Atrial Fibrillation

Atrial fibrillation is the most frequently occurring cardiac arrhythmia, and during the past few years the topic has moved to center stage in cardiology. Because of the relatively high prevalence of atrial fibrillation in the adult population and the clinical implications of this arrhythmia, increasing attention is being directed to the prevention and management of this cardiac rhythm disorder.

Atrial fibrillation has been recognized as an irregularly irregular heart rhythm since the beginning of medicine, with an appreciation for its association with rheumatic heart disease when this disease was prevalent. With the advent of the electrocardiogram a century ago, clinical documentation of atrial fibrillation and its first cousin, atrial flutter, became possible, and these arrhythmias became the subject of numerous clinical studies. Controlling the rate of atrial fibrillation with digoxin and the conversion of this arrhythmia to sinus rhythm with quinidine were prominent components of cardiac therapeutics in the mid 20^th century. During the last half of the 20^th century, there has been a sharp increase in the prevalence of atrial fibrillation, with the incidence doubling with each decade of life above 50 years. ¹ Atrial fibrillation is rare in young healthy persons, affecting only 0.5–1.0% of the general population, but it is common in older individuals affecting about 6% in the octogenarian age group. ²

Except in the young, atrial fibrillation is usually secondary to underlying valvular, ischemic, hypertensive, or cardiomyopathic heart disease. The presence of one or more of these conditions, and possibly cardiac senescence, contribute to the increased frequency of occurrence of this arrhythmia in older people. Hyperthyroidism, whether overt or apathetic in presentation, is an infrequent but easily correctable cause of atrial fibrillation in this age group. The major risk from atrial fibrillation is systemic emboli, and this arrhythmia is an important cause of stroke. In addition, this arrhythmia can precipitate and exacerbate congestive heart failure through loss of the atrial kick mechanism and the development of inappropriately fast heart rates.

Atrial fibrillation has important prognostic implications, and the presence of this arrhythmia is associated with an increased mortality risk in almost all longitudinal follow‐up studies of patients with organic heart disease. ³ In the MADIT‐II study, atrial fibrillation in patients randomized to conventional therapy was associated with more than a two‐fold risk of death during an average follow‐up of two years. It is unlikely that the atrial fibrillation rhythm per se is the determinant of the mortality risk. Rather, atrial fibrillation is an indicator of the severity of the underlying heart disease, for this arrhythmia is highly correlated with left ventricular dysfunction as manifest by a reduced ejection fraction (systolic dysfunction) or an elevated left ventricular end‐diastolic pressure from impaired ventricular compliance (diastolic dysfunction).

In younger individuals without structural heart disease, atrial fibrillation is usually paroxysmal in nature, with the intermittent events frequently triggered by alcohol, fever, drugs, or autonomic factors. These atrial fibrillation events are often self‐limited with spontaneous conversion back to sinus rhythm. If the rhythm persists, it is easily terminated with pharmacologic or electrical intervention. Electrophysiologic studies in these individuals may reflect a latent accessory pathway or an ectopic focus in the pulmonary veins at the entrance into the left atrium. Infrequently, the classical findings of the Wolff‐Parkinson‐White syndrome (short PR interval and delta wave) or the Lown‐Genong‐Levine syndrome (short PR interval) may be evident on the scalar electrocardiogram, and these disorders provide the electrophysiologic substrate for atrial fibrillation. Radiofrequency ablation of the atrioventricular nodal bypass pathway or the Mahaim accessory pathway is the treatment of choice when these disorders are the cause of recurrent atrial fibrillation.

In older patients, atrial fibrillation begins as an intermittent arrhythmia, but quickly becomes chronic and permanent. Most of these patients have a moderately enlarged left atrium on echocardiography when the arrhythmia first begins, and chronic atrial fibrillation contributes to adverse remodeling with further enlargement of the left atrial chamber. Patients who have had prior cardiac surgery for coronary or valvular heart disease are at a particularly high risk of developing chronic atrial fibrillation during long‐term follow‐up after the surgical procedure. The scar from the surgical atriotomy and/or late effects from post‐operative pericarditis may be important contributing factors to the development of atrial fibrillation in these patients. Regardless of the cause of chronic atrial fibrillation, the arrhythmia contributes to ineffective atrial contraction and further chamber enlargement—two factors that provide the substrate for mural atrial thrombi and systemic embolization.

During the past decade or more, the accepted therapy for patients with chronic atrial fibrillation was first to control the rate of the ventricular response to atrial fibrillation with digoxin, beta‐blockers, and/or calcium channel blockers, and then to convert the arrhythmia to normal sinus rhythm by electrical or pharmacologic measures. If conversion to sinus rhythm was successful, maintenance antiarrhythmic therapy was initiated in an attempt to maintain sinus rhythm. Frequently, this cycle of therapy had to be repeated with recurrence of atrial fibrillation. This approach is challenging in view of the limited efficacy of the available antiarrhythmic agents and the high potential of these drugs for adverse reactions. Nevertheless, this strategy was the preferred approach because it seemed logical that maintained sinus rhythm would increase cardiac performance and reduce embolic complications.

Two recent studies found that rate control of atrial fibrillation was associated with fewer hospitalizations and fewer adverse side effects from drugs than a rhythm‐control approach. ⁴ , ⁵ These findings are not surprising in view of the troublesome side‐effect profile of antiarrhythmic agents that are used for conversion and for maintenance therapy. The two studies further highlight the importance of optimizing anticoagulant therapy to reduce the frequency of systemic embolization regardless of rate or rhythm control.

How does the treating physician achieve adequate rate control in patients with chronic atrial fibrillation? Digitalis, beta‐blockers, and/or calcium channel blockers are the drugs of choice, but their proper prescription including dosage and frequency of administration requires full knowledge of the range of heart rates during various levels of activity throughout day and night. Periodic Holter monitoring while receiving rate‐control medication provides invaluable information into the maximum and minimum heart rates during extended time periods. Exercise testing is helpful in evaluating maximal heart rates during vigorous activity. Although rate control suggests emphasis on the prevention of inappropriate tachycardia, and this is important, one should not overlook the potential for dangerous bradycardia from high‐grade atrioventricular block that can complicate atrial fibrillation, especially in the elderly receiving one or more drugs to control fast heart rates. Thus, the recent studies that document the importance of good rate control in atrial fibrillation support the clinical usefulness of Holter monitoring in order to capture the necessary heart rate information for proper therapeutics in this most common arrhythmia.