 Good morning everyone. I am here to talk about persistent left SVC, a sinister persistence. PL SVC is the most common systemic venous anomaly which is associated with 4-8% of cardiac anomalies. It drains in the right atrium via coronary sinus. Here is a little peek into the embryology of this variant. So there are two anterior cardinal veins which drain the cranial portion of the fetus into the sinus phenosis which is the primitive atrium through common cardinal veins. There are transverse venous plexuses which connect these two. Normally there is regression of a part of left anterior cardinal vein and normal central venous anatomy with left brachycephalic vein and right SVC is formed. Regression of these transverse venous plexuses and persistent of the left anterior cardinal vein results in PL SVC. Earlier PL SVC was known to be associated with cardiac anomalies like septal defects, coronal truncal anomalies and arch abnormalities. However, there has been a change in our understanding from what we came across in the last four months with extra cardiac anomalies and systemic anomalies being more common. This is an original article published in the Journal of Ultrasonic Obstructrix Gynecology. They came across a total of 82 cases of PL SVC associated anomalies with heterotaxi and isolated cardiac anomalies being more common. Promosable anomalies were third most common. All second trimester ANC patients who were referred for anomaly scan and fetal echo were searched for PL SVC and associated anomalies. Six such cases were identified which are discussed below. The first case is a 26-year-old primie who came for anomaly scan and PL SVC was detected. A muscular VSD and diodal atria were the additional anomalies. These are the images of PL SVC lateral to the ductile arch. This is the muscular VSG with flow from right ventricle to the left ventricle and this is the transfer section of fetal abdomen showing double bubble sign suggestive diodal atria. Case two is a 28-year-old who came for anomaly scan and PL SVC was noted. This image shows PL SVC and right SVC on either side of the aortic arch. The fetal heart also shows AB valves at the same level, a single inflow and two parallel outflows which are coming from the morphological left ventricle. Here is the video showing the same a single inflow and two parallel outflows which was suggestive of unbalanced AVSG with double outlet left ventricle. Case three is a 23-year-old primie who was referred for polyhydroaminose. The fetal heart showed PL SVC, absent thymus with aortic arch flush to the sternum, a large main pulmonary artery as compared to the aorta, polyhydroaminose with ECOS and a ventricular septal defect with an overriding aorta. This video shows that the fetal heart is divided to the right and the muscular ventricular septal defect with a dilated main pulmonary artery. This also shows a large main pulmonary artery arising from the dilated right ventricle. This is the color Doppler of the scene which shows a forward jet into the main pulmonary artery with a regurgitated jet as well. With above findings a diagnosis of absent pulmonary valve syndrome variant of fallot tetralogy was made. We also suspected Dijot's syndrome in the fetus but the mother denied in this procedure. Case four was a 22-year-old multigravita who was referred in view of polyhydroaminose and PL SVC. The fetal heart showed an inlet VSD with absent septum primum, seducia partial VSD with a dilated coronary sinus. IVC was not seen and instead another vessel was noted posterior and to the left of the aorta at the level of four chamber heart which was the azygous continuation of IVC. Both the outflows were parallel arising from the right ventricle and there was pulmonary stenosis as well. These are the two parallel vessels in the fetal thorax absent IVC with all hepatitis draining into the right atrium and there was also over distended stomach. Post-intel 2D echo so it shows a double outlet right ventricle with pulmonary stenosis this is the small permeary artery and PL SVC and right SVC on both sides. Still images of the same shows PL SVC, absent IVC with dilated azygous wave posterior and to the left of the aorta and hepatic veins directly draining in the right atrium. The child was operated for gastric outlet obstruction and they found a fibrous band across D1 segment of deodenum with the pre-deodenal vein. The IC junction was also not fixed in the retroperitonium. These findings were suggestive of partial malrotation with left heterotaxi. Case 5 was an elderly primary gravita who was known to have SLE. A PL SVC was noted along with ventricle omega-L with normal spine and hepatic core calcification with normal maternal torsidus. This is the video showing persistent left SVC along with these two findings. Case 6 is a 25 year old primary gravita. Her fetus was found to have PL SVC on detail evaluation of fetal heart following anomalies were found. This was the PL SVC which was to the left of the pulmonary artery. The axis was divided to the right. The ascending aorta and the aortic arch appear small. This is the ascending aorta smaller than the main pulmonary artery and small left ventricular outflow tract. And there was also a shell flex structure at the aortic isthomas which is seen here. Shell flex structure. At 24 weeks the Z scores of the ascending aorta was minus 1.6 and at 28 weeks it further reduced to minus 2.8. There was also incidentally noted fetal peritoneal curvilinear calcification adjacent to the stomach. Hence a working diagnosis of evolving co-actation of aorta or aortic arch hypoplasia was made. At last I would like to say that PL SVC is an anatomical variant. A thorough search for cardiac and extracardial anomaly should be done. Invisive testing for genetic evaluation should be done when indicated. And in case of an isolated PL SVC the patient should be counseled and followed up for development of evolving anomalies. And most importantly it should be considered as a soft marker at the back of the mind. Thank you. These are my references.