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