C63-20 Acute Right Ventricular Failure After Patent Foramen Ovale Closure Requiring Urgent Heart and Lung Transplantation

Abstract Patent foramen ovale (PFO) is a common and often asymptomatic congenital heart defect. While PFOs usually do not cause hemodynamically significant left-to-right shunting, underlying pulmonary hypertension (PH) can lead to increased right atrial (RA) pressure that may exceed left atrial pressure and cause shunt reversal with systemic hypoxemia. PFO closure in patients with significant PH may lead to right ventricular (RV) failure and cardiogenic shock. A 43-year-old woman with chronic respiratory failure from severe emphysema due to prior cigarette smoking and obstructive sleep apnea on nocturnal bilevel positive airway pressure (BiPAP) presented with dyspnea and edema refractory to oral diuretics. She was afebrile and normotensive, but tachycardic, tachypneic, and hypoxic. Physical exam revealed signs of volume overload. Arterial blood gas (ABG) showed respiratory acidosis and hypoxemia. Imaging showed pulmonary vascular congestion and ascites. Echocardiogram showed normal left ventricle (LV) systolic function with mild diastolic dysfunction, intraventricular septum flattening, increased right ventricular systolic pressure (RVSP), and leftward bowing of atrial septum with right to left shunting. Left heart catheterization showed mild diffuse coronary artery disease with moderate to heavy calcifications. Right heart catheterization (RHC) showed elevated RA and RV pressure, elevated pulmonary artery and pulmonary capillary wedge pressure, and mildly reduced cardiac index. She was treated with corticosteroids, bronchodilators, intravenous diuretics, and BiPAP, with some improvement. She subsequently underwent PFO closure. Afterwards her respiratory status acutely worsened. Repeat echocardiogram showed an underfilled and hyperdynamic LV, severe RA and RV dilation, residual intra-atrial right-to-left shunting, and severely increased pulmonary artery systolic pressure. Repeat RHC showed worsened pulmonary artery pressure. Serial ABGs showed progressive hypercapnic respiratory failure. She was placed on mechanical ventilation and subsequently on venoarterial extracorporeal membrane oxygenation (ECMO) and transferred to our center. She underwent an expedited evaluation and received heart and lung transplantation after a few weeks and continues to do well a year after surgery. This case illustrates how underlying PH, likely group 3 in our patient, can lead to high pulmonary vascular resistance and increased RA pressure causing shunt reversal through a PFO as an adaptive mechanism to relieve RA pressure. PFO closure in this setting can be detrimental, as the acute rise in RA pressure can lead to right heart failure, decreased LV preload, and cardiogenic shock. It also demonstrates successful urgent heart-lung transplantation in such a situation. Thorough hemodynamic evaluation and treatment of PH is critical prior to any PFO closure. This abstract is funded by: None