Atrial fibrillation
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| Conduction | ||
Sinus rhythm  | Atrial fibrillation  | |
| Atrial fibrillation Classification and external resources | |
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|---|---|
| The P waves, which represent depolarization of the atria, are irregular or absent during atrial fibrillation. | |
| ICD-10 | I48. |
| ICD-9 | 427.31 |
| DiseasesDB | 1065 |
| MedlinePlus | 000184 |
| eMedicine | med/184 emerg/46 |
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 Discuss Atrial fibrillation further in the WikiDoc Cardiology Network |
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Overview
Synonyms and related keywords: AF, Afib, fib
Atrial fibrillation (AF or afib) is a cardiac arrhythmia (abnormal heart rhythm) that involves the two upper chambers (atria) of the heart. (Atrial fibrillation is a supraventricular tachyarrhythmia characterized by uncoordinated atrial activation with consequent deterioration of atrial mechanical function. The decline in mechanical function of the atrium may or may not lead to inadequate filling of the ventricle depending upon the importance of the atrial "kick" or atrial contribution to ventricular filling in a given patient.) It can often be identified by taking a pulse and observing that the heartbeats don't occur at regular intervals, but a conclusive indication of AF is the absence of P waves on an electrocardiogram (ECG). AF is the most common arrhythmia; risk increases with age, with 8% of people over 80 having AF.
In AF, the normal electrical impulses that are generated by the sinoatrial node are overwhelmed by disorganized electrical impulses that originate in the atria and pulmonary veins, leading to conduction of irregular impulses to the ventricles that generate the heartbeat. The result is an irregular heartbeat which may occur in episodes lasting from minutes to weeks, or it could occur all the time for years. The natural tendency of AF is to become a chronic condition. Chronic AF leads to a small increase in the risk of death.[1][1]
Atrial fibrillation is often asymptomatic, and is not in itself generally life-threatening, but may result in palpitations, fainting, chest pain, or congestive heart failure. Patients with AF usually have a significantly increased risk of stroke (up to 7 times that of the general population). Stroke risk increases during AF because blood may pool and form clots in the poorly contracting atria and especially in the left atrial appendage (LAA). The level of increased risk of stroke depends on the number of additional risk factors. If the AF patient has none, the risk of stroke is similar to that of the general population.[1] However, many patients do have additional risk factors and AF is a leading cause of stroke.[1]
In the presence of intact atrioventricular conduction, replacement of consistent P waves by rapid oscillations or fibrillatory waves that vary in amplitude, shape, and timing, associated with an irregular, frequently rapid ventricular response is characteristic EKG findings of atrial fibrillation.
The result of this process is an irregular heartbeat. This may be continuous (persistent or permanent AF) or alternating between periods of a normal heart rhythm (paroxysmal AF). The natural tendency of atrial fibrillation is to become a chronic condition.
Atrial fibrillation may be treated with medications which either slow the heart rate or revert the heart rhythm back to normal. Synchronized electrical cardioversion may also be used to convert AF to a normal heart rhythm. Surgical and catheter-based therapies may also be used to prevent recurrence of AF in certain individuals. People with AF are often given anticoagulants such as warfarin to protect them from stroke.
Classification
Although several clinical classification plans and protocols have been proposed, none of them fully account for all aspects of atrial fibrillation. The American Heart Association, American College of Cardiology, and the European Society of Cardiology have proposed the following classification system based on simplicity and clinical relevance:[1]
| AF Category | Defining Characteristics |
|---|---|
| First detected | only one diagnosed episode |
| Paroxysmal | recurrent episodes that self-terminate in less than 7 days |
| Persistent | recurrent episodes that last more than 7 days |
| Permanent | an ongoing long-term episode |
First detected atrial fibrillation
Any patient with new diagnosed AF is in this category, as the exact onset and chronicity of the disease is often uncertain.
Recurrent atrial fibrillation
Two or more identified episodes of atrial fibrillation are named as recurrent form of atrial fibrillation. This is further classified into paroxysmal and persistent based on when the episode terminates without therapy. Atrial fibrillation is said to be paroxysmal when it terminates spontaneously within 7 days, most commonly within 24 hours.
The term 'Persistent' or 'chronic' is used if diagnosis of atrial fibrillation established for more than seven days. Differentiation of paroxysmal from chronic or established AF is based on the history of recurrent episodes and the duration of the current AF episode.[1][1][1]
Lone atrial fibrillation (LAF)
Lone atrial fibrillation is defined as atrial fibrillation in the absence of clinical or echocardiographic findings of cardiopulmonary disease including hypertension.[1] Patients in this group are young individuals (less than 60 years old).
Historical Background
Because the diagnosis of atrial fibrillation requires measurement of the electrical activity of the heart, it was not truly described until 1874, when Edmé Félix Alfred Vulpian observed the irregular atrial electrical behavior that he termed "fremissement fibrillaire" in dog hearts.[1]
In the mid-eighteenth century, Jean-Baptiste de Sénac made note of dilated, irritated atria in people with mitral stenosis.[1] The irregular pulse associated with AF was first recorded in 1876 by Carl Wilhelm Hermann Nothnagel and termed "delirium cordis", stating that "In this form of arrhythmia the heartbeats follow each other in complete irregularity.
