There are several methods to classify CAF, one of the common ways is though identifying the drainage site of the CAF. The drainage of CAF can either be into a cardiac chamber (coronary cameral fistulas) or drainage into lower pressure venous systems (coronary arteriovenous fistulas, CAF) [4,5]. Only 7% of CAF drain into the coronary sinus [6] specifically. To date, there are no published case reports of co-existing left main/ left circumflex aneurysms with a coronary sinus fistula. The gold standard for the diagnosis of coronary artery fistulas is through cardiac catheterization, where selective coronary angiography can establish the sites of original and termination of a CAF, as well as the blood flow through it [7]. More recently however coronary computerized tomography angiography (CTA) and MR angiography have provided an alternative means of determining the anatomy of a CAF [8]. In addition to being non-invasive coronary CTAs have a higher sensitivity for the diagnosis of CAF as compared to angiography [9]. In our patient’s case, her CTA best demonstrated the arteriovenous fistula and consequent giant coronary sinus aneurysm that prolapsed into the right ventricle (a detail that would have been difficult to assert on catheterization alone). Echocardiography provides an alternative method of diagnosis, and microbubble contrast injection can help identify CAF and their course, although the limited field of view on echo can limit the assessment of a fistulous tract and other extracardiac structures [8]. Large fistulas may produce symptoms even in infancy, however more than half of adult patients may remain asymptomatic. Symptoms in adults include congestive heart failure, dyspnea, arrhythmias (due to chamber dilation) and angina (due to coronary steal phenomenon) [10-12]. Our patient presented uniquely with a large pericardial effusion. The most common etiology of pericardial effusions in the context of CAF is due to fistula rupture [13], where the pericardial effusion has a bloody appearance (hemopericardium). Our patient however had a serous transudative effusion, we therefore hypothesize that her effusion developed secondary to elevated filling pressures of the coronary sinus, directly related to the CAF. Moreover syncope can rarely be seen in some patients with CAF, and has been described secondary to extensive coronary ischemia with consequent complete heart block [14] as well as consequent ventricular fibrillation [15]. Our case is unique however in the presence of a syncopal episode despite having no arrhythmias. We hypothesize that the patient’s syncopal episode was secondary to transient right ventricular outflow tract obstruction by the prolapsing coronary sinus aneurysm. Various algorithms have been recommended to determine surgical versus transcatheter approach treatment of CAF. Due to the prolapsing nature of the aneurysm in our patient however, she was advised to undergo surgical repair, and has been doing well since that time with no recurrent pericardial effusions or syncopal events.