CONGRESS ABSTRACT

Eustachian valve is a remnant of the right venous valve of the sinus venosus represented by fold of endocardium originating from the anterior margin of the inferior vena cava (IVC) orifice, typically extends towards the lower end of the crista terminalis, while the medial horn joins the thebesian valve (valve of the coronary sinus) (Fig.1). In some instances, it persists as a mobile, elongated structure projecting several centimeters into the right atrial cavity, rarely mimicking the echocardiographic appearance of cor triatriatum. We report the case of a 70-year-old female patient presenting with Wolff-Parkinson-White (WPW) syndrome (Fig. 2a), symptomatic for episodes of paroxysmal supraventricular tachycardia (PSVT) with palpitations. Transthoracic echocardiography (TTE) revealed the presence of a prominent Eustachian valve. In anticipation of radiofrequency (RF) catheter ablation, transesophageal echocardiography (TEE) was indicated to assess the feasibility of access for the electrophysiology study (EPS) via the inferior vena cava (IVC). The TEE documented the presence of a particularly prominent Eustachian valve, while excluding the presence of cor triatriatum and confirming the patency and thus the feasibility of venous access for the EPS via the IVC (Fig. 3). The patient then underwent a fluoroless electrophysiology study (EPS) performed via femoral approach. This study revealed the presence of a left-sided accessory pathway located within the cardiac venous system, precisely at the level of the middle cardiac vein. Radiofrequency (RF) energy was delivered to the identified accessory pathway, achieving successful ablation with immediate elimination of pre-excitation as evidenced by normalization of the ECG (Fig. 2b). Although no prior reports have described a concomitant presentation of prominent Eustachian valve and WPW syndrome, the anatomical continuity of the Eustachian valve with the valve of the coronary sinus (Thebesian valve) and the ostium of the coronary sinus raises the possibility that the underlying pathophysiological mechanisms responsible for the exuberant Eustachian valve development may also contribute to the arrhythmogenic substrate observed in this patient.