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9 Atrial Fibrillation

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9

Atrial Fibrillation

Peter S. Fischbach

Atrial fibrillation is a supraventricular tachy- cardia characterized by a disorganized ac- tivation and contraction of the atrium. The characteristic “irregularly irregular” rhythm is generated by the rapid irregular bom- bardment of the atrioventricular (AV) node with electrical impulses emanating from the atrial myocardium with variable conduction of the atrial impulses through the AV node (Figure 1). The ventricular response is depen- dent on the ability of the AV node to trans- mit electrical signals (i.e., its refractory state).

This is determined by its inherent electro- physiologic properties as well as autonomic tone.

INCIDENCE

Atrial fibrillation is the most common rhythm disorder seen in man, with prevalence in the general population estimated at 0.4%.

There is a significant age-related discrepancy in the distribution of the arrhythmia with 6%

of the population greater than 80 years of age suffering from atrial fibrillation. Atrial fibril- lation remains an extremely rare arrhythmia in the pediatric population, although there have been a few reports of familial forms of atrial fibrillation (Chapter 18).

ASSOCIATED DISEASE

Atrial fibrillation commonly occurs as a co-morbid condition with other cardiovas- cular abnormalities. It is frequently asso- ciated with congestive heart failure, mitral valve stenosis and insufficiency, hyperten- sion, and hyperthyroidism. Atrial fibrilla- tion is also associated with Wolff-Parkinson- White syndrome. Atrial fibrillation occurring in conjunction with Wolff-Parkinson-White syndrome is a potentially life-threatening sit- uation due to the lack of decremental con- duction through the accessory pathway. Some accessory pathways are capable of rapidly conducting the atrial signals to the ventricle leading to ventricular fibrillation (Chapter 20, Figure 3). Following elimination of the acces- sory pathway, either surgically or via trans- catheter ablation, atrial fibrillation resolves in a large portion of these patients. Atrial fib- rillation also may be associated with several other forms of supraventricular tachycardia in young patients. Our experience has been that young patients presenting with atrial fibril- lation will frequently have other underlying mechanisms of SVT such as AVNRT, AVRT, ectopic atrial tachycardia, or atrial flutter. Ab- lation of these other tachycardia substrates results in the resolution of atrial fibrillation.

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116 ATRIAL FIBRILLATION

FIGURE 1. Paroxysmal atrial fibrillation in a 17-year-old boy. Note the low amplitude fast waveforms (atrial fib- rillatory waves) between the “irregularly irregular” QRS intervals. There are a few different QRS morphologies due to aberrant conduction. The atrial fibrillation spontaneously terminates (bottom tracing) as it frequently does in the paroxysmal form in patients without structural heart disease.

MECHANISM

The pathophysiologic mechanisms un- derlying the initiation and perpetuation of atrial fibrillation remain under investigation (Figure 2). It is possible that the mecha- nisms that support the initiation of atrial fib- rillation are different from those that sustain the arrhythmia. The three most likely mech- anisms include the multiple wavelet theory, single-circuit reentry, and multiple-circuit

reentry. In the first model, multiple reen- trant waves continuously circulate through the atrium using migrating central cores of refractory tissue to rotate around. The multi- ple wavelets circulate throughout the atrium following ever-changing pathways created by myocardium recovering from refractoriness.

A critical mass of atrial tissue in this model is necessary to support a minimum number of wavelets in order to sustain atrial fibrillation.

This has been cited as a rational for the low

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ATRIAL FIBRILLATION 117

FIGURE 2. Three electrocardiographic leads and 4 intracardiac electrograms [3 in the right atrium (RA) and 1 from the right ventricular apex (RV)] illustrating the multi-phasic variable amplitude of the atrial fibrillation wavefronts.

incidence of atrial fibrillation in infants and children, as well as in small mammals (Chap- ters 2 and 3). The second proposed mechanism for atrial fibrillation is the single circuit reen- trant model. In this model, a single “mother ro- tor” serves as the hub with multiple accessory circuits emanating from it. The third potential mechanism is atrial fibrillation arising from a rapidly discharging ectopic focus with fibril- latory conduction. This mechanism has come into favor with recent findings of excitatory loci occurring within the pulmonary veins.

Recent clinical experience has demonstrated that focal radiofrequency ablation within the pulmonary veins as well as pulmonary vein isolation has successfully treated atrial fibril- lation.

Sustained atrial fibrillation produces pro- found changes within the atrial myocardium, creating a substrate more conducive to supporting sustained atrial fibrillation. The electrical and structural remodeling of the atrium includes increasing fibrosis, as well as

alterations in the expression of gap junctions and ion channels. These changes alter the me- chanical and electrical properties of the atrial tissue by slowing the conduction velocity and shortening the refractory period in the atrium, leading to tissue that is more likely to sustain atrial fibrillation.

