Atrial Fibrillation Review

Pathophysiology - Etiology - Diagnosis - Symptoms - Treatment - Special Situations - Quick Fact Sheet

Multiple Choice Questions - Case Questions - Jeopardy Game - ACC/AHA Guidelines - Clinical Trials

Introduction

Atrial fibrillation (AF) is the most common chronic arrhythmia and is characterized by erratic atrial electrical activity with atrial rates of
400-600 beats per minute. The P wave is absent on the surface electrocardiogram which can at times be replaced with fibrillatory
waves. Atrial flutter is similar to atrial fibrillation in regards to symptoms and thromboembolic risk (including stroke), however the
pathophysiology and management differs.

The symptoms of atrial fibrillation are related to the loss of atrial mechanical activity (atrial contraction) and rapid ventricular heart rates
both of which can reduce cardiac output and lead to congestive heart failure. Thromboembolism frequently causes stroke in atrial
fibrillation patients.

Atrial fibrillation is classified into paroxysmal, persistent or permanent (the three Ps).

Paroxysmal atrial fibrillation is self-limiting and sinus rhythm restores spontaneously. Paroxysmal atrial fibrillation lasts for less than 7
days and does not require intervention to convert to a normal rhythm such as electrical or chemical cardioversion.

Persistent atrial fibrillation lasts for greater than 7 days. The term persistent is used when there is a plan to use a rhythm control
strategy and return the patient to sinus rhythm.

Permanent atrial fibrillation is present when atrial fibrillation is present 100% of the time for greater than 7 days and there are no
interventions planned to restore sinus rhythm.

The term chronic atrial fibrillation and the abbreviation PAF are no longer recommended for use. The term lone atrial fibrillation is
used when structural heart disease is not present. Atrial fibrillation has also been classified as valvular versus non-valvular in etiology.
Atrial fibrillation is termed recurrent when there have been two or more episodes.

Pathophysiology

Atrial fibrillation occurs when irritable foci cause rapid action potentials which result in an atrial heart rate between 400 and 600 beats
per minute. The foci are commonly located in the superior pulmonary veins which is important in regards to the approach to atrial
fibrillation ablation (a.k.a. pulmonary vein isolation). Less commonly, the foci of atrial fibrillation can be within the right atrium and rarely
in the superior vena cava or coronary sinus.
Atrial tissue in patients with atrial fibrillation is well known to remodel showing pathologic changes of fibrosis and inflammation the exact
mechanism of which remains unclear. Any cardiac condition that results in left atrial enlargement will increase the risk of atrial fibrillation
since the above mentioned remodeling is more prominent in this setting. The left atrium will enlarge whenever the left atrial pressure is
increased as in congestive heart failure, chronic hypertension and valvular heart disease. The larger the left atrium, the higher the risk
of atrial fibrillation. Likewise, the larger the left atrium, the less likely that maintaining sinus rhythm after cardioversion will be successful,
especially without antiarrhythmic drugs.

Fortunately, not all 400-600 atrial action potentials during atrial fibrillation conduct to the ventricles in normal individuals due to the
actions of the AV node. The AV nodal refractoriness inhibits more than half of these action potentials from reaching the ventricles and
thus the typical ventricular heart rate in patients with atrial fibrillation (in the absence of AV blocking medications) is about 100-170
beats per minute.

In patients with Wolff-Parkinson-White (WPW) syndrome who develop atrial fibrillation, an accessory pathway is present electrically
connecting the atrium to the ventricles (separate from the AV node) allowing many more action potentials to reach the ventricles
resulting in ventricular rates greater than 200 beats per minute. Blocking the AV node with medications such as beta-blockers or
calcium channel blockers paradoxically increases the ventricular heart rate since more atrial action potentials can conduct through the
accessory pathway which commonly has a short refractory period (can conduct quite fast). This paradoxical increase in ventricular
heart rates can lead to ventricular fibrillation (ventricular rates of 400-600) and death. Procainamide or electrical cardioversion is
recommended in WPW patients with AF for this reason (see management below).

The development of thrombi in the left atrial appendage can result in embolus causing stroke in susceptible individuals. When AF is
present, flow velocities are significantly decreased in the atrium including the left atrial appendage. This allows coagulation and
thrombus formation. Certain predictors can be used to identify those at higher risk for thromboembolism (see the CHADs 2 score,
the CHADS 2 Vasc score and the ACC/AHA guidelines).

