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Health See other Health Articles Title: Atrial Fibrillation: Diagnosis and Treatment CECILIA GUTIERREZ, MD, and DANIEL G. BLANCHARD, MD, University of California, San Diego, La Jolla, California Am Fam Physician. 2011 Jan 1;83(1):61-68. Patient information: See related handout on atrial fibrillation, written by the authors of this article. Atrial fibrillation is the most common cardiac arrhythmia. It impairs cardiac function and increases the risk of stroke. The incidence of atrial fibrillation increases with age. Key treatment issues include deciding when to restore normal sinus rhythm, when to control rate only, and how to prevent thromboembolism. Rate control is the preferred management option in most patients. Rhythm control is an option for patients in whom rate control cannot be achieved or who have persistent symptoms despite rate control. The current recommendation for strict rate control is a resting heart rate of less than 80 beats per minute. However, one study has shown that more lenient rate control of less than 110 beats per minute while at rest was not inferior to strict rate control in preventing cardiac death, heart failure, stroke, and life-threatening arrhythmias. Anticoagulation therapy is needed with rate control and rhythm control to prevent stroke. Warfarin is superior to aspirin and clopidogrel in preventing stroke despite its narrow therapeutic range and increased risk of bleeding. Tools that predict the risk of stroke (e.g., CHADS2) and the risk of bleeding (e.g., Outpatient Bleeding Risk Index) are helpful in making decisions about anticoagulation therapy. Surgical options for atrial fibrillation include disruption of abnormal conduction pathways in the atria, and obliteration of the left atrial appendage. Catheter ablation is an option for restoring normal sinus rhythm in patients with paroxysmal atrial fibrillation and normal left atrial size. Referral to a cardiologist is warranted in patients who have complex cardiac disease; who are symptomatic on or unable to tolerate pharmacologic rate control; or who may be candidates for ablation or surgical interventions. Atrial fibrillation is the most common cardiac arrhythmia, and its incidence increases with age.1,2 It affects about 1 percent of patients younger than 60 years and about 8 percent of patients older than 80 years.3 Atrial fibrillation is defined as a supraventricular tachyarrhythmia characterized by uncoordinated atrial activation with consequent deterioration of mechanical atrial function.4 Electrocardiographic findings include the replacement of the normal consistent P waves (which represent synchronous atrial activation) with oscillatory or fibrillatory waves of different sizes, amplitudes, and timing (Figure 1). The QRS complex remains narrow unless other conduction abnormalities exist (e.g., bundle branch block, accessory pathways). The ventricular response is often rapid, between 90 and 170 beats per minute. SORT: KEY RECOMMENDATIONS FOR PRACTICE Clinical recommendation Evidence rating References Rate control is the recommended treatment strategy in most patients with atrial fibrillation. Rhythm control is an option for patients in whom rate control is not achievable or who remain symptomatic despite rate control. A 12–14 Rhythm control of atrial fibrillation through electrical or pharmacologic cardioversion requires anticoagulation therapy three weeks before and four weeks after cardioversion. C 4,17,18 Rate control improves diastolic filling and coronary perfusion, decreases myocardial energy demand, and prevents tachycardia-mediated cardiomyopathy. The goal is to achieve a ventricular response of less than 80 beats per minute at rest and less than 110 beats per minute during exercise. C 4 Warfarin (Coumadin) is more effective than aspirin in preventing thromboembolic events in patients with atrial fibrillation, although it confers a higher risk of bleeding. Warfarin is superior to aspirin plus clopidogrel (Plavix) and confers the same risk of bleeding. Adding full-dose aspirin to warfarin should be avoided because of the increased risk of bleeding. A 23-26 Patients with nonvalvular atrial fibrillation who are at low risk of stroke can be treated with 81 to 325 mg of aspirin per day. C 16 A = consistent, good-quality patient-oriented evidence; B = inconsistent or limited-quality patient-oriented evidence; C = consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, go to www.aafp.org/afpsort.xml. Figure 1 Electrocardiogram showing atrial fibrillation. P waves are absent and replaced by irregular electrical activity. The ventricular rate is irregular and chaotic. Atrial fibrillation is a source of significant morbidity and mortality because it impairs cardiac function and increases the risk of stroke. Its most important clinical implications are shown in Figure 2. The cost of caring for patients with atrial fibrillation is about five times greater than caring for patients without it.5 Atrial fibrillation is an independent risk factor for mortality 6,7; it can also lead to or worsen heart failure and increase mortality rates in patients who have had myocardial infarction.8,9 Clinical Implications of Atrial Fibrillation Figure 2 Flowchart for clinical implications of atrial fibrillation. Pathophysiology