Eustachian valve thrombus: Critical factor in outcome of venous thromboembolism.
There are some reported cases of IVC enlargement in the setting of normal RAP, including highly trained athletes, patients with large body-surface area, young adults with history of vasovagal syncope, those on mechanical ventilation, or those with structural causes such as narrowing of the IVC-RA junction, web or tissue present in the IVC, or prominent
Eustachian valve [5, 8, 9].
Eustachian valve endocarditis (EVE) was firstly described in 1986.
Transthoracic echocardiography (TTE) and also transesophageal echocardiography (TEE) showed normal left and right ventricular size and function, mild pulmonary hypertension (systolic pulmonary artery pressure, 37 mm Hg), and dense echogenicity on the
Eustachian valve of the inferior vena cava in the right atrium and a worm-like, highly mobile echogenicity (5 x 0.4 cm) in the right ventricle attached to the free wall without valvular involvement, mostly in favor of intracardiac thrombosis (Figures 1 and 2).
This structure begins to regress during the second trimester leaving four remnants: the
Eustachian valve (EV), the Thebesian valve, Chiari network and the terminal crest.
Normally, the valve regresses by approximately 12 weeks gestation and leaves behind the crista terminalis superiorly and the
eustachian valve of the inferior vena cava and the thebesian valve of the coronary sinus inferiorly.