At the same time, the height and tension of the individual pulse waves are continuously changing".[1] Correlation of delirium cordis with the loss of atrial contraction as reflected in the loss of a waves in the jugular venous pulse was made by Sir James MacKenzie in 1904.[1]
Willem Einthoven published the first electrocardiogram showing AF in 1906.[1]
The connection between the anatomic and electrical manifestations of AF and the irregular pulse was made in 1909 by Carl Julius Rothberger, Heinrich Winterberg, and Sir Thomas Lewis.[1][1][1]
Prevalence
The prevalence of AF is estimated at 0.4% of the general population and its prevalence increases with age. Cross-sectional studies have found the prevalence to be less than 1% in those under 60 years of age. Based on limited data, the age-adjusted risk of developing AF in African-Americans appears to be less than half that in Caucasians.
In population-based studies, the frequency of atrial fibrillation in patients with no history of cardiopulmonary disease (lone AF) was less than 12% of all atrial fibrillation cases.
The median age of AF patients is about 75 years of age. Approximately 70% of patients with atrial fibrillation are between 65 and 85 years of age. The overall number of men and women with AF is about equal, but approximately 60% of AF patients over 75 years old are female. The age-adjusted prevalence of AF is higher in men, in whom the prevalence has more than doubled from the 1970s to the 1990s.
The incidence of AF increases from less than 0.1% per year in those under 40 years old to exceed 1.5% per year in women and 2% in men older than 80 years.
Epidemiology
Atrial fibrillation is the most common arrhythmia found in clinical practice.[1] It also accounts for 1/3 of hospital admissions for cardiac rhythm disturbances[1], and the rate of admissions for AF has risen in recent years.[1] Approximately 2.2 million individuals in the United States and 4.5 million in the European Union have AF.[1][1]
The incidence of atrial fibrillation increases with age. The prevalence in individuals over the age of 80 is about 8%.[1] In developed countries, the number of patients with atrial fibrillation is likely to increase during the next 50 years, due to the growing proportion of elderly individuals.[1]
Pathophysiology
Mechanisms of atrial fibrillation
Two predominant underlying pathophysiologic processes are widely accepted:
- Enhanced automaticity in 1 or several rapidly depolarizing foci
- Reentry involving 1 or more circuits.
A focal origin of AF is supported by experimental models of aconitine-induced and rapidly firing atrial foci, located most often in the superior pulmonary veins. These foci may initiate AF in susceptible patients. Patients may have more than 1 pulmonary vein focus capable of engendering AF. These foci also located in the RA and infrequently in the superior vena cava or coronary sinus. The focal origin appears to be more important in patients with paroxysmal AF than in those with persistent AF, and ablation of such foci may be curative.
Atrial Electrical Remodeling
Pharmacological or electrical cardioversion of atrial fibrillation has a higher success rate when atrial fibrillation has been present for less than 24 hours, whereas a longer duration of atrial fibrillation reduces the likelihood of restoring and maintaining sinus rhythm. These observations gave rise to the adage that “atrial fibrillation begets atrial fibrillation.”
The increasing propensity to atrial fibrillation was related to progressive shortening of effective refractory periods with increasing episode duration, a phenomenon known as electrophysiological remodeling. Calcium channel blockade may inhibit the atrial remodeling that occurs during atrial fibrillation.
Prolonged periods of atrial fibrillation may also disturb atrial contractile function, and recovery of atrial mechanical function may depend on the duration of AF. After a long period of persistent atrial fibrillation, recovery of atrial contraction can be delayed for days or even weeks after sinus rhythm has been restored. This has important implications for the duration of anticoagulation.
Etiology of atrial fibrillation
AF can be associated with underlying cardiac diseases, but it may also occur in otherwise normal hearts.
Common Causes
Complete Differential Diagnosis of Underlying Etiologies for Atrial Fibrillation
| Cardiovascular | Acute myocardial infarction • Congenital heart disease especially atrial septal defect in adults • Coronary artery disease • Heart failure (especially diastolic dysfunction and diastolic heart failure) • Hypertrophic cardiomyopathy (HCM) • Hypertension • Mitral regurgitation
Mitral stenosis (e.g. due to Rheumatic heart disease or Mitral valve prolapse) • Myocarditis • Pericarditis • Previous heart surgery • Dual-chamber pacemakers in the presence of normal atrioventricular conduction.[1] • Restrictive cardiomyopathies (such as amyloidosis, hemochromatosis, and endomyocardial fibrosis), cardiac tumors, and constrictive pericarditis |
| Congenital | |
| Dermatologic | No underlying causes |
| Drugs | Digoxin in patients with vagally mediated AF |
| Ear Nose Throat | No underlying causes |
| Endocrine | Hyperthyroidism • Hypothyroidism • Pheochromocytoma |
| Gastroenterologic | Vomiting |
| Genetic | A family history of AF increases risk by 30%.[1] Various genetic mutations may be responsible.[1] |
| Hematologic | No underlying causes |
| Infectious Disease | No underlying causes |
| Musculoskeletal / Ortho | No underlying causes |
| Neurologic | Multiple sclerosis |
| Nutritional / Metabolic | No underlying causes |
| Oncologic | No underlying causes |
| Opthalmologic | No underlying causes |
| Overdose / Toxicity | Excessive alcohol consumption ("binge drinking" or "holiday heart syndrome") • Carbon monoxide poisoning • Caffeine • Stimulants |
| Post-Op Complication | Surgery,particularly coronary artery bypass surgery • During pulmonary artery line placement and right heart catheterization trauma to the right atrium can result in atrial fibrillation |
| Pulmonary | Hypoxia of any cause • Lung cancer • Pneumonia • Pulmonary embolism • Sarcoidosis • sleep apnea syndrome |
| Renal / Electrolyte | Hypokalemia |
| Rheum / Immune / Allergy | No underlying causes |
| Trauma | Electrocution • Cardiac contusion |
| Miscellaneous | Hypothermia • Fever |
The autonomic nervous system may trigger AF in susceptible patients through heightened vagal or adrenergic tone
A. Vagal atrial fibrillation
- A prevalence that is approximately 4 times greater in men than in women;
- Age approximately 40 to 50 years at onset;
- Frequent association with lone atrial fibrillation;
- Little tendency to progress to permanent atrial fibrillation;
- Occurrence at night, during rest, after eating, or after ingestion of alcohol; and
- Antecedent progressive bradycardia
- Because heart rate is relatively slow during the episode of AF, most patients complain of irregularity rather than dyspnea, lightheadedness, or syncope.
