## 4 Discussion
Interestingly, an improvement in RV performance was consistently demonstrated at all study time periods. [PERSON] et al. also reported an improvement in RV systolic performance [22]. Such improvement could be due to a concurrent improvement in pulmonary compliance and a reduction in inflation pressures. To explore this further, we looked at the correlation of OSI and RV performance and did not find a significant relation. As such, our findings suggest that the improvement in RV performance could be independent of respiratory changes and intrinsically related to dexamethasone. Such improvement may be linked to improved ventriculo-arterial coupling and reduced RV afterload, as suggested by the longitudinal decrease in the eccentricity index. The parameters reflective of LV longitudinal systolic function in TDI were found to increase over time without changes in the LV EF or LVO. Such improvement in LV function could be driven by the RV itself based on the principles of biventricular interdependence and shared myocardial fibers, especially in the septal wall, as well as by the application of advanced imaging techniques such as TDI, which is load-independent. Both the LV EF and LVO are influenced by the loading conditions of the LV. Dexamethasone is known to increase systemic vascular resistance, thereby increasing the afterload on the LV, which could possibly explain the lack of a significant increase in the LV EF and LVO within our cohort. Alternatively, it could be a reflection of physiological maturation or a direct effect of steroids on both right and left ventricular myocytes. Animal model studies have demonstrated that dexamethasone can stimulate angiotensin-converting enzyme (ACE) activity in cardiac myocytes, potentially influencing cardiac remodeling [23]. Low-dose dexamethasone in hypertensive rat models has shown improved LV systolic and diastolic function, which may be due to LV angiogenesis and a reduction of wall collagen deposition area [24]. Several researchers have described changes such as increased LV posterior wall thickness and ventricular septal hypertrophy in response to dexamethasone administration to premature neonates [9; 10; 11]. Our results do not show any significant change in the septal and LV dimensions, possibly because our cumulative dose of dexamethasone was substantially lower than the doses used in these studies. Similar results were reported by [PERSON] et al., who used a cumulative dexamethasone dose of 0.89 mg/kg [22], which is a very similar dose range to that in our study. From the PDA perspective, 60% of the cohort had PDA prior to their dexamethasone course. This then dropped to 39% after the completion of the course, but was not statistically significant (\(p\) = 0.453). Specific PDA-related echocardiographic parameters were not further investigated in our present study. [PERSON] et al. showed significant ductal constriction post dexamethasone use, along with improvements in metrics of pulmonary over circulation [22]. There have been some other studies that have reported ductal closure with steroids [25; 26]. However, a future prospective study to analyze the effects of steroid on ductal parameters would be interesting. Given that our study period witnessed two different dose regimes, we had the opportunity to explore a dose response relationship between steroids and right heart performance. We did not see a significant interaction between the dose and the RV systolic function parameters. Furthermore, our study explored the role of these changes in predicting respiratory outcomes. Our exploratory analysis showed that the changes in echocardiographic parameters could not predict successful extubation, days on oxygen, days on mechanical ventilation, or the development of CPHTN. Our study's limitations include a small sample size and a single institution's experience, which may limit the generalizability of the findings. In addition, we did not include a long-term follow-up later in infancy to evaluate the patient's outcomes beyond discharge.