It is important to demonstrate CS anatomy as well as cardiac anatomy, as it is necessary for planning in electrophysiological procedures such as ablation, cardioplegia, stem cell therapy, and cardiac surgery [1-3].

Echocardiography, computed tomography (CT) and magnetic resonance imaging are used for imaging. However, the most useful technique is CT angiography (CTA). The delay time is typically higher than in coronary artery CTA to provides acceptable venous enhancement. In daily practice, it perform venous studies with an additional delay of 3 seconds more than used for coronary CTA [1-4].

Findings and procedure details

The radiologist who detects wide CS in a thorax CT or CTA or cardiac MRI evaluation should investigate the following pathologies:

1. Although it is more common in adults, the most common acquired cause is; It is the increase in right heart pressure caused by valvular dysfunction, volume overload, and pulmonary hypertension [1] (Fig. 1).

2. The primary cause of congenital CS enlargement is the presence of persistent left superior vena cava (PLSVC). A persistent LSVC generally drains into the CS, as the embryologic connection of the left common cardinal vein and the left horn of the sinus venosus. The 97% of PLSVC flows into the right atrium via the coronary sinus, and 3% into the left atrium. If there is no SVC on the right in the presence of PLSVC, the CS may be dilated due to increased venous return. CS expansion may be isolated or; It may be associated with cardiac pathologies such as ASD, VSD, AVSD, cor triatriatum [1-5] (Fig. 2 and 3).

3. If congenital large CS is present with findings of left-to-right shunt, unroofed CS should be investigated. Functional connection of a PLSVC with the anatomic left atrium can occur if the CS is partly or completely unroofed In this process, there is an ASD-like defect between the CS and the left atrium. It can be seen isolated or together with PLSVC. Unroofed CS may accompany multiple congenital heart defects such as abnormal pulmonary venous return, AV valve atresia, ASD, VSD, TOF, cor triatriatum [5] (Fig. 4).

4. One of the causes of CS with left-to-right shunt is abnormal pulmonary venous return anomalies. Some or all of the pulmonary veins drain directly into the CS or into the CS through a sac. Oxygenated and deoxygenated blood mix in the right atrium. Therefore, the presence of ASD is necessary for life [1-4] (Fig. 5 and 6).

5. Arteriovenous fistulas between the coronary arteries and the coronary sinus can cause extensive CS [1,2,6].

6. Ostial stenosis at the right atrium opening point of the CS creates pre-stenotic enlargement, leading to enlargement of the CS. In this case, if PLSVC is present, coronary venous blood reaches the right atrium via the retrograde route [1-3].

7. CS diverticulum, which is mostly detected incidentally, can be defined as dilated CS. However it is considered a variant [1].

8. Other less common causes of a dilated CS without a shunt include an interrupted IVC with hemiazygos continuation to an LSVC or hepatic veins connecting directly to the CS. The interrupted IVC continues as the azygos vein or in cases of left IVC as the hemiazygos vein. With visceral situs abnormalities or heterotaxysyndrome, typically the left isomerism, an interrupted left IVC with hemiazygos continuation can drain into the CS via an LSVC. In such an instance, the CS receives venous blood return from both above and below the diaphragm [1] (Fig. 7).

The most CS variants have no hemodynamic consequences. However, variable CS anatomy may pose challenges for therapeutic interventional applications. Therefore it must be defined [1].