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DOI: 10.5935/abc.20190087 Over the past years, catheter ablation (CA) for atrial fibrillation (AF) has established itself as a well-recognized strategy in the management of patients with AF and an important option for rhythm control. Although CA is more effective than antiarrhythmic drug therapy, AF recurrences are common during the follow-up.1 Late recurrence, during the first 9 months after the blanking period, occurs in 25%–40% of cases and is predominantly linked to the recovery of electrical conduction between the pulmonary veins (PVs) and the left atrium (LA), irrespective of the type of AF. The incidence of very late recurrence (after more than 12 months postablation) has been shown to be higher than previously expected, with an annual recurrence rate estimated at 7.6%.2 Bunch et al.3 reported AF recurrence rates ranging from 52% (≤ 50 years + paroxysmal AF) to 75% (> 80 years + paroxysmal AF).3 In a series of 509 consecutive patients undergoing paroxysmal AF ablation by Teunissen et al., after a single procedure, antiarrhythmic drugs free success rate was 41.3%4. The predominant mechanism of very late recurrence includes, in addition to the PV connection, the development of non-PV triggers, and development and maturation of substrate. The predictors appears to be the nonparoxysmal form of AF at baseline, organic heart disease, advanced age, and obesity. AF is often associated with atrial structural remodeling and causes LA fibrosis/scarring and dilatation. Substrate progression is a multifactorial and time-dependent response of cardiac myocytes to varying “stressors”, including electrical, mechanical, and metabolic stressors. Some components of the LA changes are reversible (adaptive), whereas others are permanent (maladaptive). Most risk factors affect AF by causing structural remodeling. Progression of atrial damage due to underlying heart disease is a major factor. Recent studies suggest that AF recurrence can be prevented by effectively managing risk factors such as sleep apnea, obesity, high blood pressure, hyperglycemia, and dyslipidemia, presumably by curtailing further damage and/or reversing existing abnormalities. Conversely, AF itself can cause progression of the substrate. In addition to complexion-channel remodeling that accelerates repolarization and alters conduction properties, rapid activation of atrial cardiomyocytes causes profibrotic changes in fibroblast function and promotes atria fibrosis.

arquivos brasileiros de cardiologia

Left Atrial Stiffness, a Marker of Atrial Cardiomyopathy, and Atrial Fibrillation - Relationships and Predictors for Procedure Success after Catheter Ablation