Atrial fibrillation overview
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Sinus rhythm  |
Atrial fibrillation  |
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Special Groups | |
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Diagnosis | |
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Treatment | |
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Cardioversion | |
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Anticoagulation | |
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Surgery | |
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Case Studies | |
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Atrial fibrillation overview On the Web | |
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Directions to Hospitals Treating Atrial fibrillation overview | |
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Risk calculators and risk factors for Atrial fibrillation overview | |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Cafer Zorkun, M.D., Ph.D. [2] Anahita Deylamsalehi, M.D.[3]
Overview
Atrial fibrillation (AF or afib) is a cardiac arrhythmia (abnormal heart rhythm) that involves the two upper chambers (atria) of the heart. Atrial fibrillation is an irregularly irregular heart beat due to chaotic firing of the impulses in the atrium. In this rhythm, the atrium is stimulated chaotically by a wide number of ectopic foci of electrical activity. Although several clinical classification plans and protocols have been proposed, none of them fully account for all aspects of atrial fibrillation. The American Heart Association, American College of Cardiology, and the European Society of Cardiology have proposed a classification system based on simplicity and clinical relevance. This classification system contains four main categories which are: first detected or diagnosed, paroxysmal, persistent, and permanent atrial fibrillation. In atrial fibrillation, the normal electrical impulses that are generated by the sinoatrial node are overwhelmed by disorganized electrical impulses that originate in the atria and pulmonary veins, leading to conduction of irregular impulses to the ventricles. This results into an irregular heartbeat which may occur in episodes lasting from minutes to weeks or continuously for many years.The most common cause of atrial fibrillation is atrial dilation associated with hypertension. Approximately 1/3 of patients have familial atrial fibrillation which is due to an underlying genetic disorder. Given the number of patients who undergo coronary artery bypass grafting in the developed world, this is an increasing underlying cause of atrial fibrillation. Other general causes include: the advancing age of the population, the hemodynamic stress of heart failure and valvular heart disease, myocardial ischemia, a variety of inflammatory disorders, pulmonary diseases, alcohol and drug abuse, and endocrine disorders.Atrial fibrillation must be distinguished from other common atrial arrhythmias which include atrial flutter, atrial tachycardia, atrioventricular nodal reentry tachycardia, paroxysmal supraventricular tachycardia, and Wolff-Parkinson-White syndrome. AF is the most common arrhythmia. The risk of atrial fibrillation increases with age, and 8% of people over the age of 80 have AF. It accounts for 1/3 of hospital admissions for cardiac rhythm disturbances,[1] and the rate of admissions for AF has risen in recent years. Atrial fibrillation (AF) affects millions of people, and the number increases with increasing age. Men are more likely than women to have the condition. In the United States, AF is more common among Caucasians than African-Americans or Hispanic Americans. The risk of AF increases with age. This is mostly because the risk for heart disease and other conditions that can cause AF also increases with increasing age. Screening for atrial fibrillation is generally not performed, although a study of routine pulse checks or electrocardiograms during routine office visits found that the annual rate of detection of atrial fibrillation in elderly patients improved from 1.04% to 1.63%. Atrial fibrillation can be complicated by embolic events including stroke and systemic embolization. The atrial kick (active filling of the left ventricle by atrial contraction) often contributes importantly to the filling of the left ventricle, and the loss of the atrial kick can be associated with the development of congestive heart failure. Atrial fibrillation is often asymptomatic, and is not in itself generally life-threatening, but may result in palpitations, fainting, chest pain, or congestive heart failure. The absence of P waves on the electrocardiogram with an irregularly irregular atrial rhythm is diagnostic of atrial fibrillation. Performing an echocardiogram in the setting of atrial fibrillation is essential to evaluate certain pathologies of the heart such as valvular heart disease, hypertrophy, presence of thrombus, presence of pericardial disease; some parameters of cardiac functionality including the size and ejection fraction of the left ventricle. Atrial fibrillation may be treated with medications which either slow the heart rate or revert the heart rhythm back to normal sinus rhythm. Synchronized electrical cardioversion may also be used to convert AF to a normal heart rhythm. Surgical and catheter-based therapies may also be used to prevent recurrence of AF in certain individuals. People with AF are often given anticoagulants such as warfarin to reduce the risk of stroke.