- Importantly, both adrenergic blocking drugs and digitalis may increase the frequency of vagally mediated AF.
B. Adrenergic Atrial fibrillation
- Age: Patients usually about 50 years at onset, and most do not exhibit structural heart disease.
- A lower incidence than vagally mediated AF;
- Onset predominantly during the daytime;
- Provocation by exercise or emotional stress
- Polyuria as a common correlate;
- Onset typically associated with a specific sinus rate for a given patient
- No significant gender differences.
- In contrast to vagally induced AF, [[beta blockers] are usually the treatment of choice for AF of the adrenergic type.
Pathophysiology
- Patchy fibrosis with juxtaposition of normal and diseased atrial fibers, which may account for non homogeneity of atrial refractoriness.
- Fibrosis or fatty infiltration may also affect the sinus node and may be a reaction to inflammatory or degenerative processes that are difficult to detect.
- The role of inflammation in AF not yet been evaluated, but histological changes consistent with myocarditis were reported in 66% of atrial biopsy specimens from patients with lone AF.
- Atrial hypertrophy and dilatation may be either a cause or a consequence of persistent AF, because progressive atrial enlargement has been demonstrated echocardiographically in patients with AF.
- Congestive heart failure (CHF) facilitates the induction of sustained AF, mediated by extensive interstitial fibrosis.
- In most patients, however, it is not possible to identify the underlying anatomic process responsible for the arrhythmia.
- A role for autoimmune mechanisms in genetically predisposed patients has been suggested by high serum levels of antibodies against myosin heavy chains in patients with paroxysmal AF without identified heart disease.
- The prevalence of heart disease is generally lower in patients with paroxysmal AF than in those with permanent AF.
Morphology
The primary pathologic change seen in atrial fibrillation is the progressive fibrosis of the atria. This fibrosis is primarily due to atrial dilatation, however genetic causes and inflammation may have a cause in some individuals.
Dilatation of the atria can be due to almost any structural abnormality of the heart that can cause a rise in the intra-cardiac pressures. This includes valvular heart disease (such as mitral stenosis, mitral regurgitation, and tricuspid regurgitation), hypertension, and congestive heart failure. Any inflammatory state that affects the heart can cause fibrosis of the atria. This is typically due to sarcoidosis but may also be due to autoimmune disorders that create autoantibodies against myosin heavy chains. Mutation of the lamin AC gene is also associated with fibrosis of the atria that can lead to atrial fibrillation.
Once dilatation of the atria has occurred, this begins a chain of events that leads to the activation of the renin aldosterone angiotensin system (RAAS) and subsequent increase in matrix metaloproteinases and disintegrin, which leads to atrial remodeling and fibrosis, with loss of atrial muscle mass.
This process is not immediate, and experimental studies have revealed patchy atrial fibrosis may precede the occurrence of atrial fibrillation and may progress with prolonged durations of atrial fibrillation.
Fibrosis is not limited to the muscle mass of the atria, and may occur in the sinus node (SA node) and atrioventricular node (AV node), correlating with sick sinus syndrome. Prolonged episodes of atrial fibrillation have been shown to correlate with prolongation of the sinus node recovery time,[1] [1][1] suggesting that dysfunction of the SA node is progressive with prolonged episodes of atrial fibrillation.
Signs and symptoms
In general, clinical manifestations are;
- Palpitations
- Chest pain
- Dyspnea
- Fatigue
- Lightheadedness
- Syncope: Syncope is an uncommon but serious complication that is usually associated with sinus node dysfunction or hemodynamic obstruction, such as valvular aortic stenosis, HCM, cerebrovascular disease, or an accessory AV pathway.
Atrial fibrillation is usually accompanied by symptoms related to the rapid heart rate. Rapid and irregular heart rates may be perceived as palpitations, exercise intolerance, and occasionally produce angina (if the rate is faster and puts the heart under strain) and congestive symptoms of shortness of breath or edema. Sometimes the arrhythmia will be identified only with the onset of a stroke or a transient ischemic attack (TIA, stroke symptoms resolving within 24 hours). It is not uncommon to identify atrial fibrillation on a routine physical examination or electrocardiogram (ECG/EKG), as it may be asymptomatic in many cases.[1]
As most cases of atrial fibrillation are secondary to other medical problems, the presence of chest pain or angina, symptoms of hyperthyroidism (an overactive thyroid gland) such as weight loss and diarrhea, and symptoms suggestive of lung disease would indicate an underlying cause. A previous history of stroke or TIA, as well as hypertension (high blood pressure), diabetes, heart failure and rheumatic fever, may indicate whether someone with atrial fibrillation is at a higher risk of complications.[1]
Diagnosis of atrial fibrillation
The evaluation of atrial fibrillation involves diagnosis, determination of the etiology of the arrhythmia, and classification of the arrhythmia. A minimal evaluation performed should be performed in all individuals with atrial fibrillation. This includes a history and physical examination, surface electrocardiogram, transthoracic echocardiogram, and routine blood work. Certain individuals may benefit from an extended evaluation which may include an evaluation of the heart rate response to exercise, exercise stress testing, a chest x-ray, trans-esophageal echocardiography, and other studies.
