Atrial Fibrillation

Atrial fibrillation is the most common abnormal heart rhythm in older people. An irregularly erratic pulse characterizes the arrhythmia. Rare in children and adolescents, its incidence increases with age from approximately 0.2% to 0.3% in individuals less than 40 years of age, to 5% in the 50-59 year old age group, to 10% among those 80 to 89 years old. In the United States, more than one and a half million persons are estimated to suffer from atrial fibrillation. The heartbeat can be too fast (high pulse rate) or too slow (low pulse rate). In atrial fibrillation, the atrial and ventricular contractions are not synchronized together. The atria may be contracting at greater than 300 beat per minutes. The electrical signals from the atria must pass through tissue called the AV or atrioventricular node. The tissue is located between the atrial and the ventricles. The AV node acts as a rate controlling device only allowing a certain number of electrical signals to past to the ventricle per minute. Therefore only some of these electrical signals to travel down the conduction pathway and stimulate the ventricles. Consequently, the heart rhythm is irregular and erratic.

Atrial fibrillation often causes a sensation of pounding or fluttering in the chest. A person may feel tired and sluggish, and climbing a short flight of stairs may make then dizzy and short of breath. They may also feel faint and experience heart palpitations (noticeable irregular heartbeats). Many people with atrial fibrillation, however, have no symptoms at all. The course of atrial fibrillation over time is variable and unpredictable. Often it occurs with episodes lasting from minutes to hours, revert spontaneously, and recur infrequently. In some persons, the episodes strike months or years apart. In many patients the episodes become more frequent and longer in duration as the time passes. For some , atrial fibrillation eventually becomes the dominant atrial rhythm.

The basic cause of atrial fibrillation is not known. Atrial fibrillation is often associated with a variety of diseases affecting the atria - coronary heart disease, hypertension, mitral valve prolapse, congestive heart failure, rheumatic heart disease, cardiomyopathy, congenital atrial malformations, and metabolic diseases. Alcohol and drug use-and especially withdrawal-are often associated with atrial fibrillation in the young and mid-adult years. "Lone" atrial fibrillation refers to atrial fibrillation that occurs in the absence of known structural heart disease or hypertension, and accounts for about 10% of cases.

Although atrial fibrillation can cause serious circulatory problems, the risk of cerebral embolism and stroke is the most feared complication. In the general population, atrial fibrillation has been shown an independent risk factor for shortened life expectancy and stroke. In many patients, this is due to the increased risk of clot formation in the atria. If left atrial clots fragment and detach, they can pass to the left ventricle and into the arterial circulation. The clots may be stuck and occlude an artery, a process known as arterial embolism. When embolic then lodge occlude a brain artery, a stroke may ensue. The overall risk of stroke increases with age and the coexistence of cardiovascular disease, but the presence of atrial fibrillation raises the risk even further. Clots may also occlude arteries in the limbs or other vital organs and necessitate emergency surgery to remove the clot and restore blood flow.

Persons with atrial fibrillation can have heart rates that are too fast or too slow. A rapid rate can make the person feel uncomfortable, get short of breath, have chest pain, or even lose consciousness. Medications can slow conduction through the atrioventricular node and thereby slow the rate of contraction of the ventricles and the pulse. In some patients the heart rate can be too fast at times and too slow at other times. This combination of rhythm abnormalities is so common that it has a name, "tachycardia-bradycardia syndrome", or "tachy-brady syndrome" for short. For these patients combination therapy of a permanent pacemaker to assure adequate heart rate and medication to keep the heart from being too fast may be needed. Tachy-brady syndrome accounts for about 25% of all pacemakers that are implanted in the United States each year. In difficult cases, destruction of the atrioventricular node with radiofrequency ablation followed immediately with implantation of a permanent pacemaker works very well to achieve rate control and may allow the discontinuation of some medications.

People usually feel better when their hearts are in "normal sinus rhythm" than when their hearts are in atrial fibrillation. Sometimes, atrial fibrillation will stop by itself. When it does not, it often can be converted with "antiarrhythmic" medications over a day or two. When these do not work, or when circumstances do not favor use of antiarrhythmic medications, the rhythm can be converted in most cases with electrical cardioversion. It is very important to realize that blood clots form on the walls of the atria during atrial fibrillation. When normal sinus rhythm is restored, these can break off the walls and fly into the brain or elsewhere in the body, causing strokes or other catastrophic problems. The risk of such events is about 5% or less of all "unprotected" cardioversions. Hence cardioversion for atrial fibrillation that has been present for more than 24 to 48 hours. Is rarely performed in this country unless the patient has been taking the anticoagulant warfarin for three or four weeks. After cardioversion, anticoagulant medication should be continued for another three to six weeks and sometimes indefinitely because the atria sometimes don't contract mechanically for some time after the electrical abnormality has been corrected.

Maintaining normal sinus rhythm after conversion from atrial fibrillation is difficult. Patients have a 70 to 80 % chance of returning to atrial fibrillation by the end of one year if not treated. Antiarrhythmic drugs reduce the chances to 30 to 50% of returning to atrial fibrillation. However, there is strong evidence that antiarrhythmic drugs may cause more deaths in these patients than if they were not treated at all with antiarrhythmic drugs. The management of atrial fibrillation with antiarrhythmic drugs should only be attempted by physicians who have broad experience in antiarrhythmic drugs.

Surgical and ablative methods have been reported for the cure of atrial fibrillation. Texas Arrhythmia Institute currently does not recommend these procedures due to the involved and often risky nature and unproven long-term outcome of these procedures. Atrial defibrillators have been developed that can detect and convert atrial fibrillation to sinus rhythm automatically. These devices are implanted like other ICD's under the skin. There are problems with the usage of current atrial defibrillators. The current levels of energies shocks required to cardiovert atrial fibrillation hurt. A more serious potential problem though not apparently reported in recent experience is the possibility of shocks in the atria causing ventricular fibrillation. It might be desirable to have ventricular defibrillation safety backup which would require a more complicated device. More the question is whether the clinical utility of such a device warrants its use to treat a normally non-life-threatening problem. There is growing evidence supporting the use of an atrial defibrillator in selected patients. While the atrial defibrillator is an exciting technology, it is unclear yet whether it will prove useful in patients.

As noted above, patients with atrial fibrillation are at increased risk for stroke and in general the risk is 3 to 6 % per year. The risk increases with age over 65 and the presence of hypertension, heart failure, previous stroke or blood clot, myocardial infarction, diabetes, mechanical valves and mitral stenosis. Several excellent studies suggest that this risk can be reduced by administering anticoagulant such as warfarin. Generally is has been suggested that persons under age 65 without any of the listed risks for stroke should take aspirin. Persons over age 65 and less than 75 without any of the listed risks should take either warfarin or aspirin depending on the patient. Person over the age of 75 should take warfarin. There has been no distinction in stroke risk between chronic atrial fibrillation and a more intermittent form of atrial fibrillation. Generally the target level for anticoagulation is an INR of 2 to 3 unless patient has mechanical valves then 2.5 to 3.5. INR should be followed instead of the simple PT measurements because of the lesser variability of the INR.

Atrial Fibrillation Links