Historical Prespetive
The first time atrial fibrillation was described was between 1696 and 2598 BC by a Chinese physician named Huang Ti. He described atrial fibrillation as a disease with irregular pulses and tremulous beats. William Harvey was the first one who found out atrium as the origin of the abnormal pulse in 1628. Jean-Baptiste de Senac (1693–1770) and Robert Adams (1827) were the first who mentioned atrium as the main origin of atrial fibrillation. For the first time in 1894 Theodor Wilhelm Engelmann introduced multi foci origins of irregular pulses in the atrial fibrillation. Disappearance of presystolic ‘a’ wave in the jugular phlebogram was first detected by Mackenzie (1853–1925). First time in 1906 an electrical tracing (ECG) of atrial fibrillation was published by Einthoven. William Withering was the first one who introduced the therapeutic properties of the digitalis leaf (digitalis purpurea) in 1785.
Classification
Although several clinical classification plans and protocols have been proposed, none of them fully account for all aspects of atrial fibrillation. Previously the American Heart Association (AHA), American College of Cardiology (ACC), and the European Society of Cardiology (ESC) had proposed a classification system based on simplicity and clinical relevance. More recently, another classification has been proposed by a task force writing group which composed of experts representing seven organizations: the American College of Cardiology (ACC), the American Heart Association (AHA), the Asia Pacific Heart Rhythm Society (APHRS), the European Cardiac Arrhythmia Society (ECAS), the European Heart Rhythm Association (EHRA), the Society of Thoracic Surgeons (STS), and the Heart Rhythm Society (HRS). Still there are some shared definitions in almost all classification systems. Atrial fibrillation that terminates spontaneously or with intervention within 7 days of onset is considered a paroxysmal atrial fibrillation. On the other hand atrial fibrillation that lasts more than 7 days is named persistent atrial fibrillation. Long standing (or permanent) atrial fibrillation is referred to a atrial fibrillation that lasts for more than a year.
Pathophysiology
Numerous triggers such as sympathetic or parasympathetic stimulation, ectopic activity in muscular sleeves, atrial stretch, premature atrial beats and accessory AV (atrio-ventricular) pathways have been responsible in initiation of atrial fibrillation. Younger patients with paroxysmal atrial fibrillation may have ectopic foci of electrical activity in the pulmonary vein. While the pulmonary vein is a common source of these ectopic foci, there may also be foci present in the atrium itself. Unfortunately the reason why the pulmonary vein turns to an arrhythmogenic foci is not fully understood. It seems that structure of the pulmonary vein makes it potential for re-entry formation which can lead to atrial fibrillation. Presence of the aformentioned triggers produce re-enterant wavelets of electrical activity due to shortened effective refractory period (ERP). Furthermore mechanosensitivity of cardiac myocytes is thought to play a pivotal role in initiation of atrial fibrillation. Mechanisms such as altered myocyte stress/strain, catecholamine release secondary to atrial stretch and activation of G-protein coupled pathways have been introduced in the pathogenesis of atrial fibrillation. Dilatation of the atria can be due to structural abnormalities such as hypertension, valvular heart disease and congestive heart failure that can cause a rise in the intra-cardiac pressures. Once dilatation of the atria has occurred, this begins a chain of events that leads to the activation of the renin aldosterone angiotensin system (RAAS) and subsequent increase in matrix metaloproteinases and disintegrin, which leads to atrial remodeling and fibrosis, with loss of atrial muscle mass. In addition any inflammatory state that affects the heart can cause fibrosis of the atria. This is typically due to sarcoidosis but may also be due to autoimmune disorders that create autoantibodies against myosin heavy chains. There are numerous evidences for presence of a relationship between autonomic nervous system and it's function and the atrial electrophysiology and atrial fibrillation development. Multiple associated genes to atrial fibrillation have been found. Connexin 40, potassium voltage-gated channels, natriuretic peptide precursor A and lamin A/C are some of the known genes that are related to atrial fibrillation pathogenesis. The presence of atrial fibrillation often reflects the presence of an underlying cardiac or lung disease. Indeed, the proportion of patients with lone atrial fibrillation is low (approximately 12% of cases). On gross pathology atrial enlargement has been found with echocardiographic evaluations as a consequence of atrial fibrillation. On microscopic pathology lateralization of gap junctional proteins (such as connexin 43 (Cx43), connexin 40 (Cx40) and N-cadherin) have been found. Furthermore there is an approximately 57% reduce in connexin 43 (Cx43) in right atrium appendages and walls.
Causes
The most common cause of atrial fibrillation is atrial dilation associated with hypertension. Atrial fibrillation can be caused by several organic cardiac diseases, but it has also been reported to have a familial etiology in some patients. Approximately 1/3 of patients have familial atrial fibrillation which is due to an underlying genetic disorder. In developed countries, hypertensive heart disease and coronary heart disease are the two most common causes of atrial fibrillation. However, rheumatic heart disease is associated with a higher incidence of atrial fibrillation in developing countries. Life threatening conditions such as acute coronary syndromes, electrolyte imbalance, dehydration, hypoxia, pulmonary embolism, myocarditis and pericarditis should be identified and promptly treated. Other general causes such as the advancing age of the population, the hemodynamic stress of heart failure and valvular heart disease, myocardial ischemia, a variety of inflammatory disorders, pulmonary diseases, alcohol, drug abuse, and endocrine disorders.
