Author Affiliations: Division of Cardiovascular Medicine, Section of Electrophysiology, University of Pennsylvania, Philadelphia (Dr Deo); and Section of Cardiac Electrophysiology, University of Colorado Denver, Colorado Cardiovascular Outcomes Research (CCOR) Group, and VA Eastern Colorado Health Care System, Denver (Dr Varosy).
Several recent studies have noted a rise in the prevalence and incidence of atrial fibrillation (AF). The population burden of AF is expected to double over the next 40 years and will likely affect between 6 to 12 million Americans by 2050.1- 3 In this issue of the Archives, Wong and colleagues4 confirm that this phenomenon is not limited to the United States. Using administrative data, these investigators demonstrate that the number of hospitalizations for AF in Australia tripled over a 15-year period between 1993 and 2007. In comparison, the number of hospitalizations for myocardial infarction and heart failure increased only modestly during this time.
What accounts for this rise in AF? As Wong and colleagues4 propose, an increasing population of older patients may explain part of this trend. Patients with coronary artery disease and congestive heart failure are surviving longer and contributing to the growing population at risk for AF. Increasing age is associated with other comorbidities, including valvular heart disease, diabetes mellitus, hypertension, and peripheral arterial disease, all of which are risk factors not only for the development of AF but also for AF-associated thromboembolic complications. Increasing use of ambulatory electrocardiography devices and implantable arrhythmia devices such as pacemakers, defibrillators, and cardiac resynchronization therapy devices have likely enhanced detection of asymptomatic and minimally symptomatic arrhythmias. These possibilities, however, likely explain only a part of the increase in AF hospitalizations.
A larger and older population with AF will increase the burden of morbidity and mortality associated with AF. Even with appropriate risk stratification and anticoagulation, the risk of thromboembolic stroke is increased in AF, especially among patients with risk factors.5 Even brief, asymptomatic episodes of AF that are detected incidentally in patients with implantable arrhythmia devices are associated with ischemic strokes or peripheral emboli.6 More ominously, incident AF is associated with an increased risk of all-cause mortality in health care professionals7 and other cohorts.8,9 These findings portend a potentially dramatic rise in hospitalizations, stroke, and AF-associated mortality by 2050 unless our therapeutic options evolve adequately to counter these challenges.
Unfortunately, no single therapeutic breakthrough alone is likely to mitigate the rising burden of AF. Although all AF is characterized by chaotic atrial electrical activity, the arrhythmia is a final common pathway of multiple heterogeneous conditions, including electrical triggers (especially in the pulmonary veins), underlying structural heart disease, long-standing hypertension, genetic disorders, cardiomyopathies, and, almost certainly, other conditions we do not yet understand. Currently, guideline-based treatment strategies for AF begin with assessment and appropriate reduction of stroke risk (with aspirin, warfarin, or other anticoagulants) followed by treatment of AF-associated symptoms beginning first with control of the ventricular response to AF. If a rate control strategy fails or is otherwise unacceptable to the patient, efforts to achieve and maintain normal sinus rhythm can include cardioversion, antiarrhythmic drugs, and/or ablation by either catheter-based or surgical approaches. Unfortunately, patients continue to be hospitalized with poor ventricular rate control despite the use of rate controlling drugs. Furthermore, even when control of the rhythm is desired, antiarrhythmic drugs have both incomplete efficacy and substantive toxicities. Although promising in some, catheter ablation in the best candidates has both nontrivial procedural risk and a likelihood of success for a first procedure on the order of 60% to 85%, even with concomitant antiarrhythmic drug therapy.10 At a fundamental level, all of these treatments address a condition that has already afflicted the heart without addressing the upstream causes.
Clearly, both in the United States and abroad, the public health burden of AF is increasing. The good news is that anticoagulation with warfarin in appropriately risk-stratified patients has reduced (but not eliminated) stroke risk, and recent randomized trials suggest that simpler regimens with new anticoagulants are as efficacious as warfarin. Better insights into the mechanisms of AF have identified patients with structurally normal hearts and pulmonary venous atrial tachycardia triggers as particularly good candidates for AF ablation. Unfortunately, though, the burden of AF is increasing despite these and other advances.
We must do better—even greater support for scientific discovery may lead to better understanding of the mechanisms leading to AF and novel therapeutic approaches. Hopefully, new strategies with better profiles of safety and efficacy than those of our current therapeutic arsenal will mitigate the future symptoms and risks of adverse AF-associated outcomes. We are even more hopeful that other strategies may eventually emerge to prevent AF. Without such advances, the burden of AF will weigh heavily on our world in the coming decades.
Correspondence: Dr Varosy, VA Eastern Colorado Health Care System, Cardiology Section (111B), 1055 Clermont St, Denver, CO 80220 (email@example.com).
Financial Disclosure: None reported.
Funding/Support: This study was funded in part by grant K23DK089118 from the National Institutes of Health (Dr Deo) and a Research Career Development Award (RCD 04-115-2) from the Veterans Administration Office of Health Services Research (Dr Varosy).
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