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Ablation of atrial fibrillation: Facts for the referring physician

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Release date: October 1, 2018
Expiration date: September 30, 2019
Estimated time of completion: 1 hour

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ABSTRACT

Radiofrequency ablation has become a safe and effective treatment for atrial fibrillation. We believe that referral to an electrophysiologist for consideration of ablation may allow for better rhythm control and outcomes by altering the natural history of atrial fibrillation progression.

KEY POINTS

  • Atrial fibrillation is increasing in prevalence with the aging of the US population and is associated with worsening quality of life and increased risk of stroke, heart failure, and death.
  • Atrial fibrillation results in adverse atrial remodeling and fibrosis, eventually leading to persistence of the arrhythmia and making rhythm control difficult.
  • Catheter ablation has evolved to be a safe procedure with technologic advancements, especially in experienced tertiary care centers.
  • The primary aim of atrial fibrillation ablation is to reduce symptoms and improve quality of life. In theory, it could also decrease the risk of stroke, heart failure, and death, but these outcomes have not been systematically evaluated in a large randomized controlled trial.


 

References

A 64-year-old man with hypertension but  without known structural heart disease presents for a second opinion on management of his atrial fibrillation. The condition was first diagnosed at age 38, when he experienced palpitations and shortness of breath on exertion; at times he also experienced decreased endurance and fatigue without overt palpitations. At first, these episodes occurred about twice a year, and the patient was managed with a beta-blocker for rate control and an oral anticoagulant.

Over the past 10 years, the episodes have become more frequent and longer-lasting and have required frequent cardioversions. He was given flecainide for rhythm control but continued to have frequent episodes, and so about 1 year ago he was switched to amiodarone, which controlled his rhythm better. However, after reading about side effects of amiodarone, he decided to seek a second opinion.

He was evaluated by our team and eventually underwent radiofrequency ablation. During the procedure, he was noted to have diffuse scarring and fibrosis of his left atrium, and afterward he continued to require antiarrhythmic drugs to maintain sinus rhythm.

Should he have been referred sooner? What factors should primary care physicians consider when referring a patient with atrial fibrillation for ablation?

THE EPIDEMIC OF ATRIAL FIBRILLATION

Atrial fibrillation is a large and growing public health problem. In 2010, it was estimated to affect 2.7 to 6.1 million people in the United States, and with the rapid aging of our population, its prevalence is expected to rise to between 5.6 and 12 million by 2050.1–3 It is associated with significant morbidity, poor quality of life, and increased risk of death, heart failure, stroke, and cognitive impairment.

The number of new cases per year has increased over the years despite research and preventive measures, which may reflect aging of the population and increased survival rates in patients with cardiovascular or comorbid conditions.1,4

Thus, atrial fibrillation is one of the most common cardiovascular conditions encountered by primary care physicians and cardiologists, putting them at the forefront of its management. Proper treatment in its early stages and referral to a specialist for advanced management may alter its natural history and improve clinical outcomes.

HOW DOES ATRIAL FIBRILLATION ARISE AND PERSIST?

Much is still unknown about the pathogenesis of atrial fibrillation, but considerable progress has been made in the past few decades, opening the door for clinical ablative strategies.

Multiple wavelet hypothesis

Until the late 1980s, the most widely accepted conceptual mechanism of atrial fibrillation was the multiple wavelet hypothesis developed by Moe et al.5 According to this hypothesis, atrial fibrillation begins with multiple independent wavelets occurring simultaneously and spreading randomly throughout both atria, and it persists if there are a minimum number of coexisting wavelets, increased atrial mass, and heterogeneous conduction delays across the atrial tissue.

The surgical maze procedure, in which a series of incisions arranged in a maze-like pattern is created in the left atrium, was predicated on this model. The theory was that these surgical lesions would compartmentalize the atria into discrete electrical segments and thereby reduce the number of circulating random wavelets.6,7

However, experimental and clinical studies suggest that although randomly propagating wavelets can contribute to maintaining atrial fibrillation, focal triggers are noted in most cases.

Focal triggers

In 1997, Jaïs et al8 observed that atrial fibrillation is often triggered by a rapidly firing ectopic focus and that ablation of that focus can eliminate it. These ectopic foci are often found at or near the ostia of the pulmonary veins or near the superior vena cava.8,9 It is now well established that ectopic foci in the pulmonary veins are crucial triggers that initiate atrial fibrillation.

Trigger-and-substrate theory

Atrial fibrillation is currently thought to arise from focal triggers

Figure 1. Atrial fibrillation is currently thought to arise from focal triggers, many of which are located in the pulmonary veins, and to be maintained by an abnormal substrate, ie, scarring and fibrosis of the left atrium.

Currently, the most widely accepted theory is that atrial fibrillation requires both a trigger and a susceptible substrate (Figure 1). Triggers consist of rapidly firing foci, most commonly located in the pulmonary veins but also in the superior vena cava, posterior wall of the left atrium, the vein and ligament of Marshall, the coronary sinus, and the left atrial appendage.

The substrate for maintaining atrial fibrillation consists of an abnormal left atrium with heterogeneous fibrosis (scarring) and conduction delays. Any heart disease that increases left atrial pressure could lead to atrial dilation and remodeling, which could be substrates for atrial fibrillation. Extensive atrial remodeling and scarring are associated with progression and persistence of atrial fibrillation and make rhythm control more challenging.

Atrial fibrillation begets atrial fibrillation

As shown in the case above, over time, paroxysmal atrial fibrillation often progresses to persistent and long-standing atrial fibrillation if not aggressively managed initially.

In 1972, Davies and Pomerance10 performed 100 autopsies and found that the people who had had atrial fibrillation for longer than 1 month had lost muscle mass in the sinus node and internodal tract, and their atria were dilated. The study introduced the concept that atrial fibrillation itself causes pathologic changes in the atrium.

Wijffels et al,11 in an experiment in goats, showed that atrial fibrillation produced by rapid bursts of atrial pacing was initially paroxysmal. However, as they continued to induce atrial fibrillation over and over again, it lasted progressively longer until it would persist for more than 24 hours. Thus, in a relatively short time, the atria went from supporting paroxysmal fibrillation to supporting persistent fibrillation.

Atrial fibrillation leads to electrophysiologic and anatomic remodeling in the atrium, which leads to a shorter action potential duration and a shorter refractory period. This in turn makes it easier for atrial fibrillation to persist.12

Because atrial fibrillation tends to progress, intervening early may improve its outcomes. Early ablation has been shown to improve the chances of staying in sinus rhythm in both paroxysmal and persistent atrial fibrillation.13–15

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