Differentiating Atrial Fibrillation from other Diseases
Atrial fibrillation has to be differentiated from other diseases such as atrial flutter, atrial tachycardia, atrioventricular nodal reentry tachycardia (AVNRT), multifocal atrial tachycardia, paroxysmal supraventricular tachycardia and Wolff-Parkinson-White syndrome. The differentiating features are largely based on both EKG findings and cardiovascular examinations.
Epidemiology and Demographics
Incidence of atrial fibrillation is approximately less than 0.1% per year in those under 40 years of age. On the other hand incidence rate increases to greater than 1.5% per year in women over 80 age and greater than 2% per year in men over 80 years of age. The atrial fibrillation prevalence in the general population is 0.4%. Prevalence of atrial fibrillation has been estimated to be even more, since many cases of atrial fibrillation remain asymptomatic for a long time. Atrial fibrillation is associated with a 1.5 to 1.9 fold increase in the risk of death. The incidence of atrial fibrillation increases with age (median age of 75 years). Prevalence of atrial fibrillation has been reported to be higher among Caucasians (European ancestry) and it is more common in males compared to females.
Risk Factors
Numerous risk factors have been found for atrial fibrillation. There are some reversible risk factors such as alcohol drinking and alcohol withdrawal, caffeine, cocaine, stimulant and smoking. Furthermore risk factors such as hypertension, diabetes, obesity and sedentary lifestyle can be considered as reversible conditions that can increase the chance of atrial fibrillation development. On the other hand risk factors such as hypertrophic obstructive cardiomyopathy, heart failure, chronic renal failure and positive familial history have been introduced as irreversible risk factors in atrial fibrillation. There are also conditions that have been recognized as risk factors for ischemic stroke or systemic embolization in patients with non-valvular atrial fibrillation, such as advanced age, impaired left ventricular systolic function, hypertension and diabetes. Male sex, diuretic use and cardiac or thoracic surgery are also among other known risk factors.
Screening
Early diagnosis of atrial fibrillation and proper prophylactic treatment can prevent numerous related complications, such as stroke and mortality. Since patients older than 65 are more prone to atrial fibrillation and the aforementioned complications, it has been recommended to perform screening at least in this age group. Electrocardiogram (12-lead ECG) has been introduced as the gold standard method for atrial fibrillation screening. Nevertheless atrial fibrillation screening can be done by simply checking pulse. The other reason to support atrial fibrillation screening is the cost effectiveness of it.
Natural History, Complications and Prognosis
The natural tendency of atrial fibrillation is to become a chronic condition. Based on epidemiological studies atrial fibrillation starts as the paroxysmal form and then evolves to the permanent form eventually in some cases. Numerous complications in association to atrial fibrillation (such as impaired cardiac output, stroke, heart failure and Cognitive disturbances) have been recognized. Although after introduction of anticoagulant treatment rate of stroke and consequently risk of death have been decreased. In a study done on Swedish patients with atrial fibrillation risk of stroke is 25 per 1,000 person/year in patients treated with anticoagulants, compared to 45 per 1,000 person/year risk of stroke in AF patients who didn't received anticoagulant therapy. The occurrence of atrial fibrillation in the setting of ST elevation MI is associated with a poor prognosis including a 40% rise in the risk of mortality in meta-analyses.
Diagnosis
History and Symptoms
Atrial fibrillation is often asymptomatic, and is not in itself generally life-threatening, but may result in palpitations, fainting, chest pain, or congestive heart failure.
Physical Examination
Atrial fibrillation is often be identified by taking the pulse and observing that the heartbeats occur at regular intervals. The pulse is classically irregularly irregular.
Electrocardiogram
The absence of P waves on the electrocardiogram with an irregularly irregular atrial rhythm is diagnostic of atrial fibrillation.
Chest X-Ray
A chest X-ray is useful in the setting of atrial fibrillation only when the cause is suspected to be pulmonary in origin.
Echocardiogram
Performing an echocardiogram in the setting of atrial fibrillation is essential to evaluate certain pathologies of the heart such as valvular heart disease, hypertrophy, presence of thrombus, presence of pericardial disease; some parameters of cardiac functionality including the size and ejection fraction of the left ventricle.
Cardiac MRI
Cardiac magnetic resonance imaging may be used to assess the structure and the function of the atria in patients with atrial fibrillation. It is also useful in the evaluation of atrial thrombi in persons with atrial fibrillation.
