© copyright annals of internal medicine, 2010 ann int med. 153 (11): itc6-1. terms of use the in...

© Copyright Annals of Internal Medicine, 2010Ann Int Med. 153 (11): ITC6-1.

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in the clinic

Atrial Fibrillation


Who is at risk for atrial fibrillation?

Most common, clinically significant cardiac arrhythmia

Occurs in <1% 60-65y; 8%-10% >80y

Higher prevalence men than women, whites than blacks

Risk for AF w/ presence & severity of underlying HF and valvular disease.

Definition of Atrial Fibrillation (AF):

When diffuse, chaotic electrical activity in atria suppresses/replaces normal sinus mechanism, leads to deterioration of mechanical function


What symptoms and signs should cause clinicians to suspect AF?

Symptoms Palpitations Shortness of breath Exercise intolerance Chest pain Malaise

Symptoms greatest at AF onset (paroxysmal episode)

Diminish over time, esp when arrhythmia persistent

Many pts asymptomatic, esp elderly silent AF (some have severe symptoms with other AF episodes)

Result from Elevated ventricular rate (either at rest or exaggerated by exercise) Irregular ventricular rate Loss atrial contrib to cardiac output

Signs on physical exam Faster-than-expected heart rate (varies greatly from pt to pt) “Irregularly irregular” time between heart sounds on auscultation Peripheral pulses that vary irregularly in rate & amplitude


Is a single electrocardiogram sufficient to diagnose or exclude atrial fibrillation?

Single ECG sufficient to Dx if recorded during arrhythmia

ECG of AF w/ rapid ventricular rate



Single ECG showing normal rhythm does not exclude Dx because AF often is paroxysmal

With daily symptoms, 24- or 48-h continuous Holter monitoring usually is sufficient to make Dx

With less-frequent symptoms, monitor longer with ECG loop recorder

Must turn on recorder when symptoms begin, so it is not useful if arrhythmias are asymptomatic or if pt doesn’t recognize symptoms

With very infrequent episodes may take yrs to confirm Dx (if symptoms nonspecific and long periods between episodes)



Newer event monitors, implanted pacemakers & defib-cardioverters with atrial leads record symptomatic & asymptomatic AF

Other new devices continuously record heart rhythms for ≥1 mo

Wirelessly send data to central monitoring station for automated interpretation and Dx


What is the role of history and physical examination in patients with AF?

Determine duration symptoms

Identify potential underlying causes

Cardiac causes

Hypertension

HF

Cardiac surgery

Murmurs indicating stenotic or regurgitant valvular disease

Other indications structural heart disease

Noncardiac causes

Pulmonary disease

Hyperthyroidism

Use of adrenergic drugs (e.g., for pulmonary disease) or other stim’ts

Alcohol use

Family Hx might identify 1st-degree relatives with AF and may someday have therapeutic implications


What other electrocardiographic arrhythmias can be confused with AF?

Sinus rhythm with frequent premature atrial contractions

Atrial flutter

Atrial tachycardia

Key ECG findings of AF

Absence of P waves

Presence of irregular ventricular rhythm without a recurring pattern

When irregular rhythm present but Dx of AF uncertain

Examine long recordings from multiple leads

Look for partially obscured P waves in deformed T waves and ST segments


What other electrocardiographic arrhythmias can be confused with AF? ECG of irregular rhythm that might be AF, but P waves

& other features ID sinus rhythm with frequent premature atrial contractions


What other electrocardiographic arrhythmias can be confused with AF? ECG of irregular rhythm that might be AF, but “saw-

tooth” P waves & varying ventricular response (2:1 to 4:1 AV conduction) identify atrial flutter


How should clinicians classify AF?

Same pt may be classified into different categories at different times. Classify to current or most common pattern

Distinctions predict responses to Tx (antiarrhythmic drug Tx less likely to succeed as pattern goes from paroxysmal to persistent to permanent)

Pts in all 3 categories require anticoagulation

Paroxysmal: Episodes spontaneously terminate < 7d Persistent: Episodes last >7d and require intervention to restore sinus rhythm Permanent: Interventions to restore sinus rhythm have either failed or have not been attempted


What lab studies should clinicians obtain in patients newly diagnosed with AF?

