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Treatment For Atrial Fibrillation
. Atrial Fibrillation
Atrial fibrillation Info



Atrial fibrillation

Atrial fibrillation
ICD-10 code: I48
ICD-9 code: 427.31

Atrial fibrillation (AF or afib) is a cardiac arrhythmia (an abnormality of heart rate or rhythm) originating in the atria. Abnormal electrical impulses in the atria cause the ventricles to contract erratically. AF is the most common cardiac arrhythmia. If rapid, it may compromise blood flow and cause fainting, orthostatic hypotension (low blood pressure on standing up) or low blood pressure. In addition, it predisposes to thrombosis and embolism to the brain, being a prime risk factor for stroke, the most feared complication of atrial fibrillation.

Contents

Signs and symptoms

Atrial fibrillation is usually accompanied by symptoms related to either the rapid heart rate or embolization. Rapid and irregular heart rates may be perceived as palpitations, exercise intolerance, and occasionally produce angina and congestive symptoms of shortness of breath or edema. Sometimes the arrhythmia will be identified with the onset of a stroke or a TIA. It is not uncommon to identify atrial fibrillation on a routine physical examination or electrocardiogram.

Paroxysmal atrial fibrillation is the episodic occurence of the arrhythmia and may be difficult to diagnose. Episodes may occur with sleep or with exercise, and their episodic nature may require prolonged ecg monitoring for diagnosis.

Diagnosis

Electrocardiogram

Image:Afib.gif

Atrial fibrillation is diagnosed on an electrocardiogram, an investigation performed routinely whenever irregular heart beat is suspected. Characteristic findings are (a "rhythm strip" of lead II is shown):

  • absence of P waves
  • unorganized electrical activity in their place
  • irregularity of R-R interval due to irregular conduction of impulses to the ventricles

Other investigations

While many cases of AF have no definite cause, it may be the result of various other problems (see below). Hence, renal function and electrolytes are routinely determined, as well as thyroid-stimulating hormone (commonly suppressed in hyperthyroidism and of relevance if amiodarone will be administered) and a blood count. A chest X-ray is generally performed. 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.

Causes

AF is linked to several cardiac causes, but may occur in otherwise normal hearts. Known associations include:

In turn, untreated AF can cause further damage to the heart muscle. This weakened condition, termed chronotropic cardiomyopathy, is usually a result of relatively long term uncontrolled heart rate.

Pathophysiology

In atrial fibrillation, the regular impulses produced by the sinus node to provide rhythmic contraction of the heart are overwhelmed by the rapid randomly generated discharges produced by larger areas of atrial tissue. It can be distinguished from atrial flutter, which is a more organized electrical circuit usually in the right atrium that produces characteristic saw toothed waves on the electrocardiogram.

Often, the rhythm produced is more rapid than normal, but the difficulty is in obtaining control of the heart rate both at rest and with exercise. Good rate control will usually require two drugs, and can only be checked by observing heart rate response to exercise.

An organized electrical impulse in the atrium produces atrial contraction; the lack of such an impulse, as in atrial fibrillation, produces stagnant blood flow, especially in the atrial appendage and predisposes to clotting. The dislodgement of a clot from the atrium results in an embolus, and the damage produced is related to where the circulation takes it. An embolus to the brain produces the most feared complication of atrial fibrillation, stroke, while an embolus may also lodge in the mesenteric circulation (the circulation supplying the abdominal organs) or digit, producing organ-specific damage.

Treatment

Rate and 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. 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 Trial2.

AF can cause a form of heart failure called tachycardia-induced cardiomyopathy. This can significantly increase mortality and morbidity. The early treatment of AF through either rate-control or rhythm-control can prevent this condition and thereby improve mortality and morbidity.

Rate control

Rate control methods include:

In refractory cases where none of the above drugs are sufficient, amiodarone may be used, accepting the small risk of their toxicities.

These medications work by slowing the generation of impulses from the atria and the conduction of those impulse from the atria to the ventricles.

In patients with AF where rate control drugs are ineffective and it is not possible to restore sinus rhythm using cardioversion, non-pharmacological alternatives are available. For example, to control rate it is possible to destroy the bundle of cells connecting the upper and lower chambers of the heart - the atrioventricular node - which regulates heart rate, and to implant a pacemaker instead. A more complex technique involves ablating groups of cells near the pulmonary arteries where atrial fibrillation is thought to originate.

