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.