DISCUSSION
LA remodelling is a common response to AF, manifesting as increased size and reduced function, deteriorating with increasing AF burden [5]. RA structure and function were not thoroughly investigated in patients with LSPSAF than compared to LA. Moreover, data on the association between RA parameters and LVA burden seem to be lacking. Therefore this study aimed to describe echocardiography determined RA dataset among LSPSAF patients and identify if any of these could predict the existence of voltage-derived LA fibrotic remodelling.
We have shown that (1) the majority of the study population presented enlarged RA, however RA volumes were larger than LA volumes in the minority of cases (2) RA enlargement had a positive correlation with the presence of mild-to-moderate TR, LVH, LA enlargement, LA area and volume (3), none of the RA indices were associated with the prediction of the absolute LVA or advanced LA fibrotic remodelling, although patients with severe LVA burden presented longer RA length and a larger area comparing to patients with a less advanced remodelling pattern.
Many studies reported that voltage-defined LA remodelling increases with LA size [6-8] however not among LSPSAF patients [2]. It was suggested that the presence of functional LA enlargement due to AF persistence exclusively, seems not translate into atrial fibrosis. Three patterns of increased LA size in the LSPSAF population were proposed i) functional and at least partially reversible as a consequence of AF itself ii) secondary to other causes e.g. valvular regurgitation (primary or functional due to annular dilatation caused by AF) iii) a combination of both [2].
In our study cohort, 76%of patients presented enlarged RA. In the vast majority of cases (83%) RA indexed volumes were lower than LA volumes, in 11% it represented half of the LA volume. As RA maximum volume and the presence of RA enlargement correlated with the presence of LA enlargement, maximum LA volume and its area may suggest that increased RA size was the consequence of increased LA size in the context of AF persistence. It was previously reported that both LA and RA enlargement can develop as a consequence of AF in patients who had no evidence of significant structural or functional cardiac abnormalities other than AF [9]. This could explain why there was no association between RA size expressed in various parameters and LVA in our dataset. However, the presence of mild-to-moderate TR and LVH that correlated with RA enlargement and CHA2DS2VASc score ≥4 that correlated with RA maximum volume could suggest that increased RA size was, at least in some cases, secondary to other scenarios than AF persistence. It is worth noting that cases where RA indexed volumes were higher than LA volumes also correlated with TR and LVH. RA enlargement is a common finding in patients with pulmonary arterial hypertension and atrial septal defect, though unlikely in our study group, and was found to be associated with the increased prevalence of AF [10]. Hypertensive LVH, very common in our cohort, is the known causative factor of diastolic dysfunction and has been shown to affect right-sided cardiac morphology and haemodynamics [11]. Therefore, it seems that increased RA size among LSPSAF patients is multifactorial.
The role of RA systolic (EF, SV) and diastolic (EI) function in the pathophysiology of AF persistence is yet to be analysed systematically. Moreover, due to the absence of established cut-off values [3]it is hard to assess RA function pattern. Accepting magnetic resonance-derived normative data [12] all patients presented severely decreased RA function. Larger RA volume index and lower RA EF have been shown to be a predictor of recurrence of AF after direct current cardioversion and were superior to LA parameters in one study [13]. In our study RA functional parameters were not associated with LVA. A clear interpretation of these findings remain unclear.