Effect of lifetime endurance training on left atrial mechanical function and on the risk of atrial fibrillation

Abstract

Background: Left atrial (LA) dilation and prolongation of the signal-averaged P-wave duration (SAPWD) are linked to the amount and intensity of training. There is growing evidence that this atrial anatomical and electrical remodeling could be the substrate for the increased risk of atrial fibrillation (AF) observed in retrospective cohort studies of athletes. The aim of this study was to evaluate the impact of LA anatomical and electrical remodeling, in the context of lifetime exercise endurance training, on its passive (conduit) and active (pump) function measured by 2-D speckle tracking echocardiography (STE), and to find a link between LA functional adaptation and AF. Methods: Amateur male runners ≥30 years old were recruited (n=109) and, after exclusion of subjects having an office blood pressure >140/90mmHg or other cardiovascular risk factors, stratified in 3 groups according to lifetime training hours: low ( 4'500 h, n=30). Baseline examination consisted of an ECG with analysis of the SAPWD, Doppler echocardiography including STE, 24-hour ambulatory ECG and BP monitoring. Results: No differences were found, between the groups, in terms of age, BP, and diastolic function. LA maximal volume index (30±5, 33±5 vs. 37±6ml/m2, p<0.001), and conduit volume index (9±3, 11±3 vs. 12±3ml/m2, p<0.001) increased significantly from the low to the high training group, unlike the STE parameters which were comparable between the groups: strain pump -15.0±2.8, -14.7±2.7 vs. -14.9±2.6%, p=0.927; strain conduit 23.3±3.9, 22.1±5.3 vs. 23.7±5.7%, p=0.455. Independent predictors of LA strain conduit function were age, maximal early diastolic velocity of the mitral annulus, heart rate and peak early diastolic filling velocity. Left ventricular end diastolic volume index and stroke volume index both increased significantly with lifetime training hours. SAPWD (135±11, 139±10 vs. 148±14ms, p<0.001) and the number of premature atrial contractions (3 [1-7], 6 [2-12], 9 [3-26], p=0.008) increased from the low to the high training group. In one runner of the high training group 4 episodes of non-sustained AF were recorded. Conclusions: The LA anatomical and electrical remodeling does not have a negative impact on atrial mechanical function. LA enlargement may be an adaptation to volume overload, which permits a greater volume delivery to the simultaneously dilating left ventricle. A possible link between these risk factors for AF and its actual, rare occurrence in this athlete population, could not be uncovered in the present study.