Renal & hepatic function blood tests (to guide selection of drug Tx)

Stool Hemoccult test (before starting anticoagulation)

Transthoracic ECHO (to measure left atrial size and assess for valvular heart disease, pericardial disease, and LV hypertrophy)

Transesophageal ECHO (excludes atrial clot and is indicated when transthoracic images are inadequate or cardioversion is planned in a pt therapeutically anticoagulated <3 wks)

Additional tests as necessary for possible PE, AMI, or HF

Serum electrolytes and TSH (for possible causes)


What underlying conditions should clinicians look for in patients with AF?

Structural heart disease causes 80% of AF

Particularly hypertensive heart disease

Also CAD, valvular heart disease, or cardiomyopathy

Atrial fibrosis often occurs with structural heart disease

May be central to arrhythmia's pathogenesis

AF in absence of heart disease is “Lone” AF

Some experts restrict Lone AF to pts <60y because it is hard to exclude structural heart disease in older pts


What underlying conditions should clinicians look for in patients with AF?

May occur without predisposing conditions, typically in men 40-50y with symptoms at night, at rest, following vigorous exercise, or with alcohol use

Other forms of AF without underlying conditions occur during waking hrs and are preceded by emotional stress or exercise

Illnesses associated with AF AMI Pulmonary embolism Thyrotoxicosis After major surgery (AF occurs in ≈40% after cardiac/thoracic surgery) During severe illness Obesity and sleep apnea


Diagnosis… Atrial fibrillation is the most common clinically significant cardiac arrhythmia, and its prevalence increases with advancing age. Typical symptoms include palpitations, shortness of breath, and exercise intolerance. However, some patients report only general malaise, and many patients are asymptomatic. Electrocardiogram recordings during episodes are the only way to confirm the diagnosis. If the diagnosis is suspected and the ECG is normal, longer monitoring with a loop recorder or a Holter monitor can be helpful. The initial assessment should include laboratory tests for electrolytes, thyroid-stimulating hormone, and renal and hepatic function to rule out underlying disorders or contraindications to therapies. An echocardiogram should be done to look for structural heart disease.

Diagnosis… Atrial fibrillation is the most common clinically significant cardiac arrhythmia, and its prevalence increases with advancing age. Typical symptoms include palpitations, shortness of breath, and exercise intolerance. However, some patients report only general malaise, and many patients are asymptomatic. Electrocardiogram recordings during episodes are the only way to confirm the diagnosis. If the diagnosis is suspected and the ECG is normal, longer monitoring with a loop recorder or a Holter monitor can be helpful. The initial assessment should include laboratory tests for electrolytes, thyroid-stimulating hormone, and renal and hepatic function to rule out underlying disorders or contraindications to therapies. An echocardiogram should be done to look for structural heart disease.


What are the complications of atrial fibrillation, and how can therapy decrease the risk for these events? Symptoms (sometimes disabling)

Usually caused by rapid ventricular rates or irregular ventricular response

Loss of atrial contribution to ventricular filling (atrial kick) is well tolerated except by pts with ventricular hypertrophy

Thromboembolism (stroke most common)

In nonvalvular AF, the annual risk of arterial thromboembolism is 5% (higher in pts >75y)

Atrial thrombi cause 75% strokes in AF

Cardiomyopathy (prevent by treating tachycardia of AF)


When should clinicians consider immediate cardioversion in patients with AF? When duration of arrhythmia is <48h (e.g., hospitalized pt

on cardiac monitoring)

May be appropriate in selected pts with

Decompensated HF

Severe angina or acute infarction

Hypotension

High risk for acute stroke

In patients with extremely rapid AV conduction mediated by the accessory pathway in Wolff-Parkinson-White syndrome

Most pts with AF don’t require immediate cardioversion


Which patients with AF should clinicians consider hospitalizing?

