-range, but rarely over 160-170. Head and neck: exophthalmos, thyromegaly, elevated jugular venous pressures, cyanosis.
Carotid artery bruits suggest peripheral arterial

disease and increase the likelihood of comorbid coronary artery disease.

Physical Examination
Pulmonary: rales, wheezes or diminished

breath sounds Cardiac: displaced point of maximal impulse or S3 suggests ventricular enlargement and elevated left ventricular pressur
prominent P2 points to the presence of pulmonary

hypertension.

Abdomen: ascites, hepatomegaly, hepatic

capsular tenderness, left upper quadrant pain

Physical Examination
Lower extremities: cyanosis, clubbing, or

edema. Neurologic: Signs of a transient ischemic attack or cerebrovascular accident may be discovered. Evidence of prior stroke and increased reflexes is suggestive of hyperthyroidism

Approach Considerations
ECG

Lab Studies

CBC count (looking for anemia, infection) Serum electrolytes and BUN/creatinine (looking for electrolyte disturbances or renal failure) Cardiac enzymes - CK and/or troponin level (to investigate myocardial infarction as a primary or secondary event) BNP (to evaluate for CHF) D-dimer (if the patient has risk factors to merit a pulmonary embolism workup) Thyroid function studies (looking for thyrotoxicosis, a rare, but not-tobe-missed, precipitant) Digoxin level (may be obtained when appropriate for subtherapeutic levels and/or toxicity; generally considered safe to give digoxin to patient with AF on digoxin for rate control without waiting for lab values if patient presents with AF with rapid ventricular response [RVR]) Toxicology testing or ethanol level

Echocardiography
Transthoracic echocardiography (TTE) is helpful for making the following determinations:
Evaluate for valvular heart disease
Evaluate atrial and ventricular chamber and wall

dimensions Estimate ventricular function and evaluate for ventricular thrombi Estimate pulmonary systolic pressure (pulmonary hypertension) Evaluate for pericardial disease

Echocardiography
Transesophageal echocardiography (TEE) is

helpful for making the following determinations:

Evaluate for LA thrombus (particularly in the LA

appendage) To guide cardioversion (if thrombus is seen, cardioversion should be delayed) When TEE is planned, the concurrent use of TTE may increase cost without providing significant additional information.

Approaches
CT and MRI Chest radiography Six-Minute Walk Test or Exercise Test Holter Monitoring or Event Recording Electrophysiology Study

Risk-Management Decisions Risk Factors for Stroke in Patients with Nonvalvular AF

Risk Factors Prior stroke or TIA History of hypertension Heart failure and/or reduced left ventricular function Advanced age 2.5 1.6 1.4 1.4 Relative Risk

Diabetes
Coronary artery disease

1.7
1.5

Table 3. Recommendations for Antithrombotic Therapy in Patients with Nonvalvular Atrial Fibrillation
Risk Category No risk factors Recommended Therapy Aspirin 81-325 mg daily

One moderate-risk Aspirin 81-325 mg daily or factor warfarin (INR 2-3) Any high-risk factor or Warfarin (INR 2-3) more than 1 moderaterisk factor

Management of New-Onset AF
an initial rate-control strategy is

"reasonable" for asymptomatic or minimally symptomatic older patients with hypertension and comorbid cardiovascular disease for younger individuals, especially those without significant comorbid cardiovascular disease, an initial rhythm-control strategy may be a better approach

Rate control
IV or PO Beta-blockers and calcium channel

blockers 1st line IV diltiazem or metoprolol - AF with a rapid ventricular response Amiodarone - class IIa recommendation from the ACC/AHA/ESC for use as a ratecontrolling agent for patients who are intolerant of or unresponsive to other agents, such as patients with CHF who may otherwise not tolerate diltiazem or metoprolol

Anticoagulation
Acute cardioversion for AF carries a risk of

thromboembolism unless anticoagulation therapy is initiated prior to the procedure and continued post procedure. The risk of thromboembolic events is greatest when AF has been present for longer than 48 hours.

Anticoagulation
IV heparin (activated partial thromboplastin time
Warfarin: INR target 2-3

[aPTT] of 45-60 seconds) or low-molecular-weight heparin (1 mg/kg bid)

Patients can be started concomitantly on warfarin in

an inpatient setting while awaiting a therapeutic INR value (2-3). Dabigatran (Pradaxa) is a newer oral anticoagulant that appears to be at least as effective as warfarin, with added expense but also added safety.
does not require serial INR (PT) blood tests not significantly affected by almost any medication or

vitamin

Cardioversion
electively or emergently to restore sinus

rhythm most successful when initiated within 7 days after onset of AF

Long-Term Management
focused on reducing the likelihood of AF

recurrence, reducing AF-related symptoms, control of ventricular rate, and reducing stroke risk

Long-Term Management
warfarin - significantly more effective than

antiplatelet therapy (relative risk of 40%) if the INR is adjusted between 2 and 3, except in patients who are at a significant risk for stroke 2011 update to ACCF/AHA/HRS guidelines:if warfarin will not be used, adding clopidogrel to aspirin may be considered

Long-Term Management
The RE-LY study evaluated the efficacy and safety of 2 different doses of dabigatran relative

to warfarin :
Dabigatran 110 mg was noninferior to warfarin for the

primary efficacy endpoint of stroke or systemic embolization dabigatran 150 mg was significantly more effective than warfarin or dabigatran 110 mg. major bleeding occurred significantly less often with dabigatran 110 mg than warfarin dabigatran 150 mg had similar bleeding to warfarin