Absent coronary venous sinus: a rare anomaly.

A 42-year-old man presented with complaints of exertional dyspnea of 2 years’ duration and occasional giddiness. The dyspnea was not progressive and there was no paroxysmal nocturnal dyspnea or orthopnea. There was very few episodes of giddy spells and none of them was associated with syncope or presyncope. The patient was normotensive, non-diabetic and a nonsmoker, and had no other symptoms. Clinical examination revealed a normally disposed individual with a normal pulse, blood pressure and heart sounds with no cardiac murmurs. There was no pedal edema and the neck veins were normal. The chest X-ray was normal and electrocardiography revealed an incomplete right bundle branch block. The echocardiograph showed a normal-sized heart with good ventricular function. The situs was normal and the infraand intrahepatic portions of the inferior vena cava were normally visualized. The pulmonary veins drained normally into the left atrium, while the interatrial and ventricular septum were intact. A treadmill exercise test showed horizontal ST segment depression in the inferolateral leads at 7 METS. A 24-hour ambulatory electrocardiogram was normal. There was no systemic desaturation and an oximetry run did not reveal any significant oxygen step-up at any level. Coronary angiography was carried out to rule out coronary artery disease. It revealed normal epicardial coronary arteries with a normal branching pattern (Fig. 1). The contrast from the coronaries during the venous phase emptied into the left ventricle through multiple small fistulous connections giving a unique striate appearance (Fig. 2). However, the coronary veins and the coronary sinus were not visualized during the venous phase (Fig. 3). A contrast injection was given into the left brachial vein to rule out associated anomalies. The left brachial, subclavian and the innominate veins were anatomically normal, but there was no left superior vena cava (SVC). The patient was advised conservative management and showed no clinical deterioration at follow-up after 3 months.