Catheter Ablation in the Treatment of Paroxysmal and Permanent Atrial Fibrillation

Catheter Ablation in the Treatment of Paroxysmal and Permanent Atrial Fibrillation

1.0 Introduction

Atrial fibrillation affects up to 5 million people in the United States, and data suggest that as the population ages, the incidence will continue to increase. According to statistics, there are 5% patients who have nonvalvular atrial fibrillation and are subject to ischemic stroke. Patients having normal sinus rhythm have half the death rate as compared to patients with atrial fibrillation. The overall cost of treating recurrent atrial fibrillation has been estimated to be more than $6.5 billion per year. [1]

Atrial fibrillation is usually a progressive disease. The natural history often begins with infrequent episodes of limited duration termed paroxysmal atrial fibrillation (often defined as episodes that terminate spontaneously within 1 week). Such episodes then tend to become more frequent and longer in duration, progressing to persistent atrial fibrillation (which fails to terminate spontaneously within 7 days and may require cardioversion) or permanent atrial fibrillation (if the arrhythmia lasts for more than 1 year and cardioversion either has not been attempted or has failed). Symptoms include palpitations, shortness of breath, and fatigue; particularly for symptomatic patients, atrial fibrillation has adverse effects on quality of life.

2.0 Pathophysiology and Effect of Therapy

The electrophysiological basis of atrial fibrillation requires both a trigger that initiates the dysrhythmia and a substrate that can sustain it. The most common triggers of atrial fibrillation are ectopic atrial beats that arise from the pulmonary veins containing muscle sleeves. These triggers may be provoked by the intrinsic activity of cardiac ganglionic plexuses, which are clustered in the vicinity of the pulmonary vein-left atrial junction. The pulmonary vein-left atrial junction and an enlarged atrium harboring fibrosis and inflammation serve as the substrate for sustaining wavelets of atrial fibrillation. With persistence of atrial fibrillation, a further electrophysiological change in the atria — namely, shortening of the refractory period of the atrial muscle — occurs and predisposes to the development of other triggers and wavelets. This process results in perpetuation of atrial fibrillation and in a greater predisposition to atrial fibrillation. Maintenance of sinus rhythm can reverse these changes and mechanisms. [2]

Atrial fibrillation ablation is a therapeutic technique that uses radiofrequency energy or freezing to destroy atrial tissue that is involved in the propagation of the dysrhythmia. Radiofrequency ablation generates an alternating electrical current that passes through myocardial tissue, creating heat energy that conducts to deeper tissue layers. At temperatures of 50°C or higher, most tissues undergo irreversible coagulation necrosis and then evolve into nonconducting myocardial scar tissue. Cryoablation destroys tissue by freezing.

The principal objective of atrial fibrillation ablation is the electrical disconnection of the pulmonary-vein triggers from the atrial substrate (often called “pulmonary-vein isolation”). To achieve this goal, ablation is performed around the pulmonary-vein orifice (Figure 1)

Figure 1. Catheter Placement during Atrial Fibrillation Ablation and Conduction Block of Pulmonary-Vein Triggers by Means of Ablation.

Source: Rodriguez LM, Geller JC, Tse HF, Timmermans C, Reek S, Lee KL, Ayers GM, Lau ...