Uncertain or unstable underlying arrhythmia

Acute MI, altered mental status, decompensated HF, or hypotension

Intolerable symptoms despite hemodynamic stability

Elective cardioversion (if monitored outpatient setting unavailable)

Acute anticoagulation for very high stroke risk high

Telemetry monitoring when initiating some drugs

For procedures such as cardiac catheterization, electrophysiologic studies, pacemakers, implantable defibrillators, or catheter or surgical ablation


Should clinicians attempt rate control or rhythm control?

Traditionally clinicians preferred rhythm control to rate control

Recently high-quality clinical trials have found that rhythm control doesn’t improve mortality, stroke, hospitalization, or QOL compared with rate control

Rate control easier to accomplish, prevents exposure to the potential adverse effects of antiarrhythmic agents

Rhythm control is useful in select pts with severe symptoms (before or after rate control failure) or younger pts without structural heart disease


What strategies should clinicians consider for rate control in patients with rapid AF?

Consider drugs to control ventricular rate in all pts with AF even those being treated for rhythm control

Traditional target heart rate has been 60-80 beats/min at rest and 90-115 beats/min during mod exercise (criteria varies by age)

Recent data found no advantage of a target of ≤80 beats/min compared to a target of ≤110 beats/min (Van Gelder et al, 2009)



Convenient IV admin in NPO pts, rapid onset action, dependable AV nodal blockade

Side effects: Bradycardia, hypotension, heart block, bronchospasm (less frequently than nonselective ß-blockers), worsening of CHF

ß-Blockers: 1st-line Tx to AV nodal conduction

Metoprolol

Short-acting, titratable on or off w/ very rapid half-life

Side effects: Bradycardia, hypotension, heart block, bronchospasm (less frequent)

Occasionally inconsistent effect in high-catecholamine states

Less bradycardia, less bronchospasm; less propensity for heart block than other ß-blockers

Side effects: Bradycardia, hypotension, heart block

Doesn’t cross blood-brain barrier, fewer CNS side effects


Lower incidence of crossing blood–brain barrier, fewer CNS side effects


Available in oral form only

Propranolol

Esmolol

Pindolol

Atenolol

Nadolol

Inexpensive, commonly avail

Side effects: Bradycardia, hypotension, heart block, bronchospasm, worsening CHF



Nondihydropyridine calcium-channel antagonists (1st-line Tx to AV nodal conduction)

Verapamil Consistent AV nodal blockade

Side effects: Hypotension, heart block, direct myocardial depression

Do not use in Wolff-Parkinson-White syndrome

Useful for rate control only with LV systolic function

Side effects: Heart block and arrhythmias; dosage adjustment required in renal impairment

Not useful for rate control during exercise or conversion of AF/aflutter to NSR

Diltiazem

Cardiac glycoside digoxin



Dronedarone

Recently approved, modestly effective, fewer side effects than amiodarone

Amiodarone Blocks AV node, not recommended as 1st-line

monotherapy for rate control because of associated toxicities

Occasionally used to ventricular response if other agents fail


What strategies should clinicians consider for rhythm control in patients with AF?

Consider rhythm control in younger patients and patients with highly symptomatic AF because trials did not include these groups

Experienced clinicians may prefer rhythm control with cardioversion for 1st episode symptomatic AF in younger patients because many such patients maintain sinus rhythm without drugs

Rhythm control is no longer the preferred strategy based on trials comparing rate vs. rhythm control Rhythm control is no longer the preferred strategy based on trials comparing rate vs. rhythm control



Direct electrical current to convert to NSR indicated if hemodynamically unstable

Antiarrhythmic drugs:

- conversion rate < direct electrical current in hemodynamically stable pts

+ deep sedation or general anesthesia not required



Either direct electrical or antiarrhythmic drug cardioversion: AF >48h or undetermined duration: establish rate control &

anticoagulation before elective cardioversion INR 2.0 – 3.0 for > 3 weeks prior and > 4 weeks after cardioversion

Alternative- Transesophageal Echo: No clot: heparin for 48 hr prior to cardioversion & warfarin for 4

wks after

Clot present: anticoagulation for 4 weeks; most confirm thrombus resolution with repeat TEE before cardioversion

Serum K level should be >4.0 mmol/L, serum Mg level >1.0 mmol/L, and ionized Ca levels >0.5 mmol/L