Etiology

Identifying the cause of atrial fibrillation can not be under emphasized as the treatment of the cause is frequently necessary to eliminate
atrial fibrillation. The classic mneumonic PIRATES encompasses a vast majority of the causes of atrial fibrillation:

Pulmonary embolus, pulmonary disease, post-operative, pericarditis

Ischemic heart disease, idiopathic (lone atrial fibrillation), intravenous central line (in right atrium)
Rheumatic valvular disease (specifically mitral stenosis or mitral regurgitation)
Anemia, alcohol (holiday heart), advanced age, autonomic tone (vagally mediated atrial fibrillation)
Thyroid disease (hyperthyroidism)
Elevated blood pressure (hypertension), electrocution
Sleep apnea, sepsis, surgery

Historically, hypertension was thought to be the most common cause of atrial fibrillation, however obstructive sleep apnea is present in
about 40% of atrial fibrillation patients and it is we

ll known that obstructive sleep apnea causes hypertension. The exact proportion of atrial fibrillation caused directly from obstructive
sleep apnea remains unclear.

Diagnosis

Diagnosing atrial fibrillation (AF) is done predominantly on the surface ECG. Sinus P waves are absent and sometimes no atrial activity
can be identified. Frequently, coarse fibrillatory waves can be seen representing the erratic atrial activity that occurs in the setting of
atrial fibrillation.
The QRS complexes are irregularly irregular as there is no pattern to their frequency. This is commonly described as varying R-R
intervals.

Note that there are three rhythms originating from the atrium that can be irregularly irregular: Atrial fibrillation, atrial flutter with variable
conduction and multifocal atrial tachycardia.

The ventricular rate is frequently elevated and when significantly so (greater than 150 beats per minute), it is frequently difficult to
determine atrial fibrillation from atrial flutter, atrial tachycardia, or atrioventricular nodal reentrant tachycardia (AVNRT). In this situation,
giving adenosine will transiently slow the ventricular rate in atrial fibrillation patients allowing a more definitive diagnosis to be made.
This should not be done in patients with Wolff-Parkinson-White syndrome (as described above) since this paradoxically increases the
ventricular rate in this setting leading to ventricular fibrillation which can be fatal.
 Below find multiple full 12-lead ECG examples of atrial fibrillation:

Atrial Fibrillation with Rapid Ventricular Rate (Example 1)

Atrial Fibrillation with Rapid Ventricular Rate (Example 2)

Atrial Fibrillation with Rapid Ventricular Rate (Example 3)

Atrial Fibrillation with Rapid Ventricular Rate (Example 4)

Atrial Fibrillation with Rapid Ventricular Rate (Example 5)

Atrial Fibrillation with Normal Ventricular Rate (Example 1)

Atrial Fibrillation with Normal Ventricular Rate (Example 2)

Atrial Fibrillation with Normal Ventricular Rate (Example 3)

Atrial Fibrillation with Bradycardia (Example 1)

Atrial Fibrillation with Bradycardia (Example 2)

Atrial Fibrillation with Bradycardia (Example 3)

On physical examination the heart rhythm will be irregularly irregular and frequently tachycardic. Findings of heart failure may be
present depending on the ventricular rate, duration of atrial fibrillation and other factors. There will never be an S4 heart sound present
during atrial fibrillation as this heart sound is produced when atrial contraction forces blood into a non-compliant left ventricle. Normal
atrial contraction is lost during atrial fibrillation.

The diagnosis of a left atrial appendage (LAA) thrombus if suspected must be done using transesophageal echocardiography (TEE) or
cardiac CT (less commonly used). It is important to note that transthoracic echocardiography does not detect left atrial appendage
thrombi in the vast majority of patients. TEE findings of a left atrial appendage thrombus includes direct visualization of a mobile
echodensity within the appendage. The echodensity should move independent of the walls of the atrium which helps to distinguish
artifact or trabeculae from thrombus. Pulse wave Doppler can be used in the left atrial appendage to determine the flow velocity. A
velocity of < 0.4 m/s indicates a higher risk in general of thromboembolism.

Symptoms

The symptoms of atrial fibrillation relate either to the irregularly irregular heartbeat causing palpitations or decreased overall cardiac
output (from loss of atrial contraction and fast ventricular rates) resulting in congestive heart failure (see congestive heart failure
symptoms). If hypotension is present from a significantly reduced cardiac output, dizziness and even syncope (loss of consciousness)
can occur.
Treatment - Alleviating symptoms

The approach to the management of atrial fibrillation patients requires the consideration of two distinct areas: Alleviating symptoms of
atrial fibrillation and preventing thromboembolism. A summary image is below.

