Age-Related Changes in Human Left and Right Atrial Conduction
Age-Related Changes in Human Left and Right Atrial Conduction
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.
Advancing age is an important independent risk factor for atrial fibrillation (AF). Population-based studies have shown that for each decade of advancing age, the risk of developing AF, including postoperative AF more than doubles. The pathological and functional changes in the atria that lead to this age-related predisposition to AF are not well understood. Although current theories of AF suggest that left atrial triggers are important in the initiation of human AF, it is not known whether the increasing prevalence with age is related to left atrial triggers or the development of an arrhythmogenic substrate.
Classical models of arrhythmogenesis predict that shortening of refractoriness and slowing of conduction are proarrhythmic. Although patients with AF accordingly demonstrate shortening of refractory periods, most previous studies of normal subjects have concluded that atrial refractoriness increases with age, which would be expected to protect from AF. Changes in atrial conduction velocity (CV) with age might therefore be expected to be proarrhythmic to offset the effects of prolonged refractoriness.
Although conduction is stochastic at the microscopic level, in the intact atrium this microscopic irregularity is smoothed out into uniform wavefronts. Wavefront propagation velocity (WPV) can only be measured accurately if the direction of the wavefront and the time taken to travel a specific distance in that direction can be determined. Previous studies measuring WPV by dividing the distance by the activation interval between two points not necessarily in line with the direction of wavefront propagation would overestimate the true velocity and introduce artefactual variation in the data. Accordingly, measurements of WPV from previous studies with endocardial mapping techniques have tended to show exaggerated CVs (up to twofold) and greater variances (up to threefold), compared with studies using simultaneous multielectrode intraoperative epicardial mapping in which the direction of wavefront propagation can be taken into account but which are subject to the limitations of studying limited areas of atrial free wall in the anesthetized patient. Unlike previous studies investigating endocardial CV, we validated an algorithm that incorporated the local vector of activation to measure WPV in the direction of wavefront propagation from three-dimensional electroanatomical maps to test the hypothesis that there are age-related alterations in WPV in both atria.
Abstract and Introduction
Abstract
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 important independent risk factor for atrial fibrillation (AF). Population-based studies have shown that for each decade of advancing age, the risk of developing AF, including postoperative AF more than doubles. The pathological and functional changes in the atria that lead to this age-related predisposition to AF are not well understood. Although current theories of AF suggest that left atrial triggers are important in the initiation of human AF, it is not known whether the increasing prevalence with age is related to left atrial triggers or the development of an arrhythmogenic substrate.
Classical models of arrhythmogenesis predict that shortening of refractoriness and slowing of conduction are proarrhythmic. Although patients with AF accordingly demonstrate shortening of refractory periods, most previous studies of normal subjects have concluded that atrial refractoriness increases with age, which would be expected to protect from AF. Changes in atrial conduction velocity (CV) with age might therefore be expected to be proarrhythmic to offset the effects of prolonged refractoriness.
Although conduction is stochastic at the microscopic level, in the intact atrium this microscopic irregularity is smoothed out into uniform wavefronts. Wavefront propagation velocity (WPV) can only be measured accurately if the direction of the wavefront and the time taken to travel a specific distance in that direction can be determined. Previous studies measuring WPV by dividing the distance by the activation interval between two points not necessarily in line with the direction of wavefront propagation would overestimate the true velocity and introduce artefactual variation in the data. Accordingly, measurements of WPV from previous studies with endocardial mapping techniques have tended to show exaggerated CVs (up to twofold) and greater variances (up to threefold), compared with studies using simultaneous multielectrode intraoperative epicardial mapping in which the direction of wavefront propagation can be taken into account but which are subject to the limitations of studying limited areas of atrial free wall in the anesthetized patient. Unlike previous studies investigating endocardial CV, we validated an algorithm that incorporated the local vector of activation to measure WPV in the direction of wavefront propagation from three-dimensional electroanatomical maps to test the hypothesis that there are age-related alterations in WPV in both atria.
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