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Back to Cardiovascular Diseases
Atrial fibrillation
Introduction
Atrial fibrillation is a condition in which there is disorganized atrial
activity resulting in loss of effective atrial contraction. The atria
beat between 350 and 600 times per minute. These rapid, irregular
impulses pass through the AV node of the heart to the ventricles and
result in a rapid and "irregularly irregular" ventricular response.
There are paroxysmal and persistent forms.
Epidemiology
Incidence and prevalence
AF is the most common sustained arrhythmia.
Approximately 2.2 million individuals in the United States and 4.5
million individuals in the European Union have atrial fibrillation.[1,2]
Gender
Men are more likely than women to develop AF, but women
diagnosed with it carry a longer-term risk of premature death.
Age
The incidence of atrial fibrillation increases with age. The prevalence
in individuals over the age of 80 is about 8%.[3] 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.[4]
Race
Blacks have half the age adjusted incidence when compared to Caucasians.
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Causes of AF
- Coronary heart disease
- Congestive heart failure
- Pericarditis
- Myocarditis
- Rheumatic heart disease
- Hypoxia
- Hypertrophic cardiomyopathy
- Hypertensive cardiomyopathy
- Dilated cardiomyopathy
- Pulmonary embolism
- Alcohol
- Lone atrial fibrillation
- Thyrotoxicosis
- Theophylline
- Blunt trauma
- Sick sinus syndrome
- Sympathomimetic toxicity
- Post-CABG surgery
Risk factors
Risk factors for development of AF include:
- Those who have had coronary heart disease, heart attack or heart
failure.
- It's also found in people with heart valve disease, an inflamed
heart muscle or lining (endocarditis) or
- Recent heart surgery
- People with atherosclerosis and angina
- Congenital heart defects
- People with chronic lung disease, emphysema and asthma
- Thyroid disorders
- Diabetes
- High blood pressure
- Excessive consumption of alcohol, cigarette or stimulant drugs,
including caffeine.
Pathogenesis
Atrial fibrillation is caused by multiple re-entrant circuits or
"wavelets" of activation sweeping around the atrial myocardium. These
are often triggered by rapid firing foci. Conduction of atrial impulses
to the ventricles is variable and unpredictable. Only a few of the
impulses transmit through the atrioventricular node to produce an
irregular ventricular response. Wavelength is critical in the
pathogenesis of AF. Increased wavelength may prevent or end AF. This can
be produced by antiarrhythmic drugs.
- Paroxysmal AF is characterized by brief episodes of the
arrhythmia, which can resolve by themselves.
- In persistent AF, the episodes require some form of intervention
to return the heart rhythm back to normal.
- For those with permanent AF, intervention (if successful at all)
only restores normal heart rhythm for a brief time.
As the uncoordinated atrial depolarizations from various places
within the atria in AF causes blood in the upper chambers of the heart
not to be carried through in a regular manner, there is a tendency for
blood clots to form in these chambers. These clots may then be swept
into the ventricles and pumped into the lungs from the right side of the
heart and into the general circulation from the left ventricle.
Sometimes, clotted blood dislodges from the atria and results in a
stroke.
Symptoms and signs
The symptoms of atrial fibrillation (AF) include palpitations,
irregular heart beat, shortness of breath, chest discomfort, dizziness
and syncopal attacks. Many patients experience feelings of weakness,
exercise intolerance, caused by the heart’s diminished pumping ability.
The awareness of a rapid and/or irregular heart beat also may lead to
anxiety.
Systemic embolization may result as well as precipitation or
intensification of heart failure.
Patients who have otherwise healthy hearts may be better able to
tolerate AF. People with underlying heart disease are generally less
able to tolerate AF without complication. Once AF becomes symptomatic,
it becomes more serious as it indicates that the heart is failing to
pump adequate amounts of blood to the body.
The ventricular rate depends on the degree of atrioventricular block,
but when 1:1 conduction occurs a rapid ventricular response may result.
Increasing the degree of block with carotid sinus massage or adenosine
may aid the diagnosis.
Complications
- Stroke: The relative risk for the development of stroke
can be determined by assessing the patient's CHADS2 score.