Conduct cardioversion in monitored hospital setting

Because antiarrhythmic drugs generally have equal efficacy, except for amiodarone, choose a drug by side effects


What strategies should clinicians consider for rhythm control in patients with AF?Class Ia antiarrhythmic drugs prolong conduction & slow repolarization by blocking inward Na+ flux

Procainamide not recommended because of frequent side effects (hypotension, nausea, vomiting, lupus-like syndrome, QT prolongation, arrhythmia)

Quinidine gluconate not recommded because of frequent side effects (proarrhythmia, nausea, vomiting, diarrhea, QT prolongation)



Disopyramide: Use in pts with hypertension & normal LV function

Adverse effects include QT prolongation, torsades de pointes, and heart block

Rarely used in current era



Propafenone is effective in paroxysmal and sustained AF

Adverse effects include atrial flutter or atrial tachycardia with rapid ventricular response

Do not use in pts with structurally abnormal hearts

Class Ic antiarrhythmic drugs block Na+ channels

Flecainide is effective in paroxysmal AF with structurally normal hearts

Adverse effects include atrial flutter and atrial tachycardia with rapid ventricular response; also VT, and VF in diseased hearts

Do not use in pts with structurally abnormal hearts



Antiarrhythmic drugs (class III)

Ibutilide prolongs action potential duration (and atrial and ventricular refractoriness)

Effective in acute & rapid conversion of AF to NSR

Adverse effects include torsades de pointes and QT prolongation



Amiodarone blocks Na+ channels

Safest agent for use in pts with structural heart disease, good efficacy maintaining NSR chronically; can be used in Wolff–Parkinson-White syndrome

Adverse effects include bradycardia, QT prolongation, hyperthyroidism, lung toxicity, blue discoloration of skin

Sotalol is a nonselective ß - and 1ß -blocking agent that prolongs action potential duration

Similar in efficacy to quinidine but with fewer adverse effects and better rate control. Initiate on telemetry

Adverse effects include fatigue, depression, bradycardia, torsades de pointes, and CHF

ß-blocking properties, but some inotropic activity; lethal arrhythmias possible; adjust dose in pts with renal insufficiency


What strategies should clinicians consider for rhythm control in patients with AF? Dofetilide prolongs refractoriness without slowing conduction

More effective than quinidine in conversion to and maintenance of NSR; initiate on telemetry

Adverse effetcs include QT prolongation and, torsades de pointes

Dose strictly according to renal function, body size, & age; contraindicated in pts with creatinine clearance <20 mL/min

Dronedarone is similar to amiodarone—blocks sodium, potassium, and calcium channels—but without iodine

Adverse effects include GI intolerance

Contraindicated for decompensated CHD; less efficacious but better tolerated than amiodarone


When should clinicians use antiarrhythmic drugs to prevent the recurrence of AF?

Have only modest effects prolonging time to recurrence

The Canadian Trial of Atrial Fibrillation randomly assigned 403 patients to amiodarone, sotalol, or propafenone and found that after mean follow-up of 16 mos, recurrence of AF was 35% for amiodarone Tx compared w/ 63% for sotalol or propafenone Tx (NEJM, 2000)

Some nonantiarrhythmic drugs (ACE-inhibitors, statins) reduce the incidence of AF in pts with HF presumably because of antifibrotic effects


When is anticoagulation indicated for patients with atrial fibrillation? When thromboembolism risk exceeds the risk for

anticoagulation-associated bleeding

For example, a >65y pt with AF and no other risk factors has ≈1% risk for thromboembolism, which approximates the risk for major bleeding on warfarin when the INR is between 2.0-3.0

Same indications for anticoagulation in pts with paroxysmal, persistent, & permanent AF

Use CHADS2 score (Cardiac Failure, Hypertension, Age, Diabetes, and Stroke [Doubled]) to identify which pts with AF warrant anticoag Tx


When is anticoagulation indicated for patients with atrial fibrillation?

CHADS2 Risk Criteria Score

Past stroke or TIA 2

Age >75 y 1

Hypertension 1

Diabetes mellitus 1

Heart failure 1

Reproduced from ACC/AHA/ESC 2006 Guidelines for theManagement of Patients with Atrial Fibrillation 2006 (PMID: 16908781) with permission from the AHA.


