CME: Primary Care
Atrial fibrillation (AF) affects more than 5 million adults in the United States, and is predicted to affect 12 million by 2030.1 This common dysrhythmia is associated with significant morbidity, including a fivefold increased risk of stroke, a threefold increased risk of heart failure, and a twofold increased risk of dementia.2 In addition, AF is correlated with a 50% increased risk of death in men and a nearly 100% increased risk of death in women.3
Because adults age 40 years and older have a one in four lifetime risk for developing AF, primary care providers will frequently encounter patients with the dysrhythmia.4 Understanding AF pathophysiology, diagnosis, treatment, and thromboembolic prevention is essential to reduce AF-related morbidity and mortality, and to improve patient outcomes.
AF is a supraventricular tachydysrhythmia characterized by chaotic atrial depolarization at a rate of 300 to 600 beats/minute, with variable and often rapid ventricular depolarization. Cardiac structural and electrical abnormalities initiate and propagate atrial ectopic impulses, which override the sinoatrial node. Automaticity of cardiomyocytes in the sleeves around the pulmonary veins is often the cause in early disease. As the heart undergoes remodeling and fibrosis, foci and frequency of ectopy increase, and electrical reentry sustains the dysrhythmia.5
AF is associated with multiple risk factors, including hypertension, obesity, obstructive sleep apnea, hyperthyroidism, diabetes, ischemic heart disease, valvular heart disease, cardiomyopathy and heart failure, left atrial enlargement, excessive alcohol consumption, and genetic predisposition. The incidence of AF increases with age, although it may appear during any decade of life.2
AF symptoms vary, and may even be absent in a third of patients.6 When present, symptoms include palpitations, dyspnea, fatigue, exercise intolerance, and lightheadedness. Impaired atrial contraction results in diminished diastolic filling, reducing cardiac output by up to 20%. Decreased cardiac output manifests as weakness and fatigue; dyspnea results from increased right atrial and pulmonary pressures.7 The incidence and severity of symptoms increase with recent onset, higher ventricular rates, and the presence of comorbid cardiovascular conditions (Figure 1).8
History and physical examination
A complete history and physical examination are essential to diagnosing AF. The history should include a careful review of symptoms, family history, and potentially modifiable risk factors.2 The most common finding on physical examination is an irregular and often rapid pulse. Patients may have signs of concomitant cardiovascular conditions such as heart failure, ischemic heart disease, or valvular heart disease. Findings may include murmur, gallop, jugular venous distension, arterial bruits, crackles, hepatomegaly, or peripheral edema.
In patients with an irregular pulse, obtain an ECG to confirm AF and determine ventricular rate. A transthoracic echocardiogram (TTE) can evaluate cardiac function and structure. Blood tests, particularly metabolic and thyroid profiles, should be performed after an initial episode of AF, or if the patient's ventricular rate is resistant to pharmacologic therapies. Ambulatory rhythm monitoring with mobile telemetry also is helpful for making the diagnosis of intermittent AF and for monitoring control of ventricular rate.
Transesophageal echocardiography (TEE) may be beneficial for evaluating the presence of thrombi, which form in the left atrial appendage; a TEE should be obtained before performing cardioversion or invasive procedures that could cause embolization.2
Management strategies and expected response to therapies depend on the patient's AF classification, which is based on the duration of the dysrhythmia (Table 1). As AF persists, electrical and structural remodeling perpetuates the dysrhythmia, increasing frequency and duration of AF episodes, and leading AF to progress from paroxysmal to persistent, even with treatment. Maintaining sinus rhythm becomes more difficult as the duration of AF increases.
Treatment for AF consists of strategies to control rate and rhythm. Rate control reduces the ventricular rate without changing the underlying cardiac rhythm. Cardioversion, antiarrhythmic medication, and catheter ablation can be used for rhythm control. Neither strategy demonstrates a benefit over the other with regard to quality of life, morbidity, or mortality. However, rhythm control is associated with increased hospitalization rates and treatment costs compared with rate control.9
The primary goal of rate control is symptom management and prevention of tachycardia-mediated cardiomyopathy. The optimal goal is undetermined, but guidelines recommend an average resting heart rate below 80 beats/minute and an ambulatory heart rate below 100 beats/minute.2 One randomized controlled trial demonstrated noninferiority with lenient rate control (resting heart rate below 110 beats/minute) compared with strict rate control (below 80 beats/minute). Therefore, consider a lenient rate control strategy in asymptomatic patients with normal left ventricular systolic function if they would be predisposed to adverse drug reactions if under strict rate control.2
Rate control is achieved by administering atrioventricular nodal blocking agents. Beta-adrenergic blockers are the most effective class of these drugs.2 Nondihydropyridine calcium channel blockers also decrease heart rate, but because of their negative inotropic effect, they should not be used in patients with systolic heart failure.2 Digoxin may add synergistic rate control when combined with beta-adrenergic and calcium channel blockers.10
Although the rate control strategy is effective for many patients, rhythm control may be preferred in those patients who have symptoms despite rate control, whose rate is difficult to control, or who develop tachycardia-mediated cardiomyopathy. Rhythm control also may be beneficial in patients who are younger, who present with a first episode of AF, or whose AF is precipitated by an acute illness. In these patients, restoring sinus rhythm may prevent irreversible electrical and structural remodeling.2
AF may terminate spontaneously, or may require chemical or electrical cardioversion. Electrical cardioversion successfully restores sinus rhythm in 75% to 90% of patients, but the correction may not last. AF recurs in 40% to 60% of patients within 3 months, and in 60% to 80% of patients within 12 months.11 Antiarrhythmic drugs have modest efficacy in maintaining sinus rhythm in about 50% of patients.12 Antiarrhythmics must be selected carefully; clinicians should take into consideration the patient's underlying cardiac disease and comorbidities, as well as the proarrhythmic and toxic potential of antiarrhythmics.2
Transvenous catheter ablation is another method of rhythm control, in which the pulmonary veins (the most common site of AF electrical triggers) are isolated with radiofrequency or cryotherapy. This treatment is an option for patients with symptomatic AF resistant to at least one antiarrhythmic drug, and prevents symptomatic AF recurrence in 70% to 80% of patients.13 Ongoing clinical trials are assessing the morbidity and mortality associated with AF ablation, and whether it will be more beneficial than antiarrhythmic and rate control therapies.