- Heart failure: Heart failure and pulmonary edema can be
precipitated or aggravated by AF.
- Cardiac ischemia: Tachy-arrhythmia can precipitate
ischemic heart disease.
Diagnosis
Atrial fibrillation can be strongly suspected simply by feeling the
pulse, but a complete diagnosis calls for full medical investigation.
EKG
One of the most important tests is the electrocardiograph (EKG),
which can also give evidence of any previous heart disease that may have
been the cause of the condition. If the AF is intermittent, it may be
necessary for the patient to wear a Holter monitor for an extended
period of time in order to catch one or more episodes of AF. Often the
EKG and Holter are used in conjunction with a chest x-ray and
echocardiogram, which shows the heart walls as they are beating. EKG
features in AF include:
- P waves absent; oscillating baseline f (fibrillation) waves
- Atrial rate 350-600 beats/min
- Irregular ventricular rhythm
- Ventricular rate 100-180 beats/min
Fast atrial fibrillation may be difficult to distinguish from other
tachycardias. The RR interval remains irregular, however, and the
overall rate often fluctuates. Mapping R waves against a piece of paper
or with calipers usually confirms the diagnosis.
Imaging
A chest X-ray
in a young patient may suggest the presence of congenital heart disease. In an older patient it can give
information on the size of the heart and whether heart failure is
present. The echocardiogram is useful in ruling out thrombus formation
as well as determining the diameter of the left atrium (> 4.5 cm).
Blood tests
Routine blood tests can also be useful in the diagnosis. They may
show anemia, which may be complicating the situation, impaired kidney
function, or thyroid gland overactivity (thyrotoxicosis).
Treatment
Left untreated, the overactive heart muscle can weaken and stretch
out. This makes it harder for the atria to contract properly, so blood
backs up even more. This problem not only increases the risk of stroke,
but it can also lead to congestive heart failure. Treating AF correctly
is the best way to reduce stroke risk. Therapy is indicated in patients
with persistent, permanent or recurrent paroxysmal AF. The goals of treatment plans for
AF are:
- Prevent blood clots from forming
- Heart rate control within a relatively normal range
- Restore a normal heart rhythm, if symptomatic
1. Medicine to prevent clots
To lower the risk of stroke either aspirin or Warfarin are generally
prescribed. Aspirin has an antiplatelet effect and is less likely to
cause abnormal bleeding, but Warfarin seems to be more effective at
preventing clot-caused strokes. Regular INR tests are carried out to
monitor the dose of Warfarin. INR should usually test between 2.0 and
3.0.
The choice of giving a patient Warfarin or aspirin depends on the
patient's risk factors for development of thromboembolic disease. This
can be determined by assessing a patient's CHADS2 score.[5]
- CHF (1 point)
- Hypertension (1 point)
- Age 75 (1 point)
- Diabetes (1 point)
- Second stroke (2 points)
A patient with a low score (0) can receive aspirin 325 mg daily for
prophylaxis against coagulation. Those with an intermediate score (1-2)
can receive either aspirin or Warfarin depending on the patient's
preference. Those with a high CHADS2 score (3 or more) should receive
Warfarin prophylaxis to maintain an INR of 2.0-3.0, unless
contraindicated (e.g., history of falls, clinically significant GI
bleeding, inability to obtain regular INR screening).
2. Rate control
- Beta-blockers (like metoprolol, carvedilol or propanolol) and
calcium-channel blockers (like verapamil or diltiazem), which slow
the heart rate;
- Digoxin, which slows the heart rate through the AV node,
therefore decreasing the rate at which the electrical impulses
conduct from the atria to the ventricles.
- In cases who are refractory to the above measures or in those
with heart failure or pre-exitation syndrome, use amiodarone,
consider cardiac consultation,
3. Rhythm control (cardioversion)
Cardioversion changes an abnormal heart rate back to a normal one.
Cardioversion can be done through medication or through electricity.
Based on the AFFIRM, RACE and STAF trials rate control with
anticoagulation is the preferred treatment. Rhythm control
(cardioversion) in asymptomatic patients does not appear to affect
survival. Electrical or chemical cardioversion may be required in
symptomatic cases or in emergency situations such as those with
cardiovascular instability and heart failure.