Rhythm control

Rhythm control methods include electrical and chemical cardioversion:

The anti-arrhythmic medications often used in either pharmacological cardioversion or in the prevention of relapse to AF alter the flux of ions in heart tissue, making them less excitable, setting the stage for spontaneous and durable cardioversion. These medications are often used in concert with electrical cardioversion. However, 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.2.

Whichever method of cardioversion is used, approximately 50% of patient relapse within one year, although the continued daily use of oral antiarrhythmic drugs may extend this period. The key risk factor for relapse is duration of AF, although other risk factors that have been identified include the presence of structural heart disease, and increasing age.

Radiofrequency ablation

Radiofrequency ablation (RFA) uses radiofrequency energy to destroy abnormal electrical pathways in heart tissue. It is used in recurrent AF. The energy emitting probe (electrode) is placed into the heart through a catheter. The practitioner first "maps" an area of the heart to locate the abnormal electrical activity before the responsible tissue is eliminated. Ablation is a newer technique and has shown some promise for cases unresponsive to conventional treatments. New techniques include the use of cryoablation (tissue freezing using a coolant which flows through the catheter), and microwave ablation, where tissue is ablated by the microwave energy "cooking" the adjacent tissue. The abnormal electrophysiology can also be modified in a similar way surgically, and this procedure referred to as the "Cox maze procedure", is commonly performed concomitantly with cardiac surgery.

This is an area of active research, especially with respect to the RF ablation technique and emphasis on isolating the pulmonary veins that enter into the left atrium.

Anticoagulation

In confirmed AF, anticoagulant treatment is a crucial way to prevent stroke. Treatment of AF patients over age 60 with warfarin (also known as Coumadin®) results in a significant reduction in the subsequent risk of stroke. Patients under age 65 who have any structural heart disease (ie: valvular heart disease, ejection fraction <= 35%, history of heart attack) also benefit from warfarin. Patients under age 65 who do not have structural heart disease do not require warfarin, and can be treated with aspirin1. Other guidelines are also used. The new anticoagulant ximelagatran has been shown to prevent stroke with equal efficacy as warfarin, without the difficult monitoring process associated with warfarin and with possibly fewer adverse haemorrhagic events. Unfortunately, ximegalatran and other similar anticoagulant drugs (commonly referred to as direct thrombin inhibitors), have yet to be widely licensed. License applications made by AstraZeneca, who developed Ximegalatran, have been rejected by both American and European licensing authorities, and its evaluation has been suspended in the UK. This is primarily due to concerns over possible liver toxicity.

References

  • Note 1: Fuster V, Ryden LE, Asinger RW, Cannom DS, Crijns HJ, Frye RL, Halperin JL, Kay GN, Klein WW, Levy S, McNamara RL, Prystowsky EN, Wann LS, Wyse DG, Gibbons RJ, Antman EM, Alpert JS, Faxon DP, Fuster V, Gregoratos G, Hiratzka LF, Jacobs AK, Russell RO, Smith SC, Klein WW, Alonso-Garcia A, Blomstrom-Lundqvist C, De Backer G, Flather M, Hradec J, Oto A, Parkhomenko A, Silber S, Torbicki A; American College of Cardiology/American Heart Association/European Society of Cardiology Board. ACC/AHA/ESC guidelines for the management of patients with atrial fibrillation: executive summary. 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 and Policy Conferences (Committee to Develop Guidelines for the Management of Patients With Atrial Fibrillation): developed in Collaboration With the North American Society of Pacing and Electrophysiology. J Am Coll Cardiol 2001;38:1231-66. ACC/AHA/ESC Fulltext. PMID 11583910.
  • Note 2: Wyse DG, Waldo AL, DiMarco JP, Domanski MJ, Rosenberg Y, Schron EB, Kellen JC, Greene HL, Mickel MC, Dalquist JE, Corley SD; Atrial Fibrillation Follow-up Investigation of Rhythm Management (AFFIRM) Investigators. A comparison of rate control and rhythm control in patients with atrial fibrillation. N Engl J Med 2002;347:1825-33. PMID 12466506.
  • Note 3: Long term management of Atrial Fibrillation

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