With aging, the pathogenesis processes of atrial fibrillation (AF) are heightened. In this article, we review the mechanisms that predispose elderly patients to AF. We also highlight the unique features in diagnosis, stroke prevention, and treatment strategies for the elderly patient with AF.
K E Y W O R D Saging, arrhythmia, atrial fibrillation 1 | BACKGROUND Atrial fibrillation (AF) is one of the most common diseases in elderly patients, and its prevalence increases with age. 1 The prevalence is estimated to be 0.3% in subjects of 40 years old, 5%-9% in those between 60 and 80 years old, and approximately 10% of patients more than 80 years old. 2 There are two primary factors that contribute to the high prevalence of AF in the elderly, the degenerative changes of the aging heart itself and the accompanying structural heart and systemic diseases, most notably coronary artery disease and hypertension, whose incidences increase cumulatively over one's life.
| ATRIAL REMODE LIN G IN AGING HEARTSThe pathogenesis processes of AF are heightened by aging. The incidence of comorbidities such as ischemic heart disease and heart failure that are risk factors for AF is significantly increased in the elderly. Aging is associated with increased p-wave duration and dispersion, reflecting intra-atrial conduction abnormalities. Changes in p-wave morphology may herald the onset of AF. 3Atrial structural remodeling predisposes aged atria to AF. Progressive atrial fibrosis is a hallmark of aging heart. 4 Atrial fibrosis is known to occur as the result of aging-related changes in the cardiac collagen matrix and predisposes patients to AF. 5,6 Aging was identified as the most significant factor in atrial fibrogenesis (Figure 1). 7 An increase in fibrotic and a decrease in hypoxic signaling and microvessel density coupled with a differential expression of matrix metalloproteinases and tissue inhibitors of metalloproteinases that favors fibrosis may contribute to age-related atrial fibrogenesis. Cellular hypertrophy of atrial cardiomyocytes occurs as a compensatory response to aging-related loss or apoptosis of atrial cardiomyocytes. 8 Hypertrophic myocytes in the rat left atrium demonstrated an increased propensity to spontaneous Ca 2+ transients with a potential to generate triggered arrhythmias. 9Electrical remodeling is an important pathophysiological mechanism that promotes the progression from paroxysmal AF to permanent AF. The shortening of the atrial action potential duration (APD), and thereby the atrial effective refractory period (AERP), potentiates the pathogenesis of AF and underlies the progression of AF as "AF begets AF." 10 However, there have been conflicting data in agerelated changes in AERP although APD seems to be shortened with aging. 11-15 Such inconsistency in data could be a reflection of the heterogeneity in AERP distribution and nonlinear nature of the correlation between the APD and AERP, as well as the limited pacing sites and pacing cycle lengths.Although it is generally recognized that intra-atrial condu...