Atrial deformation in athletes with AF: chronic adverse remodelling or transient mechanical stunning?

This editorial refers to ‘Atrial function is altered in lone paroxysmal atrial fibrillation in male endurance veteran athletes’, by A. Hubert et al., pp. 145–153. It is well established that regular physical activity is beneficial to cardiovascular health and well-being.1,2 Current physical activity guidelines recommend 30 min of moderate intensity physical activity at least 5 days/week or 25 min of vigorous activity 3 days/week, for the prevention of cardiovascular disease.3 Despite the well-known benefits of these exercise regimens, data are scarce on the upper ranges of the exercise–dose relationship. Over the last decades, there has been an increase in the number of middle‐aged and older individuals engaging in competitive sports and mass exercise events in the more economically developed countries.4 Although several studies demonstrated that endurance sports participation is associated with an increased life expectancy compared with the general population,5,6 there is increasing evidence suggesting that long-term endurance exercise is associated with an increased risk of developing some cardiac arrhythmias, especially atrial fibrillation (AF).7,8 In the general population, AF is associated with an increased risk of mortality and morbidity resulting from stroke, heart failure, and impaired quality of life, with enormous socio-economic implications.9 So far, similar hard outcome data have yet to be reported in athletic populations with AF. Nevertheless, athletes with AF seem to have a higher tendency to be symptomatic, disturbing sporting activity and exercise performance, and to progress into permanent AF.10 Therefore, early detection of paroxysmal AF would be favourable to prevent progression of the underlying substrate. Hence, it could be hypothesized that timely reduction of endurance sports participation may delay further adverse atrial remodelling, although this strategy remains unproven. In addition, targeted isolation of the pulmonary veins is more effective in paroxysmal AF, whereas more extensive lesions are required with increasing structural and electrical remodelling of the atrial tissue. Hubert et al.11 report on the use of echocardiography-derived functional assessment of the left atrium as an additional tool for the detection of atrial fibrillation among endurance athletes. The authors evaluated atrial volumes and function in a cohort of 27 veteran endurance athletes with a history of paroxysmal AF when compared with 30 age- and gender-matched endurance athletes with similar training status. The main finding of this study was that deformation measures of left atrial function outperformed volumetric measurements in the identification of athletes with a history of paroxysmal AF. Furthermore, it was found that electrocardiographic P-wave morphology during sinus rhythm did not differ between both endurance athletes with and without AF. The findings of this study may be of direct clinical utility as an adjunct to diagnosing AF in athletes in whom it is suspected. When symptoms are frequent, traditional workup using 24 h of Holter monitoring is adequate to make a diagnosis. However, most frequently events are far less common and long-term recording devices are required to detect the rhythm disturbance. However, palpitations are one of the most common complaints in athletic populations, with an incidence ranging from 0.3% to 70% depending on age and the type of sport being studied.12 In this context, the demonstration of left atrial dysfunction to identify athletes at risk of AF may be useful to select individuals in whom more advanced monitoring options should be pursued. An intriguing finding of this study is the discrepancy between volumetric and deformation measures of atrial function. Although volume measures were not accurate in distinguishing athletes with and without AF, deformation measures of reservoir, conduit, and booster function had good sensitivity and specificity to detect athletes with paroxysmal AF. Possible explanations to explain this discrepancy are that different atrial characteristics are being measured or strain is more sensitive than volume measures and identify changes in substrate at an earlier stage. It is perhaps not surprising that longitudinal atrial strain outperforms atrial volumes, because it measures function relative to size, and both are markers of atrial adverse remodelling. The motion assessed in longitudinal strain can largely be simplified to the magnitude of displacement of the mitral annulus in a manner identical to assessment of longitudinal function of the left ventricle. This raises the question as to how does strain of the atrium differ from that of the ventricle. Although the two are closely related because of the shared assessment of motion of the annular plane, they differ in that this motion is expressed as a percentage of the size of the respective chamber. Thus, if the ventricle is of normal size but the atrium is dilated then the atrial strain will be reduced more than that of the ventricle. This could prove very useful when trying to find a single measure that encapsulates the key features of atrial function. One might expect that dilation and reduced contractile motion would be the two key features of a dysfunctional atrium and strain incorporates both. Furthermore, strain assessment enables us to divide atrial function into various components: reservoir, conduit, and booster, with relative ease. The most relevant phase is the booster (also sometimes referred to as contractile) phase, because this is when changes in atrial motion and size are most dependent on atrial function as opposed to left ventricular diastolic properties. Notably, however, the two can never be completely considered in isolation. Despite the observed association between left atrial dysfunction and the occurrence of AF, it is difficult to establish cause and effect. Previous animal experiments demonstrated that even brief episodes of AF, lasting less than 60 min, result in marked depression of left atrial function, i.e. mechanical stunning.13 Therefore, it is possible that part of the functional changes in the athletes with paroxysmal AF are a consequence rather than a predictor of AF. This is an important distinction. Reductions in atrial strain that precede the onset of AF could be of critical clinical importance, as they may enable risk stratification and identify a target group in whom the efficacy of detraining in preventing AF may be tested. On the other hand, if reduced atrial strain is a post-AF consequence then it would be interesting to assess the relationship between strain and the risk of AF recurrence. It would seem that the only robust way of assessing the clinical consequences of reduced atrial strain in an unbiased fashion is to prospectively assess this parameter in a cohort or healthy athletes and follow them prospectively for incident AF (see Figure 1). This will require a large cohort and long-term follow-up, but this would seem justified, given the burden of AF on public health resources. This would not be the first occasion in which the ‘athletic model’ provides unique insights into a disease process with implications for the general population. Comparison of atrial strain in young and old endurance athletes. A 60-year-old former elite cyclist (upper panel) has reduced reservoir and booster (contractile) atrial strain relative to normal values and relative to the 17-year-old professional cyclist in the lower panel. Does this represent a risk for atrial fibriallation? Conflict of interest: None declared.