Atrial Fibrillation
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More Specific Terms
Introduction
- AF may be paroxysmal (intermittent) or persistent.
Etiology
- hypertension
- acute alcohol ingestion (holiday heart syndrome)
- ischemic heart disease
- myocardial infarction
- congestive heart failure
- valvular heart disease
- pericarditis
- sick sinus syndrome [6]
- pulmonary disease
- infections
- cardiac tumors: atrial myxoma [6]
- risk factors - [23]
- obesity
- diabetes mellitus
- high pulse pressure
- advanced age
- long-term endurance exercise (2-10 fold risk) [30] due to left atrial enlargement
- long-term glucocorticoids, as little as 7.5 mg of prednisone/day [33]
- chronic renal failure (HR=3.2 GFR <30 ml/min/1.73 m2)
- albuminuria [39]
- NSAID & COX2 inhibitors (HR=1.2-1.3; HR=1.5-1.7 for new users) [40]
Epidemiology
- most common sustained arrhythmia
- affects 10-19% of Americans over age 75
- > 98% of patients have comorbidity
Pathology
- multiple simultaneous wandering wave fronts of activation with simultaneously occurring reentrant circuits within the atria
- any disease process that increases atrial size ( left atrial enlargement) &/or decreases atrial conduction or refractory period may result in AF
- the pulmonary veins have been implicated in generating the electrical current of AF [19]
- atrial fibrillation may induce atrial cardiomyopathy [6]
- resultant atrial cardiomyopathy promotes further atrial fibrillation
Genetics
- familial atrial fibrillation associated with defect in: LMNA, KCNQ1, KCNE2
Clinical-manifestations
- may be asymptomatic
- palpitations
- irregular heart rate
- dizziness
- dyspnea
- angina
- syncope
- heart failure
- systemic embolism
- no A wave in jugular venous pulse
- pulse deficit ( auscultated pulse > palpated pulse, especially radial artery)
- variable S1 heart sound
Laboratory
- thyroid function tests
- theophylline level if indicated
- urinary metanephrines if indicated
- pulse oximetry
- digoxin level if possible exposure
Diagnostic-procedures
-
-
- deformed T waves or ST segment may hide P waves
- irregular spacing of R waves
- rule out valvular heart disease, i.e. mitral stenosis
- assess left atrial size: an enlarged left atrium is unlikely to maintain sinus rhythm if cardioverted
-
Complications
- rapid ventricular response
- thromboembolism (see risk factors for thromboembolism)
- the majority of thromboembolic strokes occur in association with AF
- stroke risk is 4%/year for untreated patients
- stroke risk for patients on aspirin alone
- 2%/year for low risk patients
- 4%/year with for any risk factor
- as high as 18%/year for high risk patients
- > 90% of atrial thrombi in patients with non-valvular atrial fibrillation are believed to originate in the left atrial appendage
- potentially serious complications with
- Wolf-Parkinson-White syndrome
- aortic stenosis or mitral stenosis
- need for atrial kick to maintain cardiac output
- non compliant ventricle, impaired ventricular filling
- cardiovascular collapse with rapid ventricular response
Differential-diagnosis
- multifocal atrial tachycardia in COPD
- digitalis toxicity - atrial tachycardia with AV block
- preexitation tachycardia
- ventricular tachycardia
- AF may appear as wide-complex tachycardia if intraventricular conduction delay ( RBBB)
Management
- general [5,12]
- hospitalize for
- hemodynamically unstable, prepare for cardioversion
- high risk for thromboembolism
- immediate anticoagulation with heparin & warfarin [5]
- correct precipitating causes
- correct hyperthyroidism prior to cardioversion [7]
- cardioversion & maintenance of sinus rhythym
- DC cardioversion (50, 100, 200, 300, 360 joules)
- more effective than chemical cardioversion [44]
-
- class 1A, 1C or 3 antiarrhythmic agents
- conversion & maintenance of sinus rhythm
- indications
- patient is unstable
- mitral stenosis
- mitral regurgitation
- new onset of atrial fibrillation within 48 hours
- atrial thrombus: delay cardioversion until completion of 4-6 weeks of anticoagulation warfarin
- IV heparin prior to emergent cardioversion if duration of AF not known [5]
- 3 weeks prior to elective cardioversion
