A. Fib
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Atrial Fibrillation (AF) is the most prevalent cardiac dysrhythmia in the United States and a substantial cause of morbidity and mortality.1 Even though AF is commonly diagnosed by clinicians; the most appropriate treatment course remains elusive. The main controversy is between controlling the rate versus the rhythm. The ventricular rate is the number of cardiac cycles (systole and diastole) in one minute, normally 60 to 100 beats per minute (bpm) in an adult; it can be determined on an electrocardiogram (ecg) by measuring the distance between R waves.2 The rate is typically pharmacologically controlled by beta or calcium channel blockers. A normal sinus rhythm demonstrates an electrical impulse generated by the sinoatrial node or “pacemaker” of the heart and maintains a consistent R-R interval on the ecg.2 AF is associated with an “irregularly irregular” rhythm due to the erratic atrial depolarization and the resulting variable ventricular response.2 AF is expressed on an ecg as a wavy baseline with an atrial rate of 400 to 600 bpm “without identifiable P waves.”2 The rhythm found in AF is controlled with electrocardioversion or antiarrhythmic drugs, such as flecainide, quinidine, and amiodarone.1
Over the last decade there have been advancements in the understanding of the pathophysiology of AF which has aided further exploration of the appropriate treatment through several key studies. For example, the Atrial Fibrillation Follow-up Investigation of Rhythm Management (AFFIRM) study concluded that there was no significant difference between the two treatment strategies.3 However, the rhythm control group was associated with slightly more adverse drug effects and hospitalizations than the rate control group studied.3 Other related key studies include the Pharmacological Intervention in AF (PIAF), Rate Control versus Electrical Cardioversion for Persistent AF (RACE), Canadian Registry of AF cohort (CARAF), How to Treat Chronic AF (HOT CAFE) and Strategies of Treatment of AF (STAF).
The objective of this paper is to do a literature review of the pertinent published works related to the treatment of AF and outline the conclusions obtained. The review will include the key studies completed in the last decade featuring AF patients comparing rate versus rhythm control. This author will explore possible subsets of AF patients for which a certain treatment is more efficacious, as well as, the cost effectiveness of the treatment. Although practitioners have long considered rhythm control to be the most effective treatment for AF, this paper will show that rate control is equal in efficacy and should be an acceptable first-line therapeutic option.
Review of Literature
Pathophysiology
AF occurs due to a focal mechanism or multiple reentry atrial circuits. As early as 1896 Englemann “proposed that AF could be the result of a single atrial focus activating the atria with a rapid rate.”4 The typical depolarization rate of the atria is between 400 and 600 beats per minute.2 As a result of the rapid rate the atrial muscles fibrillate leading to an erratic baseline on ecg “without an identifiable P wave.”2 Due to the irregular atrial depolarization and the corresponding irregular ventricular response the rhythm of AF is referred to as “irregularly irregular.”2 Jais later showed that “ablation of a single focus, most typically from one of the pulmonary veins, could stop AF.”4 During the last century, it was shown that the variable rhythm of AF can be the result of multiple reentry circuits instead of rapidly firing foci. Reentry “is not a disorder of impulse formation but rather a disorder of impulse propagation, it occurs when an impulse travels around an abnormal circuit repetitively.”5 By performing several experiments on animals and humans, Allessie et al. “confirmed multiple wavelet reentry as the cause of AF by multipolar mapping.”4 Multiple reentry as the cause of AF was further supported by the demonstration by Kumagai et al. that pathways in certain anatomic locations helped maintain AF.4 More important in AF than anatomic reentry is functional reentry in which “variations in the electrophysiologic properties of contiguous tissues, not anatomic obstacles, may serve as the boundaries” of the circuit.5 There have been several functional reentry models proposed including the leading circle, spiral wave and multiple wavelets.5 Since 1960 the multiple wavelet theory has been the most accepted and it is explained as a “critical number of wavelets, which travel throughout the atria, colliding, combining or dividing and thereby spawning daughter wavelets that perpetuate the process.”5 Any condition that alters the structure of the atria or decreases the wavelength “permit multiple wavelets and promote AF.”5 Atrial remodeling is the concept that changes in the atrium promote and maintain AF, “these changes include a shortening of the refractory period of the atrium and atrial dilationwhich may be caused by increased left atrial pressure.”1 There are three characteristic parts of the atrial remodeling process: electrical, contractile, and structural remodeling.5 Electrical remodeling is completed in the first 24 to 48 hours after onset of AF and is due to “tachycardia induced intracellular calcium overload, a downregulation of the L-type calcium channels and a subsequent reduction of sarcolemmal calcium influx.”5 Since elevated intracellular calcium can lead to toxicity homeostatic mechanisms reduce the influx of calcium that contributes to the normal duration of the action potential.5 The end result is a “shortening of the atrial refractory period and a reduction of the wavelength which increases the vulnerability of AF.”5 Further consequences of electrical remodeling include “myocyte calcium overload, atrial automaticity, dispersion of conduction, and increased sensitivity to catecholamines.”3 Contractile remodeling similar to electrical remodeling is related to calcium conduction. For example, “myofilament sliding, the cellular action responsible for muscle contraction, is intimately dependent upon intracellular calcium concentrations” and when the calcium influx is altered so are the function of the myocytes.5 As a result dilation of the atria may occur in several days to weeks.4 Structural remodeling is due to several chronic processes including “increased wall stress, a change in the distribution of connexin 40, myolysis with sacromeres replaced by glycogen, and a disruption of the sarcoplasmic reticulum” that leads to “increased fibrosis” of the atria.4 The electrical, contractile and structural remodeling of the atria helps to stabilize