There are two main approaches which can be utilized to alleviate symptoms of atrial fibrillation: A rate control strategy or a rhythm
control strategy.

The AFFIRM trial evaluated using a rate control strategy versus a rhythm control strategy. There was no difference in mortality between
these approaches and thus an individualized approach is recommended based on the degree of symptoms and the patients personal
preference.
Rate control

Commonly, controlling the ventricular rate in atrial fibrillation patients can completely resolve symptoms and no further therapy is
needed. This is done using AV blocking medications either intravenously in the acute setting or orally for long-term therapy.

Selecting the appropriate AV blocking agent requires the knowledge of other indications and contraindications for these drugs,
specifically, knowledge of the left ventricular systolic function is important. AV blocking agents used in AF include beta-blockers, non-
dihydropyridine calcium channel blockers and digoxin.

Beta-blockers (i.e. atenolol, metoprolol, carvedilol) antagonise beta-receptors which result in decreasing conduction through the AV
node reducing the heart rate in atrial fibrillation patients. Caution is advised in patients with asthma since antagonizing beta-2 receptors
can cause bronchospasm. In severe left ventricular systolic dysfunction (reduced ejection fraction), beta-blockers can acutely decrease
cardiac output leading to severe hypotension, acute heart failure and even cardiogenic shock. Despite this, beta-blockers are
considered safe when used cautiously in this setting.

Non-dihydropyridine calcium channel blockers (diltiazem, verapamil) decrease AV conduction by antagonizing voltage gated calcium
channels decreasing intracellular calcium. Since these drugs reduce left ventricular inotropy (contractility) via the same mechanism,
they are in general not advised to be used in the setting of left ventricular systolic dysfunction (reduced ejection fraction).

Digoxin blocks the sodium/potassium ATPase pump. The mechanism by which this decreases AV conduction is not clear however is
perhaps due to increased vagal tone. Intracellular calcium within the cardiac myocytes is increased by digoxin resulting in increased
inotropy (contractility) and thus digoxin is frequently used when atrial fibrillation and left ventricular systolic dysfunction coexist. Digoxin
is effective to reduce ventricular rates at rest, however not effective during physical activity and thus it is recommended to use digoxin in
combination with a beta-blocker or non-dihydropyridine calcium channel blocker.

Rarely, the above medications are not able to adequately reduce the ventricular rate and AV nodal ablation with permanent
pacemaker implantation is needed.

Rhythm Control

A rhythm control strategy is employed when rate control is not successful in completely eliminating symptoms from atrial fibrillation or if
the ventricular rate is refractory to the previously mentioned AV blocking medications. This can be done using cardioversion,
antiarrhythmic drug therapy or ablation.

The term cardioversion is used to describe an action taken to restore sinus rhythm. This can be done either electrically by delivering a
shock (direct current cardioversion or DCCV) or chemically with certain drugs (class IA, class IC or class III antiarrhythmic drugs).
Once sinus rhythm is restored, antiarrhythmic drug therapy can be utilized to maintain sinus rhythm, especially if the risk of recurrence
is high such as in severe left atrial enlargement, severe valvular heart disease or uncontrolled sleep apnea.

Antiarrhythmic drugs used to treat atrial fibrillation include the following:

Class IA (quinidine, procainamide, disopyramide): While class IA drugs are effective to treat atrial fibrillation, they are not commonly
utilized for this purpose due to side-effects and significant pro-arrhythmia except in special situations (atrial fibrillation with Wolff-
Parkinson-White or vagally mediated atrial fibrillation). These agents block cardiac sodium channels and depress phase 0 of the action
potential. Procainamide can cause drug-induced lupus erythematosus detected by measuring anti-histone antibodies. Quinidine can
cause cinchonism.

Class IB (lidocaine, mexiletine): These ARE NOT effective to treat atrial fibrillation and are used for ventricular arrhythmias.

Class IC (flecainide, propafenone, moricizine): These drugs are commonly used to maintain sinus rhythm in AF patients. Significant
coronary artery disease is a contraindication to their use as this increases the risk of proarrhythmia and sudden cardiac death. These
agents must be used in combination with an AV blocking agent in order to prevent rapid AF or atrial flutter conduction (1:1 conduction)
through the AV node resulting in very fast ventricular rates if a breakthrough episode occurs since they also act to increase AV nodal
conduction. These drugs may be proarrhythmic in the setting of left ventricular hypertrophy (wall thickness > 1.4 cm). Flecainide can be
used with a pill-in-the-pocket approach. If documented to be successful and safe while hospitalized, flecainide can be used on an as-
needed basis in the outpatient setting. Note that propafenone is hepatically cleared (not recommended with liver disease) while
flecainide is renally cleared.

