Discussion
The main finding of our study is a significant decrease in all three
left atrial strain parameters i.e. reservoir, conduit and contractile
strain suggestive of severe LA dysfunction in patients with severe
rheumatic MS when compared to healthy controls. It has been shown in a
previous study by Mahfouz et al17 on 75 patients that
the conduit and reservoir function are affected in mild MS while LA
contractile strain is well preserved. The increased LA contractile
function appears as a compensatory mechanism to counterbalance reduced
LA reservoir and conduit function in mild MS as LV filling predominantly
occurs in LA contractile phase in MS in contrast to normal filling
pattern where LA filling predominantly occurs in the early conduit
phase.18 However characterizing the various components
of LA function in MS and in other disease states requires complex
methodology.19 The speckle tracking echocardiography
provides an opportunity to quantitatively characterize various
components of LA function non-invasively. Therefore, our study
population which comprised of patients with severe MS (n = 44) and very
severe MS (n = 36) could explain the reduction in all three LA strain
parameters suggesting advanced degree of LA dysfunction. Our study shows
that in severe MS, LA contractile function is also compromised in
addition to reservoir and conduit function. Another study by Demirkol et
al on 52 asymptomatic MS patients also showed that LA reservoir and
conduit strain was significantly reduced but the contractile strain was
increased in MS patients when compared to control population. This could
similarly be explained by difference in the characteristics of study
population as in their study cohort10, MS patients had
mean MVA by planimetry of 1.38 ± 0.36 cm2 with mean
diastolic transmitral gradient of 7.9 ± 2.8 mm Hg in contrast to our
study where MS was more severe as mean MVA was 0.93 ± 0.21
cm2 and mean transmitral gradient was 12.33 ± 4.16 mm
Hg which could have compromised the contractile function.
93.75%) subjects in our study were in NYHA functional class II and III.
There was a non-significant trend of higher mean LA size, peak and mean
diastolic transmitral gradients and RVSP with increasing NYHA functional
class while mean MVA was significantly less in NYHA class III group when
compared to class II and I group (p= 0.004 between all groups). There
was trend towards stepwise decrease in LA reservoir, conduit and
contractile strain with deteriorating NYHA functional class, however
this did not reach statistical significance. Our results were different
from a study by Chien et al20 on 69 MS patients which
showed positive correlation between atrial deformation and NYHA
functional class. In their study cohort, the mean MVA by planimetry was
1.41 ± 0.50 cm2 in contrast to our study where mean
MVA was 0.93 ± 0.21 cm2 and all patients had severe MS
and none with mild/moderate MS. Hence, LA strain parameters were
markedly decreased in our study population of severe MS patients
(suggesting LA dysfunction) making further numerical fall with
deteriorating NYHA functional class inconsequential. Secondly, in their
study20, atrial fibrillation (AF) patients constituted
57% of the study population, hence LA contractile strain was not
reported. Their results of atrial deformation are based upon LA
reservoir strain in addition to reservoir and conduit strain rate. In
our study, we excluded AF patients and we systematically evaluated and
analyzed all three LA strain parameters in our study cohort.
Mitral stenosis results in obstruction to LV filling resulting in LA
pressure overload which leads to alteration in LA geometry and function
with progressive interstitial fibrosis, dilatation and remodeling of LA,
ultimately culminating in LA dysfunction.5 However, LA
remodeling is at least partially reversible and mitral valve
intervention in the form of balloon mitral valvotomy/surgery can relieve
LA pressure overload, thereby reducing LA size and improving LA function
leading to reverse remodeling.22
Our study has important clinical implication in that the patients with
severe MS regardless of severity of NYHA functional class develop severe
LA dysfunction which worsens with further decline in MVA. Therefore
patients with severe MS should be subjected to early and timely BMV so
as to improve their LA function.11,22 We also believe
that intervention may have an impact on preventing these patients to
develop atrial fibrillation (AF), RV dysfunction and improving their
prognosis. In the study by Ancona et al23 the degree
of reduced LA systolic strain in patients with rheumatic MS correlated
not only with worse cardiovascular outcomes during 3-year follow-up but
also was the most powerful predictor of new onset AF at 4-year
follow-up. In our study population of severe mitral stenosis and
pulmonary hypertension, marked LA dysfunction was present. The high RVSP
also likely contributed to LA dysfunction as higher pulmonary artery
pressures have been reported to have strong negative correlation with LA
compliance.4 Vriz et al24 showed
that reduced LA reservoir strain can predict development of RV
impairment and AF in patients with severe MS better than transmitral
gradients.
Finally, many factors could have contributed to this LA dysfunction
including chronic LA pressure overload, LA fibrosis, adverse remodeling
of LA, involvement of mitral apparatus in the rheumatic process, LV and
RV dysfunction. In fact our group has recently shown that decrease in
deformation of basal segments of LV is more compared to mid and apical
LV segments suggesting rheumatic endocarditis and scarring extend from
the mitral annulus to the surrounding basal LV myocardial
segments.25