- Screening and routine primary care visit for atrial fibrillation
- History and physical examination for atrial fibrillation
- Electrocardiogram for diagnosis of atrial fibrillation
- Chest x-ray for diagnosis of atrial fibrillation
- Echocardiography for diagnosis of atrial fibrillation
- Recorders (Holter monitors) for diagnosis of atrial fibrillation
- Exercise stress tests (Tilt-Table Test) for diagnosis of atrial fibrillation
- Electrophysiologic Testing or Electrophysiologic Studies for diagnosis of atrial fibrillation
Screening and routine primary care visit
Screening for atrial fibrillation is not generally performed, although a study of routine pulse checks or electrocardiograms during routine office visits, found that the annual rate of detection of atrial fibrillation in elderly patients improved from 1.04% to 1.63%; selection of patients for prophylactic anticoagulation would improve stroke risk in that age category.[1]
Estimated sensitivity of the routine primary care visit is 64%. This low result probably reflects the pulse not being checked routinely or carefully.[1]
History and physical examination for atrial fibrillation
The history of the individual's atrial fibrillation episodes is likely the most important part of the evaluation. Distinctions should be made to those who are entirely asymptomatic when they are in atrial fibrillation (in which case the atrial fibrillation is found as an incidental finding on an electrocardiogram or physical examination) and those who have gross and obvious symptoms due to atrial fibrillation and can pinpoint whenever they go into atrial fibrillation and revert to sinus rhythm.
Detailed history and physical examination are essential to define;
- The presence and nature of symptoms associated with AF
- The clinical type of AF (first episode, paroxysmal, persistent, or permanent)
- The onset of the first symptomatic attack or date of discovery of AF
- The frequency, duration, precipitating factors, and modes of termination of AF
- The response to any pharmacological agents that have been administered
- The presence of any underlying heart disease or other reversible conditions (e.g., hyperthyroidism or alcohol consumption)
Routine blood work
While many cases of AF have no definite cause, it may be the result of various other problems (Blood tests of thyroid function are required, especially for a first episode of AF, when the ventricular rate is difficult to control, or when AF recurs unexpectedly after cardioversion)
Hence, renal function and electrolytes are routinely determined, as well as thyroid-stimulating hormone (commonly suppressed in hyperthyroidism and of relevance if amiodarone is administered for treatment) and a blood count.[1]
In acute-onset AF associated with chest pain, cardiac troponins or other markers of damage to the heart muscle may be ordered. Coagulation studies (INR/aPTT) are usually performed, as anticoagulant medication may be commenced.[1]
Electrocardiogram
Atrial fibrillation is diagnosed on an electrocardiogram, an investigation performed routinely whenever irregular heart beat is suspected. Characteristic findings are the absence of P waves, with unorganized electrical activity in their place, and irregularity of R-R interval due to irregular conduction of impulses to the ventricles.[1]
EKG is helpful to identify;
- Rhythm (verify AF)
- LV hypertrophy
- P-wave duration and morphology or fibrillatory waves
- Preexcitation
- Bundle-branch block
- Prior MI
- Other atrial arrhythmias
- To measure and follow the RR, QRS, and QT intervals in conjunction with antiarrhythmic drug therapy
Summary of Electrocardiographic findings
- Absent P waves
- Irregularly irregular ventricular response rate. Regular RR intervals are possible in the presence of AV block or interference due to ventricular or junctional tachycardia.
- An atrial rate that ranges from 400 to 700 BPM.
- sometimes V1 may look as though there is atrial flutter. This may be because the electrode overlies a portion of the RA with rhythmic activity.
- Some authors believe that fine f waves (<.5 mm) are associated with coronary artery disease and that coarse F waves are associated with LA enlargement and rheumatic heart disease.
- the ventricular rate is usually between 100 and 180 BPM.
- if the atrial rate is greater than 200 BPM, then consider WPW or an accessory pathway.
- In the presence of AV junctional disease, the ventricular rate may be below 70 bpm.
- a rapid, irregular, sustained, wide-QRS-complex tachycardia strongly suggests AF with conduction over an accessory pathway or AF with underlying bundle-branch block.
- Complete AV block is indicated by a slow ventricular rhythm with a regular RR interval.
- In patients with electronic pacemakers, diagnosis of AF may require temporary inhibition of the pacemaker to expose atrial fibrillatory activity.
- Differential diagnosis includes tremor due to artifact. The oscillations in this case are largest in the limb leads.
When electrocardiograms are used for screening? The SAFE trial found that electronic software, primary care physicians and the combination of the two had the following sensitivities and specificities:[1]:
- Interpreted by software: sensitivity = 83%, specificity = 99%
- Interpreted by a primary care physician: sensitivity = 80%, specificity = 92%
- Interpreted by a primary care physician with software: sensitivity = 92%, specificity = 91%
If paroxysmal AF is suspected but the electrocardiogram shows a regular rhythm, episodes may be documented with the use of Holter monitoring (continuous ECG recording for 24 hours). If the symptoms are very infrequent, longer periods of continuous monitoring may be required.[1]
Chest X-ray
A chest X-ray is generally only performed if a pulmonary cause of atrial fibrillation is suggested. This may reveal an underlying problem in the lungs or the blood vessels in the chest. [1] In particular, if an underlying pneumonia is suggested, then treatment of the pneumonia may cause the atrial fibrillation to terminate on its own.