Class III (amiodarone, sotalol, bretylium, dofetilide, dronedarone, ibutilide): These drugs are also commonly used in atrial
fibrillation and act by blocking potassium channels. Amiodarone is very effective however amiodarone toxicity is a concern. The half-life
of amiodarone is 42 days. Sotalol is proarrhythmic in the setting of left ventricular hypertrophy (wall thickness > 1.4 cm). Amiodarone
and dofetilide are preferred in patients with left ventricular systolic dysfunction (reduced ejection fraction). Dronedarone is not safe with
systolic heart failure or in the setting of permanent atrial fibrillation. Bretylium is rarely used.

Atrial Fibrillation Ablation

A majority of cases of atrial fibrillation originate within the pulmonary veins. Ablation of atrial fibrillation, also known as pulmonary vein
isolation or PVI, electrically disconnects the erratic electrical activity in the pulmonary veins (which are creating action potentials at a
rate of 400-600 beats per minute) from the rest of the heart thus effectively eliminating the atrial fibrillation. Ablation for atrial fibrillation
is complex, requires multiple catheters and is performed via venous access then puncturing the interatrial septum to obtain entry to the
left atrium where the pulmonary veins empty.
The highest success rates for atrial fibrillation ablation occur in patients where the arrhythmia is paroxysmal and not persistent or
permanent. Those with smaller left atrial volumes and with shorter duration of atrial fibrillation also have higher success rates.

The indication for atrial fibrillation ablation is symptoms from atrial fibrillation and failure of at least 1 antiarrhythmic drug. An attempt at a
second antiarrhythmic drug would also be reasonable.

Treatment - Preventing Thromboembolism

Stroke related to thromboembolism occurs due to decreased flow in the left atrial appendage when atrial contraction is lost during atrial
fibrillation. This results in stagnation of blood allowing thrombus formation which can embolize not only to the brain causing stroke, but
to other organs as well.
 Determining which patient should be
fully anticoagulated and whom is safe taking only aspirin for stroke prophylaxis is determined by many factors. The most commonly
utilized method is the CHADs 2 Vasc score. CHADS stands for Congestive heart failure, Hypertension, Age ( > 65 = 1 point, > 75 = 2
points), Diabetes, and Stroke/TIA (2 points). Vasc stands for vascular disease (peripheral arterial disease, previous MI, aortic atheroma)
and female gender is also included in this scoring system. Each risk factor receives 1 point except age > 75 and stroke/tia which
receive 2 points. If 2 or more points are present, then full anticoagulation should be utilized. Those with 1 point can be treated with
either aspirin alone or full anticoagulation based on the specific individual. The more points on the CHADS 2 Vasc score, the higher the
annual stroke risk in general, which is excellent information for clinicians to discuss with their patients. The CHADS 2 score is also
sometimes used.
As a general rule, regardless of the above scoring system, if a patients atrial fibrillation is caused by valvular heart disease (severe
mitral regurgitation or mitral stenosis), then anticoagulation should be utilized.

The choice of anticoagulation should be individualized. For example, some individuals are not good candidates for coumadin therapy
which requires dietary alteration and frequent monitoring of the protime to prevent over or under anticoagulation. Dabigatran,
rivaroxaban and apixaban are relatively newer anticoagulants FDA approved for thromboembolism prophylaxis in atrial fibrillation
patients. The drugs do not require frequent monitoring, have a more predictable dosing and fewer drug/dietary interactions making
them much more convenient for patients to use.

Left atrial appendage occlusion devices have more recently been utilized to prevent thromboembolism. Percutaneously employed,
these devices essentially exclude the left atrial appendage reducing the risk of thrombus formation. They are indicated only for
individuals who have a high risk of thromboembolism and are not able to tolerate anticoagulation due to bleeding (usually
gastrointestinal bleeding) and include the Watchman device and the Lariat procedure.

