Natural History of AF
The concept of “AF begets AF” remains a cornerstone in the understanding of the natural history of AF progression.14 Increasing AF burden is associated with progressive atrial remodeling and the development of atrial fibrosis, which can contribute to the long-term persistence of AF.15 A wealth of experimental data exist regarding structural and functional atrial changes that contribute to the development, maintenance, and progression of AF. In contrast, considerably less data exist regarding the natural history of AF.16,17 This is in large part related to the difficulty in accurately assessing the underlying burden of AF in individuals and large populations. Thus, estimates of the prevalence of clinical AF subtypes and their progression have evolved with the changes in population characteristics, associated comorbidities, and development of modern arrhythmia monitoring technology. For example, the rate of progression appears to be very low in individuals with an initial diagnosis of AF who are younger than 60 years of age and who have no concomitant heart disease. Among 97 individuals followed over three decades, 21% had an isolated AF event without further recurrence, 58% had recurrent AF, and 22% developed persistent AF.18 Other longitudinal studies have demonstrated a much higher rate of AF progression. One recent study examined the rate of progression to persistent AF among 1219 paroxysmal patients with AF.13 Progression to persistent AF was observed in 15% of the patients over 12 months of follow-up. Predictors of progression included age, hypertension, prior transient ischemic attack (TIA) or stroke, and chronic obstructive pulmonary disease. Similar results were reported in another recent study that examined AF progression while waiting for an AF ablation procedure.19 Among 564 patients with PAF, 11% progressed to persistent AF during a 10-month follow-up period. In this study, heart failure (HF) and a left atrial (LA) diameter >45 mm were predictive of progression. These findings raise the possibility that the clinical progression of AF could be driven by the development of associated comorbidities as opposed to the arrhythmia itself. Moreover, recent studies using pacemaker-documented AF burden have demonstrated a more complex natural history of the arrhythmia, with persistent AF reverting to paroxysmal forms, without intervention.20 This highlights our incomplete understanding of the natural history of clinical AF and the need for larger studies focusing on the accurate assessment of AF progression and regression.