Prediction of spontaneous closure of isolated ventricular septal defects in utero and postnatal life

Abstract

BackgroundVentricular septal defect (VSD) is a highly prevalent fetal congenital heart defect, which can become spontaneously closed during infancy. The current study aims to characterize fetal VSDs that were subsequently spontaneously closed in the first 2 years of life in eastern China.MethodsBetween January 2011 and December 2013, 257 fetal patients diagnosed with isolated VSD by fetal echocardiography at Nanjing Maternity and Child Health Care Hospital, China, were enrolled in the study. Subjects were divided into three groups: group 1 = persistent VSD; group 2 = closed after birth; group 3 = closed during gestation. Fetal echocardiography data, physical features at birth and follow-up outcomes for 2 years were compared to identify factors contributing to spontaneous closure (SC) of VSD. A predictive formula was applied to patients admitted to hospital in the first quarter of 2014 (n = 23) for validation.ResultsSC occurred in 42.8% patients. Birth weight (3.095 ± 0.774, 3.174 ± 0.535, 3.499 ± 0.532 kg in groups 1, 2 and 3, respectively) and defect diameter (3.422 ± 0.972, 2.426 ± 0.599, 2.292 ± 0.479 mm, in groups 1, 2 and 3, respectively) showed statistically significant differences between the three groups (P = 0.004 and P = 0.000, respectively). Receiver operating characteristic (ROC) curves identified cut-off value for the defect diameter as 2.55 mm, and logistic regression analysis identified the SC probability = (1 + exp -[-2.151 − 0.716*birth weight + 1.393*diameter])-1. Results indicated that male fetuses, full-term birth, muscular VSD, and defects without blood flow crossing the septum, have higher incidence of SC.ConclusionsThe major determinants of SC of isolated VSD are birth weight and diameter of the defect. In addition, VSD location may also affect the SC incidence.

An Unusual Mechanism of Closure of Muscular Ventricular Septal Defects

“…Membranous VSDs close by adherence of tricuspid valve leaflets, creating an aneurysm that closes the defect [1 , 7 , 8] . It has been suggested that the spontaneous closure of muscular VSDs could be due to muscular encroachment of the septal defect along with superimposed fibrosis or by fibrous tissue formation around the margins leading to apposition of the edges of the defect [9] .…”

Clinical Presentation of Preterm Infants with Ventricular Septal Defect

“…With regards to SC of VSD, Li et al (2016) reported the frequency of cases in which VSD was diagnosed during the fetal period, and SC was confirmed within the first 2 years of life. According to this report, SC occurred in 42.8% of patients during gestation and within the first 2 years of life; birth weight and defect meter showed significant differences between the three groups (SC during gestation, SC after birth, and persistent VSD).…”

Prediction of spontaneous closure of ventricular septal defect and guidance for clinical follow‐up

“…P‐VSD closure was thought to occur as a result of damage caused by a high‐velocity jet to damage the endothelium at the edge of the VSD or the septal leaflet of the tricuspid valve, both of which can lead to accumulation of platelets and production of fibrous tissue . On the other hand, the spontaneous closure of m‐VSD was due to muscular encroachment of the septal defect along with superimposed fibrosis or fibrous tissue formation around the margins leading to apposition of the edges of the defect . Another reason may be that m‐VSD size was slightly smaller than p‐VSD.…”

“…Ventricular septal defect (VSD) is the most common congenital heart disease (CHD), accounting for almost 50% of all CHD . The estimated prevalence of VSD is 2 to 3.94 per 1000 live births diagnosed by echocardiography . Two‐dimensional (2D) combined color Doppler echocardiography makes it easy to diagnose VSD, and to measure size and position of defect, as well as to evaluate the anatomical relationship with the surrounding tissue.…”