Special Situations

Atrioventricular nodal (AVN) ablation and permanent pacing

When high doses of AV blocking drugs are not successful to lower ventricular rates in the setting of atrial fibrillation, AV nodal ablation
can be utilized. Remember that all atrial action potentials must pass through the AV node to reach the ventricle. AV node ablation
destroys this connection stopping any atrial activity from reaching the ventricle. This results in the intrinsic pacemaker of the heart
shifting from the atria to the ventricles. Unfortunately, the His-Purkinje system in the ventricles is only able to generate action potentials
at a rate of 30-40 beats per minute resulting in severe bradycardia after the AV node is ablated. Thus, a permanent pacemaker must be
implanted to prevent symptoms of bradycardia.

Vagally mediated atrial fibrillation

Atrial fibrillation triggered by situations of vagal stimulation has been well described (nausea, vomiting, abdominal pain, severe
coughing, young healthy athletes with high vagal tone etc...). In this scenario, the historical antiarrhythmic drug which has been
successful is disopyramide. This agent has significant anticholinergic activity making it more effective in this situation.

Holiday Heart

Sudden use of large amounts of alcohol (binge drinking) as frequently occurs during holidays is well known to trigger atrial fibrillation
even with a structurally normal heart. This has been termed Holiday Heart

Atrial fibrillation in hypertrophic obstructive cardiomyopathy (HOCM)

Loss of atrial contraction and fast ventricular rates are not hemodynamically tolerated well in patients with hypertrophic obstructive
cardiomyopathy. Due to the significant diastolic ventricular dysfunction in this disease, the atrial contraction is relied heavily upon to fill
the ventricles resulting in a significant decrease in cardiac output if atrial fibrillation develops. Also, since the ventricles fill during
diastole, the duration of which is significantly shortened in the setting of tachycardia, less time is present to fill the ventricles resulting in
even further decline in cardiac output. Similar hemodynamics occur when atrial fibrillation develops in patients with severe left
ventricular hypertrophy from hypertensive heart disease or aortic valve stenosis.

The treatment is frequently disopyramide as this drug is used in HOCM patients regardless of the presence of atrial fibrillation due to its
significant negative inotropic effects which are desirable to relieve the left ventricular outflow tract obstruction in these individuals.

Atrial fibrillation in Wolff-Parkinson-White

The combination of atrial fibrillation and Wolff-Parkinson-White syndrome can be fatal due to rapid conduction of the atrial activity
through the accessory pathway resulting in rapid ventricular rates causing ventricular fibrillation. AV nodal blocking agents should be
avoided in this setting since they paradoxically increase ventricular rates since more atrial activity will pass through the fast conducting
accessory pathway and fewer through the AV node itself. Procainamide is the recommended therapy or electrical cardioversion is
hemodynamic instability is present.

When atrial fibrillation is seen in a patient with Wolff-Parkinson-White, ablation of the accessory pathway is recommended to prevent
future rapid conduction to the ventricles.

The aim is to reduce the resting heart rate to under 90 beats a minute, although in some people the target is under 110 beats a
minute.
A beta-blocker (such as bisoprolol or atenolol) or a calcium channel blocker (such as verapamil or diltiazem) will be prescribed.
A medicine called digoxin may be added to help further control the heart rate. In some cases, amiodarone may be tried.
Normally just one medication will be tried before catheter ablation is considered.
Side effects
As with any medicine, anti-arrhythmics can cause side effects. Read the patient information leaflet that comes with the medicine for more
details.
The most common side effects of anti-arrhythmics are:
beta-blockers: tiredness, coldness of hands and feet, low blood pressure, nightmares and impotence
flecainide: nausea, vomiting and heart rhythm disorders
amiodarone: sensitivity to sunlight (high-protection sunscreen must be worn or skin covered up), lung problems,
changes to liver function or thyroid function (regular blood tests can check for this) and deposits in the eye (these go away
when treatment is stopped)
verapamil: constipation, low blood pressure, ankle swelling and heart failure
Medicines to reduce the risk of a stroke
The way the heart beats in atrial fibrillation means there is a risk of blood clots forming in the heart chambers. If these enter the
bloodstream, they can cause a stroke (seecomplications of atrial fibrillation for more information).
Your doctor will assess your risk to minimise your chance of a stroke. They will consider your age and whether you have a history of any of
the following:

stroke or blood clots

heart valve problems

heart failure

high blood pressure

diabetes

heart disease

You may be given medication according to your risk. Depending on your level of risk, you may be prescribed warfarin or a newer type
of anticoagulant, such as dabigatram, rivaroxaban or apixaban.

