ABSTRACT
Background: Congenital Heart Diseases (CHD) are defined as malformations of the heart and great vessels that develop in utero which may manifest at birth or later in childhood. They can be caused by numerous genetic and environmental factors. Genetic factors are nonmodifiable. However, identification of modifiable environmental risk factors is important to develop population based prevention strategies to reduce the incidence of CHD. Objectives: The primary objective of the study was to find an association of the maternal lifestyles with CHD in new-borns. The secondary outcome of the study was to identify maternal factors that can be modified for the primary prevention of CHD. Materials and Methods: This prospective study involved cardiovascular system examination of newborns after delivery in term gestations in 1394 singleton pregnancies. The maternal risk factors considered were age, prepregnancy Body Mass Index (BMI), consanguineous marriage, caffeine intake, diabetes, stress and intake of periconceptional Folic acid tablets. Results: In this study, 22 (1.58%) out of 1394 pregnancies resulted in Congenital Heart Defects. Teenage pregnancy (p value= 0.0002), consanguineous marriage (p value=0.0004), overt diabetes mellitus (p value=0.0001), caffeine intake (p value=0.0031), prepregnancy BMI>24(p value=0.0001), maternal stress (p value<0.0001, history of previous congenital malformations (p value=0.004) and non intake of folic acid tablets in the first trimester (p value=0.0023 were found to be the most likely risk factor associated with CHD. Conclusion: Community education programmes should be initiated in the high-risk population to prevent teenage pregnancies and consanguineous marriages. Maternal counseling for periconceptional control of blood glucose, adequate weight maintenance, intake of folic acid tablets, avoidance of stress and caffeine is needed to prevent CHD.
ABSTRACT
Background: Preeclampsia is defined as new onset hypertension and albuminuria in previously normotensive pregnant women after 20 weeks of pregnancy. There is no cure; management is reliant on a structured antenatal surveillance programme and antihypertensives. Recent advances in immune histochemistry study of placenta have elucidated an increased Vascular Endothelial Growth Factor (VEGF) expression in various placental bed disorders like recurrent pregnancy loss, preeclampsia, fetal growth restriction, preterm and abruption placenta. Increased release of VEGF family proteins has been attributed to atherosis and placental hypoxia. However, some studies have found normal VEGF concentrations in placenta in these disorders of feto-maternal interphase. Objectives: The study aims to analyse the VEGF expression in placental biopsy from preeclampsia and normotensive pregnancies. Materials and Methods: This prospective study involved the gross and immune histology examination of human placenta after 31-40 weeks gestation period in 20 singleton preeclampsia pregnancies. Twenty placentas of normotensive pregnancies were taken as controls. Results: In the present study, VEGF density was more in the placentas from preeclampsia pregnancies as compared to placenta from a normal pregnancy. The mean weight of placenta was smaller in preeclampsia group. Additionally, the fetal capillaries were also small in diameter and lumen was collapsed. The pulsatility index of uterine artery supplying the placenta was also higher in preeclampsia pregnancies. The high velocity blood flow can mechanically damage the tender fetal villi floating in the intervillous space. This damage collapses the fetal capillaries as evidenced by the smaller diameter of fetal capillaries in the placental biopsy. Conclusion: Placental hypoxia in cases of preeclampsia is a potent stimulus for VEGF expression. Nevertheless, the increased VEGF expression should be seen in the light of collapsed fetal vessels in a small placenta.