As a summary a chest radiograph is required to evaluate;
- The lung parenchyma, when clinical findings suggest an abnormality
- The pulmonary vasculature, when clinical findings suggest an abnormality
Echocardiography
Performing an echocardiogram is essential to identify;
- Valvular heart disease
- Left and right atrial size
- LV size and function
- Peak RV pressure (pulmonary hypertension)
- LV hypertrophy
- LA thrombus (low sensitivity)
- Pericardial disease
Transthoracic echocardiography (TTE)
A transthoracic echocardiogram is generally performed in newly diagnosed AF, as well as if there is a major change in the patient's clinical state. This ultrasound-based scan of the heart may help identify valvular heart disease (which may increase the risk of stroke manifold), left and right atrial size (which indicates likelihood that AF may become permanent), left ventricular size and function, peak right ventricular pressure (pulmonary hypertension), presence of left ventricular hypertrophy and pericardial disease.[1]
Significant enlargement of both the left and right atria is associated with long-standing atrial fibrillation and, if noted at the initial presentation of atrial fibrillation, suggests that the atrial fibrillation is likely of a longer duration than the individual's symptoms.
Transesophageal echocardiography (TEE)
A normal echocardiography (transthoracic or TTE) has a low sensitivity for identifying thrombi (blood clots) in the heart. If this is suspected - e.g. when planning urgent electrical cardioversion - a transesophageal echocardiogram (TEE) is preferred.[1]
The TEE has much better visualization of the left atrial appendage than transthoracic echocardiography. This structure, located in the left atrium, is the place where thrombus most commonly is formed in the setting of atrial fibrillation or flutter. TEE has a very high sensitivity for locating thrombus in this area and can also detect sluggish bloodflow in this area that is suggestive of thrombus formation.
If no thrombus is seen on TEE, the incidence of stroke immediately after cardioversion is performed is very low.
Ambulatory Holter monitoring
A holter monitor is a wearable ambulatory heart monitor that continuously monitors the heart rate and heart rhythm for a short duration, typically 24 hours. In individuals with symptoms of significant shortness of breath with exertion or palpitations on a regular basis, a holter monitor may be of benefit to determine if rapid heart rates (or unusually slow heart rates) during atrial fibrillation are the cause of the symptoms.
Exercise stress testing
Some individuals with atrial fibrillation do well with normal activity but develop shortness of breath with exertion. It may be unclear if the shortness of breath is due to a blunted heart rate response to exertion due to excessive AV node blocking agents, a very rapid heart rate during exertion, or due to other underlying conditions such as chronic lung disease or coronary ischemia. An exercise stress test will evaluate the individual's heart rate response to exertion and determine if the AV node blocking agents are contributing to the symptoms. As a summary the main benefits of performing an exercise stress testing;
- If the adequacy of rate control is in question (permanent AF)
- To reproduce exercise-induced AF
- To exclude ischemia before treatment of selected patients with a type IC antiarrhythmic drug
Electrophysiologic Testing or Electrophysiologic Studies
Electrophysiologic (EP) testing or EP studies (EPS) help to confirm specific arrhythmias and determine where in the heart they begin. This testing, which is performed in an EP lab by a cardiac electrophysiologist, makes it possible to reproduce troubling arrhythmias in a controlled setting. Though it is more invasive than an ECG or ECHO, EP testing is helpful in determining the type of arrhythmia, its origin, and potential response to therapy. In general, performing an EPS required;
- To clarify the mechanism of wide-QRS-complex tachycardia
- To identify a predisposing arrhythmia such as atrial flutter or paroxysmal supraventricular tachycardia
- seeking sites for curative ablation or AV conduction block/modification
- The cause of AF may be a rapidly firing focus, commonly in or near the pulmonary vein(s), or the result of a regular supraventricular tachycardia such as AV reentry, AV node reentry, or atrial flutter that degenerates into AF (tachycardia-induced tachycardia). Rate control by catheter ablation or modification of AV conduction requires electrophysiological study, as does selection of patients for pacemaker therapy to prevent AF.
EP testing is a relatively painless, nonsurgical procedure performed under local anesthesia. Following an initial puncture, an introducer sheath is inserted into a blood vessel. A diagnostic catheter is then inserted through the introducer sheath. Monitors make it possible for the electrophysiologist to view the catheter moving up through the body and into the right chambers of the heart. Once inside the heart, the catheter stimulates the heart and records where abnormal impulses start, how fast they travel, and where they bypass the normal conduction pathway. Treatments may be administered to determine if they are effective in stopping the arrhythmia. After the testing is done, the catheter and the introducer sheath are removed, and the insertion site is closed with stitches or by applying pressure at the site.
Treatment of atrial fibrillation
- Pharmacological treatment
- Invasive treatment
- Surgical treatment
Pharmacological treatment of atrial fibrillation
The main goals of treatment of atrial fibrillation are to prevent temporary circulatory instability and to prevent stroke. Rate and rhythm control are principally used to achieve the former, while anticoagulation may be required to decrease the risk of the latter.[1] In emergencies, when circulatory collapse is imminent due to uncontrolled tachycardia, immediate cardioversion may be indicated.[1]
The primary factors determining atrial fibrillation treatment are duration and evidence of hemodynamic instability. Cardioversion is indicated with new onset AF (for less than 48 hours) and with hemodynamic instability. If rate and rhythm control cannot be maintained by medication or cardioversion, electrophysiological studies with pathway ablation may be required.[1]
Antithrombotic Strategies for Prevention of Ischemic Stroke and Systemic Embolism
Meta-analysis showed that adjusted-dose oral anticoagulation is highly efficacious for prevention of all stroke (both ischemic and hemorrhagic), with a risk reduction of 61%. This reduction was similar for both primary and secondary prevention.
