A63-50 A Hole in the Heart of Cirrhosis

Abstract Introduction Portopulmonary hypertension (POPH), a form of pulmonary arterial hypertension occurring in the setting of portal hypertension, affects up to 10% of patients with advanced cirrhosis. The progressive elevation of right atrial pressures in POPH can exceed left atrial pressures, resulting in the functional reopening of a patent foramen ovale (PFO) and intracardiac right-to-left shunting. This interplay between hepatic and cardiopulmonary physiology not only worsens hypoxemia but also profoundly impacts liver transplant eligibility and survival. Given the exclusion of most POPH patients from major pulmonary hypertension trials, evidence-based management remains challenging, underscoring the importance of recognizing such presentations early. Case Presentation A 39-year-old male with alcoholic cirrhosis, hypertension, and hyperlipidemia presented in 2021 with severe exertional dyspnea and hypoxemia (SpO2 87%). Transthoracic echocardiogram (TTE) demonstrated preserved left ventricular (LV) systolic function (EF 65-70%), moderate concentric LV hypertrophy, paradoxical septal motion, right heart dilation, and estimated pulmonary artery systolic pressure (PASP) of 60-65 mmHg. Transesophageal echocardiogram (TEE) confirmed a PFO with right-to-left shunt and moderate tricuspid regurgitation. Right heart catheterization revealed severe precapillary pulmonary hypertension (PASP 70 mmHg, mean PA 48 mmHg, PCWP 10 mmHg, RA 18 mmHg), consistent with PoPH. By 2023, the patient experienced further decompensation, presenting with worsening hypoxemia (SpO2 86% on room air), jaundice, and generalized weakness. Laboratory evaluation revealed worsening liver function (MELD 23, total bilirubin 10.3 mg/dL, INR 1.5, platelets 49,000). Repeat TTE showed progression: marked right atrial and ventricular enlargement, severe tricuspid regurgitation, paradoxical septal motion, and further elevation of PASP (100 mmHg). Despite diuresis and pulmonary vasodilator therapy (sildenafil), hypoxemia persisted, requiring high-flow oxygen, pt eventually died a year later from complications of decompensated cirrhosis. Discussion This case highlights a rare yet clinically significant interaction between hepatic and cardiopulmonary pathophysiology, where POPH-induced pressure overload functionally reopened a PFO, resulting in intracardiac shunting and refractory hypoxemia. Recognition of this dynamic physiology is crucial, as premature PFO closure in uncontrolled pulmonary hypertension may precipitate hemodynamic collapse. The case underscores the importance of early screening for pulmonary hypertension in cirrhotic patients, a high index of suspicion for functional PFO reopening in unexplained hypoxemia, and timely multidisciplinary management involving cardiology, hepatology, and pulmonary hypertension specialists. Early detection and individualized intervention remain key to improving outcomes in this complex patient population. TEE with bubble study demonstrating PFO. This abstract is funded by: None