Atrial fibrillation (AF)—the most common supraventricular tachycardia—affects as many as 6.1 million adults in the United States.1 It is associated with a 5-fold increased risk of stroke,2 a 3-fold increased risk of heart failure (HF),3 and about a 2-fold increased risk of dementia4 and mortality.2 The prevalence of AF increases with maturity, from 2% in people <65 years of age to 9% in those ≥65 years,5 and that prevalence is expected to double over the next 25 years as the population ages.1
The primary goals of treatment are to alleviate symptoms and prevent thromboembolism. Strokes related to AF are more likely to result in severe disability or death when compared with those unrelated to AF.6 And yet anticoagulation remains underutilized.7
The net clinical benefit of oral anticoagulation appears to be greatest in patients with the highest risk of bleeding, since these patients are also at the highest risk for stroke.8 Patients at increased risk of stroke are more likely to receive oral anticoagulation; however, for unknown reasons, more than half of people with the highest risk of stroke are not prescribed these important anti-blood-clotting medications.7 One theory is that physicians may be relying on their gut rather than objective risk scores, and underuse of validated schemata leads to poor estimation of risk.
For example, results from the ORBIT-AF (Outcomes Registry for Better Informed Treatment of Atrial Fibrillation) trial, which involved over 10,000 people with AF, found that although 72% (n=7251) had high-risk CHADS2 scores (≥2), only 16% were assessed as having a high risk of stroke by physicians.9 Along the same lines, a recent study of Canadian primary care physicians showed that stroke risk and bleeding risk were not evaluated with validated tools in 58% and 81% of patients, respectively, leading to both significant underestimation and overestimation of risk.10
This review provides the tools to identify when anticoagulation is indicated, reports the advantages and disadvantages of the currently available anticoagulants, and discusses the selection and implementation of rate- vs rhythm-control strategies. But first, a word about the etiology, classification, and diagnosis of AF.
AF: The result of any number of cardiac and non-cardiac causes
AF is characterized by uncoordinated activation of the atria, which results in ineffective atrial contractions and an irregular, often rapid, ventricular response. It is the ultimate clinical manifestation of multiple diseases that alter atrial tissue through inflammation, fibrosis, or hypertrophy.5 The most common causes are hypertension, coronary artery disease, HF, cardiomyopathies, and valvular heart disease, all of which stimulate the renin-angiotensin-aldosterone system, leading to increased susceptibility to arrhythmia.5 Atrial ectopic tachycardia, Wolff-Parkinson-White (WPW) syndrome, and atrioventricular (AV) nodal reentrant tachycardia also may precipitate AF.5 In these cases, AF usually resolves after catheter ablation (CA) of the primary arrhythmia.11 Unrecognized AF may trigger atrial flutter, and more than 80% of patients who undergo radiofrequency ablation for atrial flutter experience AF at some point in the subsequent 5 years.12
Non-cardiac causes of AF include sleep apnea, obesity, hyperthyroidism, drugs, electrocution, pneumonia, and pulmonary embolism.5 An association between binge drinking and AF (“holiday heart syndrome”) has long been recognized. The evidence now suggests that alcohol increases the risk of AF in a dose-dependent manner with intakes of ≥1 drink per day (12 g per drink).13
Classification schema no longer includes “lone AF”
AF is classified in terms of the duration of episodes:5
- Paroxysmal AF is characterized by brief episodes that terminate spontaneously or with intervention within 7 days of onset. These episodes recur with variable frequency.
- Persistent AF refers to AF that is continuously sustained for more than 7 days.
- Longstanding persistent AF refers to continuous AF that lasts longer than 12 months.
- Permanent AF is not an inherent pathophysiologic attribute of AF, but rather an acceptance of AF where the patient and physician abandon further efforts to restore and/or maintain sinus rhythm.
- Nonvalvular AF occurs in the absence of a valve replacement (mechanical or bioprosthetic), rheumatic mitral stenosis, or mitral valve repair.
Although paroxysmal and persistent AF may occur in the same individual, the distinction is still clinically relevant, as outcomes of certain therapies, such as CA, are superior in patients with paroxysmal AF.14 With a more complete understanding of AF pathophysiology, guidelines now discourage use of the potentially confusing term “lone AF,” which has historically been applied to younger patients with no known clinical risk factors or echocardiographic abnormalities. As a result, therapeutic decisions are no longer based on this nomenclature, according to the 2014 AF practice guideline from the American College of Cardiology (ACC)/American Heart Association (AHA)/Heart Rhythm Society (HRS).5