Atrial fibrillation is the most common sustained arrhythmia and can occur in virtually all forms of cardiac disease, but it can also affect patients with no detectable structural abnormalities. Its presence is associated with significant long-term morbidity, including congestive heart failure, stroke, and increased mortality.1

After 30 years of follow-up in the Framingham study, 7.2% of subjects had developed atrial fibrillation. The incidence was age dependent and increased 5-fold in the presence of cardiovascular disease.2 It is estimated that some 2.2 million people in the United States suffer from atrial fibrillation.

Historically, most atrial fibrillation was associated with valvular disease often secondary to rheumatic heart disease. In the present era, at least in Europe and North America, this has been superseded by hypertension and coronary artery disease. The condition is likely to become even more common with the current epidemic of obesity and diabetes; more patients surviving cardiac surgical procedures, ischemic heart disease, congestive heart failure, and cardiomyopathy; and the growing number of senior citizens.

Although atrial fibrillation is not a life-threatening arrhythmia, it does adversely affect quality of life due to symptoms of palpitations, breathlessness, and fatigue, coupled with reduced functional capacity. Comorbidities such as congestive heart failure may also be worsened. Several factors account for the reduction in functional capacity: loss of atrial contraction reduces ventricular filling by an average of 20%, causing a reduction in stroke volume, resulting in an increase in heart rate to maintain cardiac output. Ventricular contractions are not only more rapid but also irregular, resulting in variable ventricular filling as demonstrated clinically by fluctuating pulse pressure, with some contractions failing to produce a palpable pulse. Stroke volume is thus further reduced, requiring an even greater increase in heart rate to maintain cardiac output. Very rapid heart rates may themselves impair ventricular filling, resulting in congestive heart failure. Maximal oxygen uptake is reduced, with ventilatory threshold occurring at lower work rates, and ventilation is increased. Recent research by Takahashi et al3 has shown that endothelial nitric oxide availability is reduced, impairing the peripheral vascular response to exercise, and an additional study by Cai et al4 found that atrial fibrillation is associated with a marked decrease in endothelial nitric oxide synthase expression and nitric oxide bioavailability and an increase in plasminogen activator inhibitor 1 expression in the left atrium. The authors conclude that loss of this antithrombotic enzyme contributes to the thromboembolic phenomena commonly observed in atrial fibrillation.

Physiologically, cardioversion to sinus rhythm and maintenance of sinus rhythm would seem to be the treatment of choice, but 2 recent studies5,6 found similar symptomatology burden, mortality, and stroke rates when comparing rate control with rhythm control. The longer atrial fibrillation persists, the less likely it is that the patient can be converted to and maintained in sinus rhythm. Medications used for both rhythm and rate control may have undesirable side effects, which influence the patient's management. A substantial number of patients end up with chronic atrial fibrillation, and then rate control is the goal of treatment.

Exercise training has been extensively studied in healthy people7 and in patients with coronary artery disease.8 Beneficial effects include reduction of heart rate at rest and exercise, reduction of blood pressure, increased peripheral oxygen extraction, increased maximal oxygen uptake, increase in ventilatory threshold, decreased blood coagulability, improved endothelial function,9and,inafewstudies,increasedstokevolume. Quality of life is improved both in patients with coronary artery disease and congestive heart failure.

Although medications will remain a corner stone of treatment, the physiological adaptations to exercise training would appear to address most of the negative changes associated with atrial fibrillation and, because exercise training is not associated with deleterious side effects, would seem to be a useful adjunct in the management of patients with chronic atrial fibrillation. Rate control is, of course, an important prerequisite for exercise training.

Two previous retrospective studies10,11 published in the Journal of Cardiopulmonary Rehabilitation have documented that a training effect can be obtained in these patients and that although they start at a lower level, functional capacity is improved by the same amount as in patients without atrial fibrillation. In both studies, there were no deleterious effects associated with the exercise training. In this issue, a third study is published which adds to our knowledge base. This study by Hegbom et al is the first randomized, controlled study to examine the effects of exercise training on functional capacity, quality of life, and AV conduction in patients with chronic atrial fibrillation. The authors confirm the previously documented increase in functional capacity and find both an improved quality of life and an improvement in heart rate variability, suggesting an increase in vagal tone accounting for the decrease in resting and exercise heart rates. A number of studies have documented heart rate variability before and after cardioversion, or prior to the onset of atrial fibrillation, but this is the first to my knowledge that has looked at heart rate variability in chronic atrial fibrillation before and after exercise training. Subjects in this study, as the authors point out, were relatively asymptomatic, and it is therefore not surprising that improvements in quality of life were modest. A reliable and validated tool to measure changes in symptoms needs to be developed to augment the current quality-of-life measures in the more symptomatic patients.

Patients with chronic atrial fibrillation are a major cost to the healthcare system, accounting for a significant number of hospital admissions and substantial drug bills. Further research documenting the benefits of exercise training, looking not only at quality of life, functional capacity, and symptom relief but also at the potential reduction in hospital and drug costs, is needed. We also need to know what are the optimum type, duration, frequency, and intensity of exercise to prescribe. At the present time, chronic atrial fibrillation is not a reimbursable diagnosis for cardiac rehabilitation in the United States, unless it is associated with a recent myocardial infarction, coronary artery bypass surgery, or stable angina. In order to bring the benefits of cardiac rehabilitation to this group of patients, we need to demonstrate the cost effectiveness of exercise training as part of their treatment.

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