- if atrial fibrillation < 48 hours, then may proceed with cardioversion without prior anticoagulation [6]
- trans-esophageal echocardiography ( TEE) may be use to determine presence of atrial thrombosis; if none then may proceed with cardioversion without prior anticoagulation [6]
- continue for 4 weeks after successful cardioversion
- antiarrhythmic therapy for maintenance of sinus rhythm
- may or may not be needed
- class III agents
- amiodarone (most commonly used)
- 400 mg for 30 days, then 200 mg QD
- especially useful with structural heart disease
- 1st line agent for AF if ischemic heart disease & LV dysfunction [5]
- sotalol in patients with CAD
- dronedarone ( Multaq) [31]
- class 1C agents, if no structural heart disease
- flecainide 100 mg BID, or
- propafenone 150-225 mg TID
- 30-50% of patients will maintain sinus rhythm after 1-2 years
- PRN flecainide or sotalol for paroxysmal atrial fibrillation
- control ventricular rate via AV nodal blocking agents is generally the preferred strategy (excluding WPW)# [11,13]
-
- not very effective in controlling ventricular response during exercise
- add calcium channel antagonist or beta-blocker in patients controlled at rest, but with tachycardia during exercise
- do not use as single agent for rate control [5]
- lenient rate control (< 110/min) with outcomes similar to standard control (< 80/min) [36]
- anticoagulation [16] (see CHADS score)
-
- patients < 60-75* years of age without risk factors (see Complications) [6]
- patients unable or unwilling to take warfarin
- see risk factors for thromboembolism
- reduces risk 50% [10] & lessens severity of stroke [9]
- 50% of patients benefit from anticoagulation [32]; patients with < 2 risk factors for stroke will not benefit
- risk of stroke on warfarin - 1.6%/year mean age 71 [10] - 2.6%/year mean age 81 [17]
- in elderly (> 75 years of age), stroke scores with poor predictive value [41]
- in elderly (> 75 years of age), risk of hemorrhage is high
- risk of major hemorrhage 10%/year
- risk of life-threatening hemorrhage 5%/year,
- risk of fatal hemorrhage 1%/year [17]
- increased risk of intracranial hemorrhage associated with INR > 3.5, age > 85
- reduces overall mortality 4.5 vs 5.3 per 100 person years [10]
- low risk of bleeding (2%), in elderly [25] <same as aspirin>
- risk scheme to predict warfarin-associated hemorrhage described in [43]
- thrombin inhibitor ( dabigatran) [8]
- factor Xa inhibitor rivaroxaban not inferior to wafarin in preventing embolic stroke [42]
- clopidogrel no better than aspirin [19]
- clopidogrel + aspirin inferior to warfarin [24]
- clopidogrel + aspirin better than aspirin alone but associated with increased risk of GI bleed (see ACTIVE A trial) [29]
- left atrial appendage closure is an investigational procedure with promise for prevention of left atrial thromboembolism
- AV node ablation with permanent ventricular pacing
- refractory ventricular rate [27]
- radiofrequency ablation of focal atrial fibrillation in younger patients [35]
- radiofrequency ablation in connection with pulmonary vein isolation may become 1st line therapy [18,20,21,22,27]
- maze procedure may be useful for patients undergoing cardiac surgery for other reasons [5]
- cardiac pacemaker
- sick sinus syndrome accompanying AF
- symptomatic patients with paroxysmal AF
- * aspirin may not be effective in patients > 75 years of age
- # in patients with WPW, rhythm control is indicated; procainamide is the drug of choice (see Wolf-Parkinson-White syndrome)
- % exception is rheumatic heart disease, INR=2.5-3.5 [5]
More General Terms
Additional Terms
- Atrial Fibrillation Follow-up Investigator of Rhythm Management (AFFIRM)
- Atrial Fibrillation Suppression Trial (AFIST)
- atrial flutter
- cardiac conduction system
- cardioversion
- pharmaceutical agents for treatment of atrial fibrillation
- risk factors for thromboembolism associated with atrial fibrillation
- Wolff-Parkinson-White (WPW) syndrome
Internet Database
OMIM: 607554
References
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- Saunders Manual of Medical Practice, Rakel (ed), WB Saunders, Philadelphia, 1996, pg 272
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