Patient age and the intensity of anticoagulation are the most powerful predictors of major bleeding.
The target intensity of anticoagulation involves a balance between prevention of ischemic stroke and avoidance of hemorrhagic complications. It is important to target the lowest adequate intensity of anticoagulation to minimize the risk of bleeding, particularly for elderly AF patients.
Maximum protection against ischemic stroke in AF is probably achieved with an international normalized ratio (INR) of 2 to 3, whereas an INR range of 1.6 to 2.5 appears to be associated with incomplete efficacy, estimated at approximately 80% of that achieved with higher intensity anticoagulation.
In patients with AF who do not have mechanical valves, anticoagulation can be interrupted for a period of up to 1 week for procedures that carry a risk of bleeding, without substituting heparin. In high-risk patients, or when a series of procedures requires interruption for a period longer than 1 week, unfractionated heparin or low molecular weight heparin can be administered intravenously or subcutaneously, respectively.
Aspirin offers only modest protection against stroke for patients with AF
The effect is less consistent than that of oral anticoagulation. Aspirin might be more efficacious for AF patients with hypertension or diabetes and for reducing non cardioembolic versus cardioembolic ischemic strokes. Cardioembolic strokes are, on average, more disabling than non cardioembolic strokes.
Oral Anticoagulation (Coumadin) versus Dual Antiplatelet Therapy (ASA/Clopidogrel)
In the ACTIVE W trial, dual antiplatelet therapy with aspirin(75-100 mg per day) and clopidogrel (75 mg per day) was found to be statistically inferior to coumadin therapy (target INR 2.0 to 3.0) in the management of patients with atrial fibrillation who had one or more risk factors for stroke[1]. The primary endpoint of ACTIVE W was the first occurrence of stroke, non-CNS systemic embolus, myocardial infarction, or vascular death. The annual risk in the coumadin group was 3.93% per year, and in the Aspirin/Clopidogrel group it was 5.60% per year yielding a relative risk of 1.44 (1.18-1.76; p=0.0003). The efficacy was not as great among patients who were coumadin naive, although the p-value for the interaction was negative. There was no excess bleeding among patients treated with coumadin, and in fact there was an excess of minor bleeds among patients treated with ASA and clopidogrel (13.6% / yr vs 11.5% year, p=0.0009).
When examining the data from atrial fibrillation trials, it is critical to evaluate the results in patients who were previously treated with coumadin separate from those patients who were naive to coumadin. Patients previously treated with coumadin are likely to be those patients who best tolerate coumadin and have passed their "bleeding stress test" and have a lower rate of bleeding on coumadin. Those patients who bleed while on coumadin have already been culled out from the population. When the data in ACTIVE W were evaluated including only those patients previously treated with coumadin(again a population to be anticipated to be at low risk of bleeding), the risk of major bleeding was indeed statistically significantly lower among patients previously treated with coumadin (p=0.03) than patients not previously treated.
The majority of the reduction in events was due to a reduction in stroke and non-CNS emolization associated with [[coumadin therapy. The pathophysiology of stroke among patients with atrial fibrillation is thought to be embolization from clot in the left atrium. The data from ACTIVE W suggest that platelet activation and its treatment may not play a pivotal role in the treatment of mural thrombus and embolization in atrial fibrillation. Coumadin was more effective in the reduction of non-disabling stroke rather than disabling stroke. There were more fatal hemorrhagic strokes (which may more often be fatal), and this may explain in part why coumadin was not associated with a reduction in mortality in the study.
While clopidogrel plus aspirin has been found to reduce the risk of recurrent myocardial infarction among patients with presumed plaque rupture and acute coronary syndromes, it is notable in ACTIVE W that the risk of myocardial infarction tended to be higher among patients treated with aspirin plus clopidogrel versus coumadin (0.86% vs 0.55%,p=0.09)[1].
Conversion to sinus rhythm and thromboembolism
Randomized studies of antithrombotic therapy are lacking for patients undergoing cardioversion of AF or atrial flutter, but the risk of thromboembolism was between 1% and 5% in case-control series.
There is no solid clinical evidence that cardioversion of AF followed by prolonged maintenance of sinus rhythm effectively reduces thromboembolism.
Patients in whom LAA thrombus is identified by TEE appear to be at high risk of thromboembolism after cardioversion of AF or flutter, and they should be treated with anticoagulation for at least 3 to 4 weeks before and after either pharmacological or electrical cardioversion.
The clinical benefit of the TEE approach is limited to saving time before cardioversion.
Electrical & mechanical dissociation
Conversion of AF to sinus rhythm results in transient mechanical dysfunction of the LA and LAA, known as “stunning.” This occurs after spontaneous, pharmacological, or electrical conversion of AF and after radiofrequency catheter ablation of atrial flutter.
The loss of atrial function can be associated with spontaneous echo contrast. Recovery of mechanical function can be delayed for several weeks, depending in part on the duration of AF before restoration of sinus rhythm. This could explain why some patients with no demonstrable LA thrombus on TEE before cardioversion subsequently experience thromboembolic events. Presumably, thrombus forms during the period of stunning and is expelled after the return of mechanical function, which explains the clustering of thromboembolic events in the first 10 days after cardioversion.
Anticoagulation is recommended for 3 to 4 weeks before and after cardioversion for patients with AF of unknown duration or that has lasted more than 48 hours.
