The current study aimed to observe any changes in intrinsic LV systolic function by GLS after BMV in rheumatic MS. We found that in our patients with successful BMV, there was a continuous improvement of the LV GLS until six months to 1 year of follow-up compared to baseline, which was not found in the LVEF. It supports other studies which suggest that the LVEF is less sensitive to evaluate LV function when compared to GLS.  To the best of our knowledge, this is the first study to assess subclinical LV function using GLS in rheumatic MS patients and to evaluate GLS immediately after BMV and 6-12 months after BMV.
Although at baseline, all of our patients had relatively normal LVEF (57.28 ± 3.84%), there was a significant reduction in LV GLS (-14.34± 3.06 %). This finding is similar to some reports of the previous studies [1, 6–8]. There are some hypotheses that explain the presence of LV systolic dysfunction in rheumatic MS. In the initial attack of rheumatic carditis, all three layers of the heart may involve.  Chronic inflammation may then occur, leading to fibrosis and scarring of the myocardial and subvalvular apparatus. This “myocardial factor” may cause wall motion abnormalities . Another study also suggests a contribution of the “hemodynamic factors," include: LV filling reduction, reduced LV compliance, increased afterload, and abnormal septal interaction due to pulmonary hypertension . Further study is needed to understand the true mechanism causing the LV dysfunction in rheumatic MS.
Early after BMV, we found that LV GLS increased significantly compared to baseline, from -14.34 ± 3.06% to -15.84 ±3.11 %, respectively. Similar findings were also reported by several studies. [1, 6–8]. In our study, no correlation was found between changes in GLS early after BMV with changes in hemodynamic variables from echocardiography (LVEDV, LVESV, LAVi, TRVmax, MVG, and MVA) in contrast to previous studies [1, 6–8]. After 6-12 months of follow up, even though there were insignificant changes in hemodynamic echocardiography parameters, we found that compared to early after BMV, the LV GLS was improving further significantly, with GLS -15.84± 3.11 to -17.29 ± 2.81%, respectively and there was still no correlation was found between changes in GLS long-term after BMV with hemodynamic echocardiography parameters. Our study suggested that improvement on hemodynamic factors or loading conditions were less likely to contribute to the improvement of GLS early after BMV nor in the long-term after BMV.
A plausible explanation is that other than the amount of diastolic filling, how the ventricle is filled also affects LV systolic function. [13, 14]. In a normal heart, the flow follows a certain sequence of spiral rings or vortices; this special pattern of filling is important to maintain systolic and diastolic performance . The BMV may alter the ventricle filling, which might be associated with the continuous improvement of GLS, but unfortunately, how the ventricle is filled is not explored in our study, so it needs a further study to prove it.
Another hypothesis suggests a process analogous to stunning -as in coronary artery disease- may occur in post BMV. Stunning myocardium in coronary artery disease is viable myocardium salvaged by coronary reperfusion that exhibits prolonged post-ischemic dysfunction after reperfusion.  Reperfusion precipitates a burst of reactive oxygen species formation and alterations in excitation-contraction coupling, which interact and cause contractile dysfunction.  There is a gradual recovery of contractile function after reperfusion on myocardial stunning. For MS patients, BMV could be analog to “reperfusion” as in coronary artery disease, and it might induce reactive oxygen and cause LV dysfunction, so it required some time for LV to recover, as could be seen with gradual improvement on GLS after BMV in our study. However, it needs further study to prove those hypotheses.
This study provides answer to limitation from previous similar studies regarding whether a longer follow-up period normalized GLS. Our study showed that even though GLS improved when the follow-up period was extended until one year after BMV, it still has not reached the normal values. We suspect that myocardial factors may prevent the normalization of GLS in MS patients. A study by Rousdhy et al. and Mahajan et al. showed that the GLS in the basal segment is much lower than the mid and apical segment; this may be due to the formation of fibrotic tissue due to the rheumatic process of endocarditis that started from mitral annulus extending to basal segment and decreased as it approached the apical segment [7, 1]. A study by Soesanto et al. proved that myocardial factor is also associated with LV dysfunction in rheumatic MS, as a significant negative correlation between GLS and late gadolinium enhancement on MS patients was found, suggesting a higher degree of fibrosis and worse LV systolic dysfunction . A longer follow-up is also needed to prove a further improvement in GLS.
Study Limitations and Recommendations
There are several limitations to this study. We did not compare the GLS in our subjects with the MS population who did not undergo BMV. However, a study by Mehta et al. found that no significant changes in GLS were found in MS patients who did not undergo BMV at 1-month follow-up. The number of patients lost to follow-up was quite large due to the COVID-19 pandemic, although the target study sample was achieved in the end. The high prevalence of AF in this study may have affected measurements, even though care has been taken to avoid unreliable data. Another limitation is that diagnosis of coronary artery disease was based only on the patient history obtained from the electronic medical record, symptoms, and electrocardiography. We did not perform cardiac catheterization or coronary multislice computed tomography.
Further studies with a longer duration of follow-up are needed to assess whether GLS improvement will sustain. It is necessary to conduct a study to explore the relationship between intrinsic ventricular systolic dysfunction as measured by GLS and its changes after BMV with clinical importance such as treatment and prognosis.