Warfarin
People with atrial fibrillation who have a high or moderate risk of a stroke are usually prescribed warfarin, unless there is a reason they
cannot take it.
Warfarin is an anticoagulant, which means it stops the blood from clotting. There is an increased risk of bleeding in people who take
warfarin, but this small risk is usually outweighed by the benefits of preventing a stroke.
It's important to take warfarin as directed by the doctor. People on warfarin need to have regular blood tests and, following these, their dose
may be changed.
Many medicines can interact with warfarin and cause serious problems, so check that any new medicines are safe to take with warfarin.
Whilst taking warfarin, do not drink more than three units of alcohol a day if you are a man or two units a day if you are a woman. It is also
not safe to binge drink by saving up units to have on one day. Drinking cranberry juice can also affect your warfarin and is not recommended.

Aspirin

Aspirin should not be prescribed as a way of preventing strokes caused by atrial fibrillation.
Newer anticoagulants

Rivaroxaban, dabigatran and apixaban are newer anticoagulants that may be used as an alternative to warfarin.
The National Institute for Health and Care Excellence (NICE) has approved these drugs for use in atrial fibrillation.
Compared to warfarin, rivaroxaban, dabigatran and apixaban do not have the same interactions with other medications, and don't require
regular blood tests.

Calcium channel blockers,

also known as "calcium antagonists," work by interrupting the movement of calcium into heart and blood vessel tissue. Besides being used to
treat high blood pressure, they're also used to treat angina (chest pain) and/or some arrhythmias (abnormal heart rhythms).

Some commonly prescribed calcium channel blockers include (generic name first; common brand names in parentheses read
drug brand name disclaimer above):

Amlodipine (Norvasc, Lotrel)

Diltiazem (Cardizem, Cartia, Dilacor, Diltia, Tiazac)

Felodipine (Plendil)

Isradipine (Dynacirc)

Nicardipine (Cardene)

Nifedipine (Adalat, Procardia)

Nimodipine (Nimotop)

Nisoldipine (Sular)

Verapamil (Calan, Covera, Isoptin, Verelan)

Beta-blockers

decrease the heart rate and cardiac output, which lowers blood pressure by blocking the effects of adrenalin. They're also used with therapy
for cardiac arrhythmias and in treating angina pectoris.
Some commonly prescribed beta-blockers include (generic name first; common brand names in parentheses read drug brand
name disclaimer above):

Acebutolol (Sectral)

Atenolol (Tenormin)

Betaxolol (Kerlone)

Bisoprolol/hydrochlorothiazide (Zebeta, Ziac)

Carteolol (Cartrol)

Esmolol (Brevibloc)

Metoprolol (Lopressor, Toprol)

Nadolol (Corgard)

Penbutolol (Levatol)

Pindolol (Visken)

Propranolol (Inderal)

Timolol (Blocadren)

Anticoagulants
(blood thinners) work by making it harder for the blood to clot, or coagulate. They aren't designed to dissolve existing blood clots. They
prevent new clots from forming or existing clots from getting larger. Because a common type of stroke is caused by a blood clot obstructing
blood flow to the brain, anticoagulants are often prescribed for people with certain conditions to prevent the occurrence of a first stroke or to
prevent the recurrence if the patient has already had a stroke. Anticoagulants are also given to certain people at risk for forming blood clots,
such as those with artificial heart valves or who have atrial fibrillation.

Warfarin (brand name Coumadin read drug brand name disclaimer) is one of the most commonly-prescribed anticoagulant
drugs. Aspirin is frequently recommended in addition to or instead of prescription anticoagulants.

Both these drugs interfere with your blood's clotting ability. Aspirin has an antiplatelet effect. That means it makes your blood platelets less
likely to stick together and form clots. Aspirin is less likely to cause abnormal bleeding, but warfarin seems to be more effective at preventing
clot-caused strokes.

Warfarin is an anticoagulant or blood thinner. That means it reduces your blood's ability to clot (coagulate). Stroke can be prevented in most
AF patients by using blood thinners. Most people over age 60 who have atrial fibrillation can be treated with a blood thinner. These drugs
must be very carefully monitored because too much blood thinner can cause abnormal bleeding.

To be sure you're getting the right amount of blood-thinning medication, your doctor will do a test called a Prothrombin Time. (This test is
also called "ProTime" or "PT.") The results of this test may be reported to you as an "INR" number. By using an INR (International Normalized
Ratio), your doctor can keep your blood clotting at a safe and effective level. Your INR should usually test between 2.0 and 3.0.