THERAPY

Atrial fibrillation has proven to be an ex- tremely difficult arrhythmia to manage with pharmacological therapy, achieving far less than optimal results. Multiple large clini- cal trials have been performed using nearly all of the currently available antiarrhythmic drugs, each of them with disappointing re- sults. Large trials have also been performed comparing rate control (inhibition of conduc- tion through the AV node) with rhythm con- trol (restoration of sinus rhythm) for the ideal therapy. These studies have demonstrated no

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118 ATRIAL FIBRILLATION

significant difference between these treatment options using total mortality, congestive heart failure, and re-hospitalization as end points.

Much of the difficulty with pharmacological therapy lies in the ever-present risk of ventric- ular proarrhythmia.

There are several non-pharmacological treatment strategies that have recently emerged. The Cox maze procedure creates multiple surgical incisions that are then re- paired in the atrium in an attempt to chan- nel the electrical signal between the sinus node and the AV-node while minimizing the formation of a reentrant loop. The surgical maze procedure has proven to have a rea- sonably high success rate, albeit with con- siderable associated surgical morbidity. An attempt to recreate this treatment principle using radiofrequency ablation has been at- tempted using long linear lesions, but with relatively poor results. The understanding of the role of rapidly discharging ectopic foci residing within the pulmonary veins has re- focused the trans-catheter therapies. Applica- tion of radiofrequency energy or cryotherapy (the later particularly in the operating room) are now directed at either electrically isolat- ing the pulmonary veins from the left atrium or at directly ablating the ectopic focus within the veins. A recent large study has demon- strated rhythm control (return to normal sinus rhythm) using radiofrequency ablation tech- niques that is superior to either rate control or rhythm control using pharmacological agents.

The difference between rhythm control using radiofrequency ablation or pharmacological agents likely rests in the proarrhythmia asso- ciated with pharmacological therapy.

Finally, pacemakers and implanted de- fibrillators have been used in an attempt to treat atrial fibrillation or to prevent its onset.

To date, no significant improvement has been achieved relative to pharmacological thera- pies.

In conclusion, while atrial fibrillation is a common arrhythmia in older patients, it

remains rare in pediatric and young adult patients. When encountered in pediatric pa- tients, it often is the paroxysmal form with spontaneous remission and infrequent episodes. In addition, it can occur in the set- ting of other forms of supraventricular tachy- cardia, which are amenable to radiofrequency ablation therapy, resulting in the resolution of the atrial fibrillation. For older patients with symptomatic or hemodynamic consequences, new ablation strategies aimed at eliminating or isolating the triggers within the pulmonary veins appear promising. Due to the infre- quency of this arrhythmia in the young, tran- scatheter treatment targeted directly to atrial fibrillation is rarely indicated or necessary.

SUGGESTED READING

1. Allessie M, Ausma J, Schotten U. Electrical, con- tractile and structural remodeling during atrial fibril- lation. Cardiovasc Res 2002;54:230–246.

2. Nattel S. Therapeutic implications of atrial fib- rillation mechanisms: can mechanistic insights be used to improve AF management. Cardiovasc Res 2002;54:347–360.

3. Wijffels MC, Kirchhof CJ, Dorland R, Allessie M.

Atrial fibrillation begets atrial fibrillation: a study in awake chronically instrumented goats. Circulation 1995;92:1954–1968.

4. Scheinman MM, Morady F. Non-pharmacologic approaches to atrial fibrillation. Circulation 2001;103:2120–2125.

5. Jais P, Haissaguerre M, Shah DC, et al. A focal source of atrial fibrillation treated by discrete radiofre- quency ablation. Circulation 1997;95:572–576.

6. Hohnloser SH, Kuck KH, Lilienthal J. Rhythm or rate control in atrial fibrillation—Pharmacological Inter- vention in Atrial Fibrillation (PIAF): a randomised trial. Lancet 2000;356:1789–1794.

7. The Atrial Fibrillation Follow-up Investigation of Rhythm Management (AFFIRM) Investigators. A comparison of rate control and rhythm control in patients with atrial fibrillation. N Engl J Med 2002;347:1825–1833.

8. Pappone C, Rosanio S, Augello G, et al. Mortality, morbidity, and quality of life after circumferential pulmonary vein ablation for atrial fibrillation: out- comes from a controlled nonrandomized long-term study. J Am Coll Cardiol 2003;42:185–197.

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