Medicines include amiodarone, dofetilide, disopyramide, flecainide
and procainamide.
Electrical cardioversion is typically used to treat cases of persistent
or permanent AF, and it is often used with medication.
There are two types of electrical cardioversion: external and
internal. For external cardioversion, two external paddles are placed on
the patient’s chest or on the chest and back. A high-energy electrical
shock is sent through the patches, through the body to the heart. The
energy shocks the heart out of AF and back into normal rhythm.
Internal cardioversion uses a similar approach, but instead of using
paddles on the outside of the body, a catheter is inserted through a
vein to the heart. The electrical energy is delivered through the
catheter to the inside of the heart to stop the AF. Internal
cardioversion has met with high success and provides an alternative to
external cardioversion.
4. Ablation
Cardiac ablation is a medical procedure performed to prevent abnormal
electrical impulses from ever beginning in the first place. In an
ablation procedure, the electrophysiologist first does mapping, which
means the precise area in the heart at which the abnormal signals start
are pin-pointed. The electrophysiologist then eliminates the small area
of tissue that is causing the arrhythmia.
There is also a procedure called AV nodal ablation. This involves
ablating the AV node, keeping the abnormal impulses from traveling to
the heart’s lower chambers. A pacemaker is used to regulate the
heartbeat after this therapy.
5. AF Suppression
AF Suppression is designed to suppress atrial fibrillation (AF). An
implanted pacemaker stimulates the heart in a way that preempts any
irregular rhythms.
A clinical study has found that a software-based AF Suppression
algorithm can suppress symptomatic paroxysmal and persistent AF better
than standard pacing. The AF Suppression algorithm is available in
certain ICDs and pacemakers manufactured by St. Jude Medical.
Prognosis and survival
Prognosis is related to the underlying cause; it is excellent when
due to idiopathic atrial fibrillation and relatively poor when due to
ischemic cardiomyopathy. Healthy life style, regular checks on blood
pressure and treatment for raised blood pressure can reduce the chances
of developing the heart problems that cause atrial fibrillation.
Some study results
Among people with atrial fibrillation who not are taking the
anticoagulant drug Warfarin, women are more likely to form dangerous
blood clots than men, according to a study.
Men who explode with anger or expect the worst from people are more
likely to develop an irregular heart rhythm called atrial fibrillation,
according to another study report.
References
1. Fuster V, Rydén LE, Cannom DS, et al (2006). "ACC/AHA/ESC 2006
Guidelines for the Management of Patients with Atrial Fibrillation: a
report of the American College of Cardiology/American Heart Association
Task Force on Practice Guidelines and the European Society of Cardiology
Committee for Practice Guidelines (Writing Committee to Revise the 2001
Guidelines for the Management of Patients With Atrial Fibrillation):
developed in collaboration with the European Heart Rhythm Association
and the Heart Rhythm Society". Circulation 114 (7): e257-354.
2. Go AS, Hylek EM, Phillips KA, et al (2001). "Prevalence of diagnosed
atrial fibrillation in adults: national implications for rhythm
management and stroke prevention: the AnTicoagulation and Risk Factors
in Atrial Fibrillation (ATRIA) Study". JAMA 285 (18): 2370–5.
3. Furberg CD, Psaty BM, Manolio TA, Gardin JM, Smith VE, Rautaharju PM
(1994). "Prevalence of atrial fibrillation in elderly subjects (the
Cardiovascular Health Study)". Am. J. Cardiol. 74 (3): 236-41.
4. Go AS, Hylek EM, Phillips KA, Chang Y, Henault LE, Selby JV, Singer
DE (2001). "Prevalence of diagnosed atrial fibrillation in adults:
national implications for rhythm management and stroke prevention: the
AnTicoagulation and Risk Factors in Atrial Fibrillation (ATRIA) Study".
JAMA 285 (18): 2370-5.
5. Gage BF, Waterman AD, Shannon W, Boechler M, Rich MW, Radford MJ
(2001). "Validation of clinical classification schemes for predicting
stroke: results from the National Registry of Atrial Fibrillation". JAMA
285 (22): 2864-70.
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