Atrial Fibrillation
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Wikipedia-Article "Atrial Fibrillation"
| Atrial fibrillation | ||
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| 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, the erratic wall motion of the atria leads to blood stasis which predisposes to thrombosis, leading to embolism of the resulting blood clot to the brain and other areas. AF is a prime risk factor for stroke, the most feared complication of atrial fibrillation.
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Classification
Paroxysmal atrial fibrillation is defined as attacks of arrhythmia lasting less than seven days separated by prolonged periods of sinus rhythm. Chronic AF is AF established for more than seven days. Differentiation of paroxysmal from chronic or established AF is based on the history of recurrent episodes and the duration of the current episode of AF.[1][2]
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 occurrence 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 (e.g. a Holter monitor) for diagnosis.
Diagnosis
Electrocardiogram
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
If paroxysmal AF is suspected, episodes may be documented with the use of Holter monitoring (continuous ECG recording for 24 hours or longer).
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 is administered for treatment) 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:
- High blood pressure
- Mitral stenosis (e.g. due to rheumatic heart disease or mitral valve prolapse)
- Mitral regurgitation
- Heart surgery
- Coronary artery disease
- Hypertrophic cardiomyopathy
- Excessive alcohol consumption ("binge drinking" or "holiday heart")
- Hyperthyroidism
- Hyperstimulation of the vagus nerve, usually by having large meals ("binge eating")
- Lung pathology (such as pneumonia, lung cancer, pulmonary embolism)
- Pericarditis
In turn, AF with a rapid rate that goes untreated can cause further damage to the heart muscle. This weakened condition, termed chronotropic cardiomyopathy, is usually a result of a long period of tachycardia (fast heart rate).
Pathophysiology
The normal electrical conduction system of the heart allows the impulse that is generated by the sinoatrial node (SA node) of the heart to be propagated to and stimulate the myocardium (muscle of the heart). When the myocardium is stimulated, it contracts. It is the ordered stimulation of the myocardium that allows efficient contraction of the heart, thereby allowing blood to be pumped to the body.
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
The main goals of treatment of atrial fibrillation are to prevent circulatory instability (in the short term) and to prevent stroke. Rate and rhythm control are principally used to achieve the former, while anticoagulation may be required to decrease the risk of the latter.[3]
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 Trial (Wyse et al., 2002).
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:
- Beta blockers (e.g. metoprolol)
- Digoxin
- Calcium channel blockers (e.g. verapamil)
In refractory cases where none of the above drugs are sufficient, a variety of other antiarrhythmic drugs, most commonly including quinidine, flecainide, propafenone, disopyramide, sotalol, or amiodarone may be used. Of these, only propafenone, sotalol, and amiodarone (which possess some beta blocking activity) control the ventricular rate; the others may maintain sinus rhythm, but may actually increase the ventricular rate. Many of these drugs are less frequently used today than in the past. All (with the possible exception of amiodarone) increase the risk of ventricular tachycardia, which can be fatal. In symptomatic patients with normal heart function, however, the small increase in risk is usually felt to be acceptable. In the presence of heart failure, the only antiarrhythmic drugs thought to be safe are amiodarone and dofetilide.
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, or creating more extensive lesions in an attempt to prevent atrial fibrillation from establishing itself.
Rhythm control
Rhythm control methods include electrical and chemical cardioversion:
- Electrical cardioversion involves the restoration of normal heart rhythm either through the application of a DC electrical shock (electrical cardioversion)
- Chemical cardioversion is performed with drugs, such as amiodarone, propafenone or flecainide.
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.[4]
The main risk of cardioversion is systemic embolization by a bloodclot from the previously fibrillating left atrium. It should not be performed without adequate anticoagulation in patients who have been in atrial fibrillation for more than 48 hours.
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. More recently, minimally invasive surgical variations on the Cox Maze procedure ("minimaze" procedures) have also been developed.
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.
Cox maze Procedure
James Cox, MD, and associates developed the Cox maze procedure, an open-heart surgical procedure intended to eliminate atrial fibrillation, and performed the first one in 1987. "Maze" refers to the series of incisions made in the atria (upper chambers of the heart), which are arranged in a maze-like pattern. The intention was to eliminate AF by using incisional scars to block abnormal electrical circuits (atrial macroreentry) that AF requires. This procedure required an extensive series of endocardial (from the inside of the heart) incisions through both atria, a median sternotomy (vertical incision through the breastbone) and cardiopulmonary bypass (heart-lung machine). A series of improvements were made, culminating in 1992 in the Cox maze III procedure, which is now considered to be the "gold standard” for effective surgical cure of AF. The Cox maze III is sometimes referred to as the “traditional maze”, the “cut and sew maze”, or simply the "maze".
Minimaze surgical procedures
Minimaze surgery is minimally invasive cardiac surgery intended to cure atrial fibrillation. Minimaze refers to "mini" versions of the original maze procedure. These procedures are less invasive than the Cox maze procedure and do not require a median sternotomy (vertical incision in the breastbone) or cardiopulmonary bypass (heart-lung machine). These procedures use microwave, radiofrequency, or acoustic energy to ablate atrial tissue near the pulmonary veins.
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 (i.e. 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 aspirin.[5] 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 for ximelegatran (made by AstraZeneca) 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.
Prognosis
Atrial fibrillation can usually be controlled with treatment. The natural tendency of atrial fibrillation, however, is to become a chronic condition. Chronic AF leads to an increased risk of death.[6]
Epidemiology
Atrial fibrillation is common among older adults. 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.[7]
References
- ^ Levy S (1998). Epidemiology and classification of atrial fibrillation. J Cardiovasc Electrophysiol 9 (8 Suppl): S78-82. PMID 9727680
- ^ Levy S (2000). Classification system of atrial fibrillation. Curr Opin Cardiol 15 (1): 54-7. PMID 10666661
- ^ Prystowsky EN (2000). Management of atrial fibrillation: therapeutic options and clinical decisions. Am J Cardiol 85 (10A): 3D-11D. PMID 10822035
- ^ Wyse DG, Waldo AL, DiMarco JP, Domanski MJ, Rosenberg Y, Schron EB, Kellen JC, Greene HL, Mickel MC, Dalquist JE, Corley SD (2002). A comparison of rate control and rhythm control in patients with atrial fibrillation. N Engl J Med 347 (23): 1825-33. PMID 12466506
- ^ 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 (2001). 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 38 (4): 1231-66. ACC/AHA/ESC Fulltext PMID 11583910
- ^ Benjamin EJ, Wolf PA, D'Agostino RB, Silbershatz H, Kannel WB, Levy D (1998). Impact of atrial fibrillation on the risk of death: the Framingham Heart Study. Circulation 98 (10): 946-52. PMID 9737513
- ^ 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. PMID 11343485
- Levy S, Breithardt G, Campbell RW, Camm AJ, Daubert JC, Allessie M, Aliot E, Capucci A, Cosio F, Crijns H, Jordaens L, Hauer RN, Lombardi F, Luderitz B (1998). Atrial fibrillation: current knowledge and recommendations for management. Working Group on Arrhythmias of the European Society of Cardiology. Eur Heart J 19 (9): 1294-320. PMID 9792255
- Greenlee RT, Vidaillet H (2005). Recent progress in the epidemiology of atrial fibrillation. Curr Opin Cardiol 20 (1): 7-14. PMID 15596953