INTRODUCTION: Advancing age is an independent risk factor for atrial fibrillation (AF), which is considered to be initiated by ectopic triggers and maintained by an arrhythmogenic substrate. It is not known whether substrate changes produce this age-related increase in propensity toward AF. We addressed the hypothesis that advancing age is associated with changes in biatrial electrophysiology even in patients with no history of atrial arrhythmias. METHODS AND RESULTS: Patients with left-sided accessory pathways and requiring routine electrophysiological studies were recruited. Electroanatomic mapping was performed in the left and right atria of 23 patients (age ranging from 17 to 75 years) with structurally normal hearts and no history of AF during sinus rhythm and pacing. Unlike previous studies, a trigonometric method was used to quantify wavefront propagation velocities (WPV) precisely in the direction of propagation. Refractoriness was measured at 2 cycle lengths, at three different atrial sites. Both right (r =-0.77, P < 0.0001) and left (r =-0.79, P < 0.001) atrial WPV demonstrated strongly inverse correlation with age. Furthermore, left and right WPVs were highly correlated (r = 0.66, P < 0.01), with velocities being 6.4 +/- 2.2 cm/sec higher in the right atria (P < 0.01). Refractoriness was significantly correlated with increasing age only at the septum (r = 0.53, P < 0.01). Left atrial wavelength was inversely correlated with increasing age (r =-0.56, P = 0.03). P wave duration was associated with age (r = 0.42, P = 0.04) and left atrial size (r = 0.44, P = 0.04) but not atrial WPV. CONCLUSION: Aging human atria demonstrate progressive decline in WPV and increase in septal refractoriness. These age-related changes in biatrial electrophysiology are likely to be important factors in the age-related increase in AF prevalence.
INTRODUCTION: Advancing age is an independent risk factor for atrial fibrillation (AF), which is considered to be initiated by ectopic triggers and maintained by an arrhythmogenic substrate. It is not known whether substrate changes produce this age-related increase in propensity toward AF. We addressed the hypothesis that advancing age is associated with changes in biatrial electrophysiology even in patients with no history of atrial arrhythmias. METHODS AND RESULTS:Patients with left-sided accessory pathways and requiring routine electrophysiological studies were recruited. Electroanatomic mapping was performed in the left and right atria of 23 patients (age ranging from 17 to 75 years) with structurally normal hearts and no history of AF during sinus rhythm and pacing. Unlike previous studies, a trigonometric method was used to quantify wavefront propagation velocities (WPV) precisely in the direction of propagation. Refractoriness was measured at 2 cycle lengths, at three different atrial sites. Both right (r =-0.77, P < 0.0001) and left (r =-0.79, P < 0.001) atrial WPV demonstrated strongly inverse correlation with age. Furthermore, left and right WPVs were highly correlated (r = 0.66, P < 0.01), with velocities being 6.4 +/- 2.2 cm/sec higher in the right atria (P < 0.01). Refractoriness was significantly correlated with increasing age only at the septum (r = 0.53, P < 0.01). Left atrial wavelength was inversely correlated with increasing age (r =-0.56, P = 0.03). P wave duration was associated with age (r = 0.42, P = 0.04) and left atrial size (r = 0.44, P = 0.04) but not atrial WPV. CONCLUSION: Aging human atria demonstrate progressive decline in WPV and increase in septal refractoriness. These age-related changes in biatrial electrophysiology are likely to be important factors in the age-related increase in AF prevalence.
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