A63-47 Severe Main Pulmonary Artery Dilation (7.2 Cm) Associated With Pulmonary Hypertension: A Case Report

Abstract Pulmonary artery (PA) dilation is an uncommon but potentially life threatening finding, most often secondary to pulmonary hypertension (PH). A diameter exceeding 4 cm is considered enlarged, while dilation beyond 5 cm is rare and may predispose to complications such as rupture, dissection, or compression of adjacent structures. PA aneurysms larger than 7 cm are exceedingly uncommon, with limited data available on their natural history or management. We present the case of a 80 year-old female with a history of pulmonary arterial hypertension (PAH) who presented with progressive dyspnea on exertion, orthopnea, and bilateral lower extremity edema. On examination, blood pressure was 110/70 mmHg, heart rate 95 bpm, respiratory rate 20/min, and oxygen saturation 92% on room air. Physical examination revealed elevated jugular venous pressure, a loud P2, right ventricular heave, and peripheral edema. A contrast-enhanced CT chest demonstrated a markedly dilated main pulmonary artery measuring 7.2 cm without evidence of dissection. Transthoracic echocardiogram showed severe right atrial and right ventricular enlargement, septal flattening consistent with pressure overload, and an estimated pulmonary artery systolic pressure of 55 mmHg. Right-heart catheterization confirmed a mean pulmonary artery pressure of 52 mmHg and elevated pulmonary vascular resistance. No evidence of pulmonary embolism or congenital shunt was identified. This case highlights the relationship between severe pulmonary hypertension and progressive pulmonary artery dilation. Chronic pressure overload leads to remodeling and weakening of the arterial wall, which may result in extreme dilation. Although often asymptomatic, massive PA enlargement can lead to serious complications including coronary or airway compression, recurrent laryngeal nerve palsy, hemoptysis from bronchial artery hypertrophy, and potential rupture or dissection. Surgical or endovascular repair is generally reserved for patients with symptoms or evidence of rapid expansion, while conservative management focuses on optimizing pulmonary hypertension therapy, including prostacyclins, endothelin receptor antagonists, and phosphodiesterase-5 inhibitors. This case underscores the importance of recognizing extreme PA dilation as a marker of advanced disease and the need for multidisciplinary management involving pulmonology, cardiology, and cardiothoracic surgery to guide surveillance and treatment decisions. This abstract is funded by: None