Other Imaging Studies
Other diagnostic studies include the holter monitor to assess symptomatic episodes of atrial fibrillation over a 24 hour period, and exercise stress testing to assess a how a patient's heart rate responds to exertion. The main benefits to performing an exercise stress test are to reproduce exercise induced atrial fibrillation, and to exclude ischemia before initiating treatment with type 1C antiarrhythmic medications.
Treatment
Atrial fibrillation may be treated with medications which either slow the heart rate or revert the heart rhythm back to normal sinus rhythm. Synchronized electrical cardioversion may also be used to convert AF to a normal heart rhythm. Surgical and catheter-based therapies may also be used to prevent recurrence of AF in certain individuals. People with AF are often given anticoagulants such as warfarin to reduce the risk of stroke.
Among patients in whom there is normal atrioventricular conduction, fibrillatory or irregular impulses that vary in timing, amplitude and shape are present which are in turn associated with the rapid irregular ventricular response that characterizes atrial fibrillation.
Cardioversion
Cardioversion is a medical procedure by which an abnormally fast heart rate (tachycardia) or cardiac arrhythmia is converted to a normal rhythm, using electricity or drugs.
Anticoagulation
Oral anticoagulation is a mainstay of atrial fibrillation management. For both primary and secondary prevention of stroke, there is a 61% relative risks reduction in the incidence of all cause stroke (both ischemic and hemorrhagic) associated with adjusted-dose oral anticoagulation.[2]
Rate Control
Atrial fibrillation with rapid ventricular rate is a common finding in many hospitalized patients. The ventricular rate may be increased up to 150-170. It is essential to bring the ventricular rate down to less than 100 because a rapid ventricular response can cause hemodynamic instabilities and tachycardia mediated cardiomyopathies (heart failure). 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. This can significantly increase mortality and morbidity, which can be prevented by early and adequate treatment of the AF.
Rhythm Control
Prophylactic antiarrhythmic drug therapy may be required to maintain sinus rhythm, reduce frequency of symptoms, improve hemodynamic function and exercise capacity and prevent tachycardia-induced cardiomyopathy secondary to atrial fibrillation. In patients with heart failure, pharmacological maintenance of sinus rhythm has shown to reduce morbidity.[3][4]
Surgery
Radiofrequency Ablation
Ablation is a newer technique and has shown some promise for cases of recurrent AF that are unresponsive to conventional treatments. Radiofrequency ablation (RFA) uses radiofrequency energy to destroy abnormal electrical pathways in heart tissue. The energy emitting probe (electrode) is placed into the heart through a catheter inserted into veins in the groin or neck. Electrodes that can detect electrical activity from inside the heart are also inserted, and the electrophysiologist uses these to map an area of the heart in order to locate the abnormal electrical activity before eliminating the responsible tissue.
Maze Procedure
A surgical option for some patients with atrial fibrillation is the maze procedure. In this procedure, a series of incisions in a cross like pattern are made on the atria, which blocks the abnormal atrial circuits, hence eliminating the atrial fibrillation. A number of improvements have been made to this surgical procedure since it was first invented.
Secondary Prevention
In patients with paroxysmal atrial fibrillation, or after conversion of persistent AF, dronedarone is a medication that may be used to decrease the need for hospitalization, and can be started as an outpatient therapy. It cannot be given in patients with class IV heart failure, decompensated heart failure, or depressed left ventricular function. A permanent pacemaker is not recommended in patients who do not have another indication for placement of a pacemaker.
References
- ↑
- ↑ Hart RG, Benavente O, McBride R, Pearce LA (1999). "Antithrombotic therapy to prevent stroke in patients with atrial fibrillation: a meta-analysis". Ann. Intern. Med. 131 (7): 492–501. Unknown parameter
|month=ignored (help) - ↑ Torp-Pedersen C, Møller M, Bloch-Thomsen PE, Køber L, Sandøe E, Egstrup K et al. (1999) Dofetilide in patients with congestive heart failure and left ventricular dysfunction. Danish Investigations of Arrhythmia and Mortality on Dofetilide Study Group. N Engl J Med 341 (12):857-65. DOI:10.1056/NEJM199909163411201 PMID: 10486417
- ↑ Deedwania PC, Singh BN, Ellenbogen K, Fisher S, Fletcher R, Singh SN (1998) Spontaneous conversion and maintenance of sinus rhythm by amiodarone in patients with heart failure and atrial fibrillation: observations from the veterans affairs congestive heart failure survival trial of antiarrhythmic therapy (CHF-STAT). The Department of Veterans Affairs CHF-STAT Investigators. Circulation 98 (23):2574-9. PMID: 9843465