Although LA thrombus and systemic embolism have been documented in patients with AF of shorter duration, the need for anticoagulation in such patients is less clear.
When acute AF produces hemodynamic instability, immediate cardioversion should not be delayed, but intravenous heparin or low molecular weight heparin should be administered first. Protection against late embolism might require continuation of anticoagulation; the duration of anticoagulation after the procedure depends on the likelihood that AF will recur and on the patient’s intrinsic risk of thromboembolism.
Management Strategies
New diagnosed or First Episode of Atrial Fibrillation
In patients who have self-limited episodes of paroxysmal AF, antiarrhythmic drugs to prevent recurrence are usually unnecessary, unless AF is associated with severe symptoms related to hypotension, myocardial ischemia, or HF. Whether these individuals require longterm or even short-term anticoagulation is not clear, and the decision must be individualized for each patient based on the intrinsic risk of thromboembolism.
Persistent Atrial Fibrillation
In patients with persistent AF, one option is to accept progression to permanent AF, with attention to antithrombotic therapy and control of the ventricular rate. Although it might seem reasonable to make at least 1 attempt to restore sinus rhythm, this is not in the best interest of all patients.
An example is the older man without risk factors for thromboembolism in whom asymptomatic AF is discovered on routine examination and control of the ventricular rate is readily achieved. Here, the potential toxicity of antiarrhythmic drugs might outweigh the benefit of restoration of sinus rhythm.
If the decision is made to attempt to restore and maintain sinus rhythm, anticoagulation and rate control are important before cardioversion. Although long-term antiarrhythmic therapy might not be needed to prevent recurrent recurrent AF after cardioversion, short-term therapy might be beneficial. In patients with AF of more than 3 months’ duration, early recurrence is common after cardioversion. Antiarrhythmic medication can be initiated before cardioversion (after adequate anticoagulation) in such cases to reduce the likelihood of recurrence, and the duration of drug therapy would be brief (e.g., 1 month).
Recurrent Paroxysmal Atrial Fibrillation
In patients who experience brief or minimally symptomatic recurrences of paroxysmal AF, it is reasonable to avoid antiarrhythmic drugs, but troublesome symptoms generally call for suppressive antiarrhythmic therapy.
Rate control and prevention of thromboembolism are appropriate in both situations. In any given patient, several different antiarrhythmic drugs might be effective, and the initial selection is thus based mainly on safety.
For individuals with no or minimal structural heart disease
Recommended as initial antiarrhythmic therapy, well tolerated, devoid of extracardiac organ toxicity.
When one or another of these drugs is ineffective or is associated with side effects, then second or third line choices which may have greater potential for adverse reactions:
A non pharmacological approach is appropriate for some patients, and this should be considered before amiodarone therapy is begun.
Vagally mediated Atrial fibrillation
Adrenergically induced Atrial Fibrillation
Beta blockers (sotalol)
Congestive Heart Failure
amiodarone or dofetilide to maintain sinus rhythm.
Ischemic heart disease
Beta-blocker medication, then sotalol (has both beta-blocking activity and primary antiarrhythmic efficacy) is considered first unless the patient has HF. Amiodarone and dofetilide are considered secondary agents in this situation. The clinician may consider disopyramide, procainamide, or quinidine on an individual basis.
Hypertension without LVH
Flecainide and propafenone, which do not prolong repolarization and the QT interval, might offer a safety advantage and are recommended first. If these agents either prove ineffective or produce side effects, then amiodarone, dofetilide, and sotalol represent appropriate secondary choices. Disopyramide, procainamide, and quinidine are considered third-line agents in this situation.
Left ventricular hypertrophy
Hypertrophied myocardium is prone to proarrhythmic toxicity and development of the torsade de pointes type of ventricular tachycardia.
Amiodarone is first-line therapy in patients with LVH (wall thickness greater than or equal to 1.4 cm).
Recurrent Persistent AF
Patients with minimal symptoms who have undergone at least 1 attempt to restore sinus rhythm can remain in AF with therapy for rate control and prevention of thromboembolism.
Alternatively, those with symptoms favoring sinus rhythm should be treated with an antiarrhythmic agent (in addition to medications for rate control and anticoagulation) before cardioversion.
The selection of an antiarrhythmic drug should be based on the same algorithm used for patients with recurrent paroxysmal AF.
Permanent AF
The designation given to cases in which sinus rhythm cannot be sustained after cardioversion of AF or when the patient and physician have decided to allow AF to continue without further efforts to restore sinus rhythm. It is important to maintain control of the ventricular rate and to use antithrombotic antithrombotic therapy, as outlined elsewhere in this document, for all patients in this category.'
Anticoagulation
Patients with atrial fibrillation, even lone atrial fibrillation without other evidence of heart disease, are at increased risk of stroke during long term follow up.[1] A systematic review of risk factors for stroke in patients with nonvalvular atrial fibrillation concluded that a prior history of stroke or TIA is the most powerful risk factor for future stroke, followed by advancing age, hypertension, diabetes.[1] The risk of stroke increases whether the lone atrial fibrillation was an isolated episode, recurrent, or chronic.[1] The risk of systemic embolization (atrial clots migrating to other organs) depends strongly on whether there is an underlying structural problem with the heart (e.g. mitral stenosis) and on the presence of other risk factors, such as diabetes and high blood pressure. Finally, patients under 65 are much less likely to develop embolization compared with patients over 75. In young patients with few risk factors and no structural heart defect, the benefits of anticoagulation may be outweighed by the risks of hemorrhage (bleeding). Those at a low risk may benefit from mild (and low-risk) anticoagulation with aspirin (or clopidogrel in those who are allergic to aspirin). In contrast, those with a high risk of stroke derive most benefit from anticoagulant treatment with warfarin or similar drugs.
