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.

Causes of AF

1. Coronary heart disease
2. Congestive heart failure
3. Pericarditis
4. Myocarditis
5. Rheumatic heart disease
6. Hypoxia
7. Hypertrophic cardiomyopathy
8. Hypertensive cardiomyopathy
9. Dilated cardiomyopathy
10. Pulmonary embolism
11. Alcohol
12. Lone atrial fibrillation
13. Thyrotoxicosis
14. Theophylline
15. Blunt trauma
16. Sick sinus syndrome
17. Sympathomimetic toxicity
18. Post-CABG surgery

Risk factors

Risk factors for development of AF include:

1. Those who have had coronary heart disease, heart attack or heart failure.
2. It's also found in people with heart valve disease, an inflamed heart muscle or lining (endocarditis) or
3. Recent heart surgery
4. People with atherosclerosis and angina
5. Congenital heart defects
6. People with chronic lung disease, emphysema and asthma
7. Thyroid disorders
8. Diabetes
9. High blood pressure
10. 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.

• Chemical cardioversion

Medicines include amiodarone, dofetilide, disopyramide, flecainide and procainamide.

• Electrical cardioversion

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.