Embolic risk stratification and prevention
Stroke prevention is a primary goal in AF management. Patients with AF are at a fivefold increased risk for stroke. In addition, strokes related to AF are more severe, more debilitating, and twice as likely to be fatal than strokes in patients who do not have AF.2 The increased stroke risk is thought to be due to decreased blood flow velocity in the left atrial appendage, which allows thrombus formation (Figure 2).14 The appendage is an irregularly shaped extension of the left atrium. High-velocity blood flow during normal sinus rhythm usually protects the appendage from thrombus formation.14 Patients with AF often are prescribed anticoagulants to prevent strokes if their CHA2DS2-VASc scores indicate they are high-risk (Table 2).15
Because anticoagulants significantly increase the risk of bleeding, including gastrointestinal bleeding and intracranial hemorrhage, current AF guidelines recommend an individualized approach when balancing the benefits of anticoagulants and risks of bleeding.2 The HAS-BLED (Table 3) bleeding score is effective for quantifying bleeding risk.15 Patients with a HAS-BLED score of 3 or greater are at increased bleeding risk; therefore, those on anticoagulants should be closely observed for bleeding, or therapy should be avoided if risks outweigh potential benefits.
Antithrombotics and left atrial appendage exclusion
No matter which type of AF patients have, their risk of stroke is substantially increased because blood flow in the left atrial appendage is reduced even in paroxysmal AF.2,16 Therefore, the decision for anticoagulant therapy should not be based on a patient's AF classification but on overall stroke risk. Once the need for anticoagulant therapy is determined, selection of agents depends on patient characteristics and preferences.
The two types of oral anticoagulants, vitamin K antagonists and target-specific anticoagulants, reduce the risk of AF-related stroke by two-thirds.17
Warfarin, a vitamin K antagonist, is the standard therapy for stroke prophylaxis in patients with AF. Effective and inexpensive, warfarin has few contraindications, and reversal agents are available if the patient develops serious bleeding. Unfortunately, warfarin's narrow therapeutic index means that patients need routine blood monitoring, and the drug is affected by drug and dietary interactions.
Target-specific anticoagulants approved for stroke prevention in patients with nonvalvular AF include the direct thrombin inhibitor dabigatran, and factor Xa inhibitors rivaroxaban, apixaban, and edoxaban.2 A meta-analysis demonstrated decreased risk of stroke and systemic embolism, all-cause mortality, and intracranial hemorrhage with target-specific anticoagulants compared with warfarin.18 Target-specific anticoagulants require a dose adjustment in patients with moderate-to-severe chronic kidney disease, although they are an alternative to vitamin K antagonists. Target-specific anticoagulants are contraindicated in patients with bioprosthetic and mechanical heart valves, previous mitral valve repair, or end-stage renal disease.18 Although more expensive than generic warfarin, target-specific anticoagulants are associated with lower medical costs due to indirect savings through reduced laboratory costs and reduced iatrogenic complications.19
These drugs inhibit platelet aggregation and have a limited role in AF-related thromboprophylaxis.
Aspirin and adenosine diphosphate receptor inhibitors are inferior to anticoagulants at reducing stroke when used as monotherapy or in combination with anticoagulants or cyclooxygenase inhibitors, such as clopidogrel, prasugrel, and ticagrelor.2 Although antiplatelets are associated with a decreased risk of intracranial hemorrhage, several studies showed no significant difference in the overall risk of major bleeding between oral anticoagulants and antiplatelets.2 For most patients, antiplatelets are not the preferred therapy for prevention of AF-related stroke.
Left atrial appendage exclusion
An emerging strategy in thromboprophylactic prevention is left atrial appendage exclusion. Because the left atrial appendage is a common source of thrombus in patients with AF, removal or occlusion of the appendage reduces the risk of embolism.20 Methods of excluding the appendage include excision at time of cardiac surgery, thorascopic left atrial appendectomy, minimally invasive ligation, and percutaneous transcatheter occlusion with a closure device. Exclusion of the left atrial appendage is indicated only in patients who are not candidates for anticoagulation.20 Complications include risk of incomplete appendage occlusion causing thromboembolic events, and occlusion-device dislodgement.
AF is a common condition that is increasing in frequency. Although the dysrhythmia is associated with significant morbidity and mortality, evidence-based AF management improves patient outcomes. In particular, anticoagulation in high-risk patients, as determined by the CHA2DS2-VASc score, reduces the risk of AF-related stroke. Clinicians must select appropriate rate control and rhythm control therapies to minimize patient symptoms and adverse reactions. Knowing current AF management strategies helps primary care providers manage AF and minimize its sequelae.
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Keywords:Copyright © 2016 American Academy of Physician Assistants
atrial fibrillation; rate control; rhythm control; thromboembolic prevention; anticoagulation; primary care