When is anticoagulation indicated for patients with atrial fibrillation? Consider long-term anticoagulation in pts with

High risk for recurrent AF

Asymptomatic AF

Intracardiac thrombus

Known risk factors for thromboembolism (age ≥75y, recent HF, LV dysfunction, diabetes mellitus, hypertension, previous thromboembolism)

Many clinicians use cutoff of 65 rather than 75 yrs to initiate warfarin Tx when pt also has CAD

Genetic tests can identify pts who require different warfarin dosing, but the tests are not recommended because they have not been shown to improve pt outcomes


What anticoagulation regimens should clinicians use in patients with AF?

Warfarin is the preferred drug. Adjust the dose to an INR of 2.0-3.0 (2.5-3.5 for patients with prosthetic valves)

Aspirin is an alternative to warfarin when there are contraindications to warfarin; no previous stroke or transient ischemic attack; no hypertension, diabetes, or HF, and the patient is < 75

Aspirin + clopidogrel together prevent more strokes than aspirin alone but are not as effective as warfarin and have a bleeding risk that is equivalent to warfarin

Dabigatran recently has been approved by the FDA to prevent stroke and systemic embolism in pts with AF & creatinine clearance ≥30 mL/min


When should clinicians consider nondrug therapies for patients with AF?

AV nodal catheter ablation inactivates parts of the atrium where AF begins

Use when drug Tx doesn’t achieve rate control (usually because of drug intolerance in the elderly or in pts with advanced HF or COPD, which limits β-blocker use) Highly effective but requires pacemaker insertion, can lead to progressive LV dysfunction Pacing therapy without AV nodal ablation has little effect on burden of AF (but may help with paroxysmal AF and symptomatic bradycardia, a side effect drug Tx)

Prevents recurrent symptomatic AF in highly selected patients, ideally young, otherwise healthy person without structural heart disease & with paroxysmal AF May be reasonable when antiarrhythmic drug Tx fails in highly symptomatic pts with paroxysmal AF

Selected high-risk pts not candidates for oral anticoagulation therapy Additional studies needed to verify the safety & effectiveness of these devices

Occlusion of the left atrial appendage to prevent strokes


How should clinicians monitor patients with atrial fibrillation?

Regular follow-up to

Determine effectiveness of Tx

Monitor warfarin anticoagulation

Check if symptoms adequately controlled (ask about palpitations, easy fatigability, dyspnea on exertion)

If on amiodarone, check liver and thyroid function every 6 months and order chest x-ray annually (otherwise routine tests for drug side effects unnecessary)


Treatment… Atrial fibrillation treatment goals include reducing the frequency and severity of symptoms, preventing stroke, and preventing tachycardia-related cardiomyopathy. Selection of patients for anticoagulation with aspirin or warfarin should be based on the CHADS2 score. Focus treatment first on rate control by using beta-blockers or calcium-channel antagonists aiming for a resting rate between 60 and 110 beats per minute. Rhythm control may be reasonable in patients who do not respond to rate control. Atrial ablation and atrioventricular nodal ablation therapy may be appropriate for selected patients with highly symptomatic AF despite drug therapy.

Treatment… Atrial fibrillation treatment goals include reducing the frequency and severity of symptoms, preventing stroke, and preventing tachycardia-related cardiomyopathy. Selection of patients for anticoagulation with aspirin or warfarin should be based on the CHADS2 score. Focus treatment first on rate control by using beta-blockers or calcium-channel antagonists aiming for a resting rate between 60 and 110 beats per minute. Rhythm control may be reasonable in patients who do not respond to rate control. Atrial ablation and atrioventricular nodal ablation therapy may be appropriate for selected patients with highly symptomatic AF despite drug therapy.


What do professional organizations recommend with regard to the management of patients with AF?

American College of Physicians & American Academy of Family Physicians guideline on AF mgmt (2003)

American Heart Association & American College of Cardiology guideline on AF mgmt (2006)

European Society of Cardiology guideline on AF mgmt (2010)

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