Surgical closure of ventricular septal defect significantly decreased left atrial reservoir, conduit, and contractile strain at 3 months compared to preoperative baseline (P<0.001, P=0.026, P<0.001).
Observational (n=40)
No
Does surgical closure of VSD alter left atrial function and myocardial deformation in pediatric patients?
Surgical closure of VSD in pediatric patients leads to significant postoperative reductions in left atrial strain and left ventricular global longitudinal strain at 3 months.
p-value: p=<0.001
Abstract Background: Ventricular septal defect (VSD) is the most prevalent form of congenital heart disease (CHD) in children and the second-most prevalent form of CHD in adults, following a bicuspid aortic valve. Large VSDs can lead to significant complications, including heart failure and ventricular dysfunction. Assessing cardiac function in patients with VSD is an essential component of clinical evaluation both before and following surgery. The left atrium (LA) is a critical structure in cardiac physiology, serving as a dynamic chamber that plays a pivotal role in left ventricular filling by actively contributing during various phases of the cardiac cycle through its mechanical functions. Our aim is to validate alterations in LA function and myocardial deformation before and after surgical closure of VSD using speckle-tracking echocardiography. Patients and Methods: A prospective observational study with paired comparisons included 40 VSD patients who were assessed preoperatively and had short-term follow-up after 3 months at a tertiary university-based pediatric hospital. Results: Infants with hemodynamically significant VSD show impaired growth. Postsurgery, VSD cases demonstrated a significant elevation in weight and body surface area ( P < 0.001). LA function assessment with speckle-tracking echocardiography showed a decrease in LA reservoir, LA conduit (CD), and LA contractile (CT) strain ( P < 0.001, P = 0.026 and < 0.001, respectively). VSD cases showed that E/E’ and MV E/A ratios decreased postsurgery ( P < 0.001 and 0.045), whereas deceleration time increased ( P < 0.001), indicating improved diastolic dysfunction. VSD cases showed a systolic function decline in septal S’ ( P = 0.034), and both two-dimensional (2D) and 3D echocardiography revealed significant drops in left ventricle (LV) volumes, whereas 3D echocardiography showed decreased ejection fraction postsurgery ( P < 0.024 and P < 0.001, respectively). LV global longitudinal strain significantly decreased postoperatively ( P < 0.001). Both left ventricular end-diastolic diameter and left ventricle end diastolic volume (LVEDV) by 2D and 3D LVEDV and LV end-systolic volume decreased significantly with surgery by 2D and 3D ( P < 0.05). Right ventricle (RV) volumes by 3D conversely increased postoperatively as 3D right ventricle end diastolic volume (RVEDV) and right ventricle end systolic volume (RVESD) increased ( P = 0.003 and 0.002, respectively). Conclusion: Preoperative VSD cases demonstrated higher LA R, CD, and CT function compared to postoperative cases.
Sheta et al. (Fri,) conducted a observational in Ventricular septal defect (n=40). Surgical closure of VSD vs. Preoperative baseline was evaluated on Left atrial reservoir, conduit, and contractile strain (p=<0.001). Surgical closure of ventricular septal defect significantly decreased left atrial reservoir, conduit, and contractile strain at 3 months compared to preoperative baseline (P<0.001, P=0.026, P<0.001).