Two mechanisms have been identified in triggering and maintaining atrial fibrillation: enhanced automaticity in one or more depolarizing foci, and reentry involving one or more aberrant circuits. If it persists, atrial fibrillation can cause atrial remodeling, which is characterized by patchy fibrosis; abnormal and excessive deposition of collagen; fatty infiltration of the sinoatrial node; molecular changes in ion channels; changes in depolarization pattern and cellular energy use; and apoptosis.10,11 Chronic remodeling leads to irreversible atrial enlargement. The longer the heart remains in atrial fibrillation, the more difficult it is to restore normal sinus rhythm. After a critical point is reached, paroxysmal atrial fibrillation self-perpetuates and becomes persistent.10,11 Definitions Different types of atrial fibrillation have different prognoses, morbidity rates, mortality rates, and treatment options (Table 1).4 For example, valvular atrial fibrillation, which is caused by structural changes in the mitral valve or congenital heart disease, carries the highest risk of stroke (i.e., 17 times that of the general population and five times the risk of stroke with nonvalvular atrial fibrillation).6 Secondary atrial fibrillation is caused by an underlying condition and is reversible if the condition is treated. The most common underlying conditions are listed in Table 2. Atrial fibrillation may occur immediately after cardiac and thoracic surgery. It is usually self-limited, but should be treated aggressively if it persists because of the increased risk of stroke. Lone atrial fibrillation occurs in patients younger than 60 years who have no underlying cardiac disease and no identifiable cause. The prognosis is very good in patients with lone atrial fibrillation. Paroxysmal atrial fibrillation refers to episodes of intermittent atrial fibrillation that terminate spontaneously. Chronic atrial fibrillation is continuous and either cannot be converted back to normal sinus rhythm or a decision has been made not to attempt cardioversion. Persistent atrial fibrillation does not self-terminate, but may be terminated by electrical or pharmacologic cardioversion. Table 1 Classification of Atrial Fibrillation Type of atrial fibrillation Characteristics Chronic/permanent Continuous atrial fibrillation that is unresponsive to cardioversion; cardioversion will not be reattempted Lone Occurs in persons younger than 60 years and in whom no clinical or echocardiographic causes are found Nonvalvular Not caused by valvular disease, prosthetic heart valves, or valve repair Paroxysmal Episodes that terminate spontaneously Persistent Paroxysmal atrial fibrillation sustained for more than seven days, or atrial fibrillation that terminates only with cardioversion Recurrent Two or more episodes of atrial fibrillation Secondary Caused by a separate underlying condition or event (e.g., myocardial infarction, cardiac surgery, pulmonary disease, hyperthyroidism) Information from reference 4. Table 2 Secondary Causes of Atrial Fibrillation Cardiac Cardiothoracic surgery Congenital heart disease Heart failure Infiltrative disease (e.g., amyloid heart disease) Longstanding hypertension Myocardial infarction Myocarditis Pericarditis Valvular disease Wolff-Parkinson-White syndrome Noncardiac Alcoholism Cor pulmonale Drug abuse Hyperthyroidism Pneumonia Pulmonary embolism Sleep apnea Clinical Presentation Atrial fibrillation has a wide spectrum of clinical presentations. Some patients may be asymptomatic. Others may present with stroke, overt heart failure, or cardiovascular collapse. Patients most commonly report palpitations, dyspnea, fatigue, lightheadedness, and chest pain. Because symptoms are nonspecific, they cannot be used to diagnose and determine the onset of atrial fibrillation.4 If electrocardiography does not demonstrate atrial fibrillation and a strong suspicion persists, a Holter or cardiac event monitor may be needed to document the arrhythmia. Evaluation The first goal is to determine the patient's cardiac stability and provide emergency stabilization if needed. If the patient is unstable because of hypotension, ongoing ischemia, severe heart failure, or cerebrovascular events, emergency electrical cardioversion is warranted. If the patient is clinically stable, the history, physical examination, and diagnostic testing should focus on potential causes, triggers, and comorbid conditions. Standard tests used to evaluate cardiac function and identify common comorbid conditions include electrocardiography, complete blood count, complete metabolic profile, thyroid-stimulating hormone measurement, chest radiography, and echocardiography (Table 3). Echocardiography provides information about heart size, chamber sizes, valvular anatomy and function, wall motion abnormalities, systolic and diastolic function, and pericardial disease. If there is clinical suspicion of myocardial ischemia, creatine kinase isoenzyme and troponin levels should be obtained. Select patients may need additional tests, such as stress testing and electrophysiology studies.4 Table 3 Initial Evaluation of Atrial Fibrillation Test Purpose Chest radiography Identify possible pulmonary disease (e.g., pneumonia, vascular congestion, chronic obstructive pulmonary disease) Complete blood count Identify