The atrium: central part of a building—a definition, cardiologists should not forget (2024)

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This editorial refers to ‘Left atrial enlargement and its association with left atrial strain in University athletes participated in 2015 Gwangju Summer Universiade’ by J.-H. Park et al., pp. 865–872.

The left atrium (LA) is fundamental and its size has been proposed as the ‘haemoglobin A1c’ of LV filling pressure and diastolic function.1

The atrial wall is thin and more sensitive to the increase in load than the ventricle. Looking at the atrium is thus a more sensitive approach to appreciate the consequences of risk factors, diseases, or endurance training. Park et al.2 have to be congratulated. They did an extremely important work by looking at LA enlargement in highly trained university athletes and its association with LA strain (influenced by function, geometry, and loading conditions). They demonstrated that 19.1% of the athletes have LA enlargement while only 5.2% have decreased LA reservoir function. Importantly, those with a decrease in reservoir function did not necessarily have LA enlargement. They defined two parameters for describing significant LA remodelling: Indexed LA volume > 42 mL/kg and LA reservoir strain < 27.6%. Not only the indexed LA volume but also LA reservoir strain might be considered in the future, as a means for reporting on LA remodelling in echo reports.

Up to recent years, it has been somewhat imprecise to quantify LA function and its three components: the reservoir function (that we are focusing on a lot nowadays, linked to the atrial compliance), the conduit function and the atrial booster pump function (that is key but more challenging to quantify).3^,4 Recently, numbers of publications have brought to light the robust ability of imaging techniques, mainly echocardiography and magnetic resonance imaging, to measure the size and the function of the atria. Echocardiographic techniques including the automated border detection in 2D and 3D, the speckle (or feature) tracking for quantifying the deformation of atrial walls over the cardiac cycle are largely available at present. Meanwhile, visualization and quantification of atrial fibrosis are becoming more feasible for clinical use by means of magnetic resonance imaging.3^,5 We might also be able to use ultrafast imaging or flow imaging very soon. These will provide more clues about the atrium and its key role as the central part of the building.

In athletes, the LA enlargement is not necessarily a pathologic finding. LA is dilated in endurance athletes with high cardio-respiratory fitness. It has been reported that left atrial volume index (LAVI) was >34 mL/m² in 39% of participants of a Norwegian athletic cohort, and LAVI was positively associated with VO_2peak. Therefore, it is probably appropriate to use LA strain in addition to LA volume, for a more accurate quantification of LA remodelling.6 Previously, we demonstrated that LA and right atrial sizes were unable to predict the development of atrial fibrillation in athletes whereas the reservoir strain was extremely powerful in that goal.6 Indeed, LA reservoir strain seems key to best understand LA function.

The typology of the patients, we now see, has changed. Twenty years ago, it was hardly believed that a significant mitral regurgitation could be linked to a LA disease.7 Today, we understand that a proportion of patients with heart failure and preserved ejection fraction, have mainly symptoms related to LA failure.8 Furthermore, secondary tricuspid regurgitation (TR) (major challenge for the management of patients in the upcoming years) is mainly driven by RA remodelling and consequently the tricuspid annular enlargement and flattening.9 Atrial remodelling could strongly impact the atrio-ventricular annulus. For instance, Figure1 illustrates how tricuspid annulus and RA geometry are influenced by loading conditions. According to the clinical context, atrial remodelling can be spherical or oblong. Some patients will have a severe resounding on atrio-ventricular annulus while some will not. Similarly, why some athletes have a LA remodelling as observed by enlargement and reduced deformation and some do not despite having the same level of training and similar level of performance? Probably intrinsic factors such as fibrosis that impacts the distensibility and contraction capability of the atria intervene. This is the reason why one should not limit the quantification of LA remodelling to LA dimensions.

Some patients without identified cardiomyopathies develop ‘lone’ paroxysmal AF. Most of these patients have abnormal LA strain despite normal LA size and morphology, underlining the fact that those atria are not completely healthy. Abnormal LA reservoir function has been associated with recurrence of AF after cardioversion, low success rate of ablation therapies, and higher risk of cardio-embolic events.10–12 The stretch of the atrium can lead to severe enlargement or less important dilatation but myocardial fibrosis and risk of recurrent arrhythmias.

Recently, atrial size has been underscored in the guidelines for the indication of mitral valve surgery or for estimating the risk of hard events including sudden cardiac death and ventricular arrhythmias, in hypertrophic cardiomyopathies.13^,14 In addition accumulating evidence related to cryptogenic stroke, success of ablative therapy in lone atrial fibrillation, ischaemic heart disease, and in heart failure encourages the recommendation of reporting not only the LA volume but also LA reservoir strain in many clinical conditions.4^,15^,16

LA is the central part of the building… It is excessively prone to volume and/or pressure overload,17 and once LA dysfunction is established, pulmonary capillary veins lack the haemodynamic damper and consequently HF symptoms are more evident.18 As such, LA failure may be the result of intrinsic atrial myopathy,19 altered loading forces (i.e. hypertension, congestion, valvular heart disease), or other maladaptive compensatory mechanisms.20

There is also a gender issue as reflected in the CHAD₂DS₂-VASC score for thrombo-embolic risk assessment. Women have a high cardio-embolic risk linked to the lower stroke volume perhaps but also, one should probably look more carefully at the atrial remodelling and not only the volume as underlined above. There might be geometrical differences between men and women. Park et al.2 showed that LA diameter and volumes were higher in men and strain was higher in women. The main registries having demonstrated the higher risk of stroke in women did not take into account LA dimensions and function.21^,22 Two important projects from the European Association of Cardiovascular Imaging (EACVI); the EURO-Afib registry initiated by Galderisi et al., and the MASCOT Registry lead by Cameli et al., both conducted in large series, will provide important data for our understanding of LA remodelling and its relationship to atrial fibrillation and thrombo-embolic risk.23

Historically, echocardiographic reports were including only the LA anteroposterior diameter. Today, quantification of LA indexed volume (>42 mL/kg) and LA reservoir strain (<27.6%) as shown in this study by Park et al.2 corroborate certainly a better description of LA remodelling. Also, large validation studies are awaited.23

Conflict of interest: none declared.

The opinions expressed in this article are not necessarily those of the Editors of EHJCI, the European Heart Rhythm Association or the European Society of Cardiology.

References

Published on behalf of the European Society of Cardiology. All rights reserved. © The Author(s) 2020. For permissions, please email: journals.permissions@oup.com.

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