In the United Kingdom, the NICE guidelines recommend using a clinical prediction rule for this purpose.[1] The CHADS/CHADS2 score is the best validated clinical prediction rule for determining risk of stroke (and therefore who should be anticoagulated); it assigns points (totaling 0-6) depending on the presence or absence of co-morbidities such hypertension and diabetes. In a comparison of seven prediction rules, the best rules were the CHADS2 which performed similarly to the SPAF[1] and Framingham[1] prediction rules. [1]
To compensate for the increased risk of stroke, anticoagulants may be required. However, in the case of warfarin, if a patient has a yearly risk of stroke that is less than 2%, then the risks associated with taking warfarin outweigh the risk of getting a stroke. [1][1]
Acute anticoagulation
If anticoagulation is required urgently (e.g. for cardioversion), heparin or similar drugs achieve the required level of protection much quicker than warfarin, which may take several days to reach adequate levels.
In the initial stages after an embolic stroke, anticoagulation may be risky, as the damaged area of the brain is relatively prone to bleeding (hemorrhagic transformation).[1] As a result, a clinical practice guideline by National Institute for Health and Clinical Excellence recommends that anticoagulation should begin two weeks after stroke if no hemorrhage occurred.[1]
Chronic anticoagulation
Among patients with "non-valvular" atrial fibrillation, anticoagulation with warfarin can reduce stroke by 60% while antiplatelet agents can reduce stroke by 20%. [1][1]. There is evidence that aspirin and clopidogrel are effective when used together, but the combination is still inferior to warfarin.[1]
Warfarin treatment requires frequent monitoring with a blood test called the international normalized ratio (INR); this determines whether the correct dose is being used. In atrial fibrillation, the usual target INR is between 2.0 and 3.0 (higher targets are used in patients with mechanical artificial heart valves, many of whom may also have atrial fibrillation). A high INR may indicate increased bleeding risk, while a low INR would indicate that there is insufficient protection from stroke.
An attempt was made to find a better method of implementing warfarin therapy without the inconvenience of regular monitoring and risk of intracranial hemorrhage. A combination of aspirin and fixed-dose warfarin (initial INR 1.2-1.5) was tried. Unfortunately, in a study of AF patients with additional risk factors for thromboembolism, the combination of aspirin and the lower dose of warfarin was significantly inferior to the standard adjusted-dose warfarin (INR 2.0-3.0), yet still had a similar risk of intracranial hemorrhage.[1]
Elderly patients
The very elderly (patients aged 75 years or more) may benefit from anticoagulation provided that their anticoaguation does not increase hemorrhagic complications, which is a difficult goal. Patients aged 80 years or more may be especially susceptible to bleeding complications, with a rate of 13 bleeds per 100 person-years.[1] A rate of 13 bleeds per 100 person years would seem to preclude use of warfarin; however, a randomized controlled trial found benefit in treating patients 75 years or over with a number needed to treat of 50.[1] Of note, this study had very low rate of hemorrhagic complications in the warfarin group.
Rate control versus rhythm control
AF can cause disabling and annoying symptoms. Palpitations, angina, lassitude (weariness), and decreased exercise tolerance are related to rapid heart rate and inefficient cardiac output caused by AF. Furthermore, AF with a persistent rapid rate can cause a form of heart failure called tachycardia induced cardiomyopathy. This can significantly increase mortality and morbidity, which can be prevented by early and adequate treatment of the AF.
There are two ways to approach these symptoms: rate control and rhythm control. Rate control treatments seek to reduce the heart rate to normal, usually 60 to 100 beats per minute. Rhythm control seeks to restore the normal heart rhythm, called normal sinus rhythm. Studies suggest that rhythm control is mainly a concern in newly diagnosed AF, while rate control is more important in the chronic phase. Rate control with anticoagulation is as effective a treatment as rhythm control in long term mortality studies, the AFFIRM Trial.[1]
The AFFIRM study showed no difference in risk of stroke in patients who have converted to a normal rhythm with anti-arrhythmic treatment, compared to those who have only rate control.[1]
Rate control
Rate control is achieved with medications that work by increasing the degree of block at the level of the AV node, effectively decreasing the number of impulses that conduct down into the ventricles. This can be done with:[1]
- Beta blockers (preferably the "cardioselective" beta blockers such as metoprolol, atenolol, bisoprolol)
- Cardiac glycosides (i.e. digoxin)
- Calcium channel blockers (i.e. diltiazem or verapamil)
In addition to these agents, amiodarone has some AV node blocking effects (particularly when administered intravenously), and can be used in individuals when other agents are contraindicated or ineffective (particularly due to hypotension).
Cardioversion
Rhythm control methods include electrical and chemical cardioversion:[1]
- Electrical cardioversion involves the restoration of normal heart rhythm through the application of a DC electrical shock.
- Chemical cardioversion is performed with drugs, such as amiodarone, dronedarone[1], procainamide, ibutilide, propafenone or flecainide.
The main risk of cardioversion is systemic embolization of a thrombus (blood clot) from the previously fibrillating left atrium. Cardioversion should not be performed without adequate anticoagulation in patients with more than 48 hours of atrial fibrillation. Cardioversion may be performed in instances of AF lasting more than 48 hours if a transesophogeal echocardiogram (TEE) demonstrates no evidence of clot within the heart.[1]
Whichever method of cardioversion i