comorbid conditions (e.g., anemia, infection) Complete metabolic profile Identify electrolyte abnormalities that may cause or exacerbate atrial fibrillation Assess kidney and liver function and blood glucose level Echocardiography Assess heart size and shape; chamber sizes and pressures; valve structure and function; presence of pericardial effusion; wall motion abnormalities; systolic and diastolic function Electrocardiography Diagnose atrial fibrillation and identify other arrhythmia (e.g., atrial flutter, atrial tachycardia) Identify other cardiac conditions (e.g., left ventricular hypertrophy, ischemia, strain, injury) Thyroid-stimulating hormone measurement Identify hyperthyroidism Management Two main strategies have been compared in the treatment of atrial fibrillation: rhythm control and rate control. Data show that patients assigned to rhythm control have more hospitalizations from adverse cardiovascular events, more serious adverse effects from medications, and the same rate of thromboembolic events compared with patients assigned to rate control.12–15 Therefore, rate control is recommended in most patients. Rhythm control remains an option when rate control is unsuccessful or when symptoms persist despite rate control.4,16 Both strategies require anticoagulation therapy to prevent stroke. RHYTHM CONTROL Cardioversion to restore normal sinus rhythm can be achieved electrically or pharmacologically. Anticoagulation therapy, before and after cardioversion, is recommended with either strategy to prevent thromboembolism. Guidelines recommend initiating anticoagulation therapy three weeks before and four weeks after cardioversion, because thrombi may form as soon as 48 hours after the onset of atrial fibrillation (Figure 3), and atrial function does not return to normal immediately after cardioversion to normal sinus rhythm.4 The atria are often “stunned,” and the risk of stroke is high for several weeks if warfarin (Coumadin) is not used.17,18 Figure 3 Transesophageal echocardiographic image of thrombi (arrows) in the left atrial appendage. (LA = left atrium; LV = left ventricle; RA = right atrium.) Pharmacologic cardioversion and maintenance of normal sinus rhythm are difficult to achieve because of the limited long-term effectiveness of medications, the risk of triggering ventricular arrhythmias, and the risk of long-term adverse effects from medication use. Medications commonly used for cardioversion include ibutilide (Corvert), flecainide (Tambocor), dofetilide (Tikosyn), sotalol (Betapace), propafenone (Rythmol), and amiodarone (Cordarone).4 Older agents such as quinidine, procainamide, and disopyramide (Norpace) are rarely used because of adverse effects. Dronedarone (Multaq), which is a noniodinated derivative of amiodarone, has been shown to reduce atrial fibrillation without the long-term serious adverse effects of amiodarone, but there are concerns about safety in patients with severe heart failure.19,20 The choice of medication depends on the patient's cardiac history. For example, flecainide and propafenone are preferred in patients with minimal or no heart disease and preserved left ventricular systolic function, whereas amiodarone and dofetilide are preferred in patients with heart failure.4 Patients with paroxysmal atrial fibrillation may use the “pill-in-the-pocket” approach with flecainide or propafenone, which involves taking a pill when an episode begins. This method is often effective in converting the rhythm to normal, and obviates the need to take antiarrhythmic medications long term. Table 4 lists the most commonly used antiarrhythmic medications, potential adverse effects, and costs. Table 4 Antiarrhythmic Medications for the Treatment of Atrial Fibrillation Medication Suggested dosage Cost of generic (brand)* Comments Amiodarone (Cordarone) 600 to 1,200 mg per day for one to two weeks, then taper to lowest possible dosage $29† ($136) for maintenance dosage Potential adverse effects include abnormal cardiac conduction, anaphylaxis, heart failure, pulmonary toxicity, ocular toxicity, thyroid abnormalities, hypersensitivity reaction, liver failure, lupus, thrombocytopenia, Stevens-Johnson syndrome 200 mg per day for maintenance dosage Disopyramide (Norpace) 400 to 800 mg per day in divided doses $63 ($198) Potential adverse effects include torsades de pointes, drug-induced lupus, hepatotoxicity, hypoglycemia, heart failure Dofetilide (Tikosyn) 500 mcg orally every 12 hours at initiation of therapy, titrate downward based on QT response NA ($234) Potential adverse effects include prolonged QT interval and various proarrhythmias Use is restricted to trained prescribers and facilities In-hospital electrocardiographic monitoring required for at least three days Flecainide (Tambocor) 100 to 150 mg taken at onset of atrial fibrillation $58 ($146) Potential adverse effects include various proarrythmias, torsades de pointes May also be taken twice per day for prevention of atrial fibrillation Not recommended for use in patients with chronic atrial fibrillation Ibutilide (Corvert) A one-time 1 mg intravenous dosage, may repeat once after 10 minutes if no response $336 ($452) for 1 mg per 10 mL vial‡ Potential adverse effects include polymorphic ventricular tachycardia, hypotension, headache Caution is needed in patients with QT prolongation, hypokalemia, hypomagnesemia, bradycardia Continuous electrocardiographic monitoring required for four hours after last dosage Procainamide Up to 50 mg per kg per day in divided dosages $37 (NA) for 500 mg every six hours‡ Potential adverse effects include agranulocytosis, aplastic anemia, coagulation disorder, arrhythmia, hepatotoxicity, drug-induced lupus Propafenone (Rythmol) 225 to 425 mg orally every 12 hours $80 ($340) Potential adverse effects include granulocytosis, angina, chest pain, heart failure, atrioventricular block, bradyarrhythmias, hypotension, palpitations, sinus arrest, drug-induced lupus, bronchospasm Quinidine 324 to 648 mg; one to two tablets every eight to 12 hours $60 (NA) Potential adverse effects include various proarrhythmias, torsades de pointes, hepatoxicity, kidney disease, myelosuppression, drug-induced lupus Sotalol (Betapace) 80 to 160 mg twice per day $21† ($249) Potential adverse effects include torsades de pointes, various proarrhythmias, heart failure, bradycardia, heart block, asthma Continuous electrocardiographic monitoring required for three days after initiation of therapy Avoid in patients with renal insufficiency NA = not available in designated form. *—Estimated retail price of one month's treatment based on information obtained at www.drugstore.com (accessed September 8, 2010), except where noted. Generic price listed first; brand price listed in parentheses. Prices based on lowest suggested dosage. †—May be available at discounted prices ($10 or less for one month's treatment) at one or more national retail chains. ‡—Estimated cost to the pharmacist based on average wholesale prices in Red Book. Montvale, N.J.: Medical Economics Data; 2010. Cost to the patient will be higher, depending on prescription filling fee. RATE CONTROL Decreasing the ventricular response rate, known as rate control, improves diastolic filling and coronary perfusion, decreases myocardial energy demand, and prevents tachycardia-mediated cardiomyopathy. Current guidelines recommend aiming for a ventricular response of less than 80 beats per minute at rest and less than 110 beats per minute during exercise.4 However, a recent randomized controlled trial showed that lenient rate control, defined as a ventricular rate of less than 110 beats per minute at rest, was not inferior to strict rate control in preventing cardiac death, heart failure, stroke, and life-threatening arrhythmias.21 Beta blockers (e.g., metoprolol, esmolol [Brevibloc], propranolol [Inderal]) and nondihydropyridine calcium channel blockers (e.g., diltiazem, verapamil) are often used for rate control. Beta blockers are generally first-line agents. Digoxin is no longer considered a first-line agent for atrial fibrillation, because studies have shown that it has little effect during exercise.4 However, it may be used in conjunction with beta blockers or calcium channel blockers. Digoxin slows the ventricular rate mostly via enhancing vagal tone. ANTICOAGULATION In patients with atrial fibrillation, the estimated risk of stroke without anticoagulation therapy is 5 percent per year.22 Paroxysmal and chronic atrial fibrillation, treated by rate or rhythm control, require long-term anticoagulation therapy unless the risks of anticoagulation use exceed the benefits.4,16 Warfarin, aspirin, and clopidogrel (Plavix) are the most commonly used oral agents for anticoagulation. Several trials and a Cochrane review have demonstrated that warfarin is more effective than aspirin but confers a higher risk of bleeding; that warfarin is superior to aspirin plus clopidogrel, with the same risk of bleeding23–25; and that adding full-dose aspirin to warfarin should be avoided because of an increased risk of bleeding.26 Post Comment Private Reply Ignore Thread Top • Page Up • Full Thread • Page Down • Bottom/Latest
#1. To: Tatarewicz (#0)
(Edited)
I have AF and appreciate your posting this. Mine was caused by a bad valve. I had a valve replacement 9 years ago -- then a hideously painful and traumatic experience -- very recent inventions make valve replacement only a little more troublesome than root canal (just my luck). Even so, the surgery did not cure the AF, so I am now on a handful of pills morning and again at night, including warfarin (better known as rat poison). To keep the warfarin level effective I have to be tapped for a blood test every few weeks and sometimes get my dosage adjusted. I also got a pacemaker - not to start my heart but to keep a computerized record of my AF episodes. The primary reason for the warfarin is to keep clots from forming in my bloodstream, such clots could be jarred loose and cause strokes. Side effects are that I am very intolerant of temperature changes, I bruise easily and the bruises seem to last longer than normal, cuts and nicks take longer to stop bleeding. If I took much too much warfarin the result would be like hemophilia. AF is very debilitating. The slightest physical exertion requires me to stop and catch my breath. Before the surgery crossing the street before the light changed was practically an athletic challenge, now walking a full block has that effect.
Eating shredded coconut occasionally seems to minimize hemorrhaging for me. Don't know its effect on clotting.
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