Inhaled nebulized epoprostenol in high-risk pulmonary embolism was associated with higher in-hospital mortality (46.7% vs 16.1%, p=0.0341), likely reflecting its use in the sickest patients.
Observational (n=46)
No
Does adjunctive inhaled nebulized epoprostenol improve clinical and echocardiographic outcomes in patients with high-risk acute pulmonary embolism?
In a retrospective cohort, adjunctive inhaled epoprostenol was predominantly used as a bridge to definitive therapy in the sickest patients with high-risk pulmonary embolism, resulting in higher observed mortality and ICU length of stay without differences in right heart strain improvement.
Absolute Event Rate: 46.7% vs 16.1%
p-value: p=0.0341
Abstract Introduction Pulmonary embolism (PE) remains a major cause of cardiovascular morbidity and mortality, primarily due to right ventricular (RV) overload and failure from increased pulmonary vascular resistance. Management traditionally focuses on anticoagulation with thrombolysis or thrombectomy depending on risk stratification. However, in cases with hemodynamically significant RV dysfunction, targeted pulmonary vasodilation with inhaled nebulized epoprostenol, a prostacyclin analog, has been proposed to reduce RV afterload. This single-center study describes practice patterns and outcomes of epoprostenol use among patients with high-risk PE. Methods A retrospective observational analysis was conducted using an institutional Pulmonary Embolism Response Team database at a tertiary academic center. High-risk PE was defined by hemodynamic instability, RV dysfunction, and/or elevated cardiac biomarkers per guideline criteria. Data were obtained from the electronic medical record. Among 46 high-risk PE cases identified, 15 received inhaled nebulized epoprostenol. Descriptive analyses were used to compare illness severity, demographics, and outcomes in both groups. Results Among those receiving epoprostenol, 93.3% had RV dysfunction and required vasopressor support. Median duration of therapy was 1.36 days. 4/15 underwent catheter-directed intervention, 4/15 underwent surgical thrombectomy, and 5/15 underwent systemic thrombolysis. One received anticoagulation only and one died prior to intervention. Those who eventually received epoprostenol had longer ICU LOS (9.33 vs 5.07 days, p = 0.020) and more likely required high-flow oxygen or mechanical ventilation (73.3% vs 29.0%, p = 0.010). They were more likely to have previously experienced cardiac arrest from PE although this was not significant (40% vs 16.1%, p = 0.14). In-hospital mortality was higher (46.7% vs 16.1%, p = 0.0341). Among those who underwent follow-up echocardiogram after thrombolysis/thrombectomy, there was no difference in improvement in right heart strain (RHS) between the two groups (80% vs 78.6%, p = 1). Discussion This review highlights that epoprostenol is predominantly being used in our sickest PE patients as a bridge to definitive therapy. Most of these patients had RV dysfunction and vasopressor dependence, higher oxygen requirements, longer ICU stays, and higher in-hospital mortality. The severity of illness likely contributes to the lack of observed difference in improvement of RHS on follow-up imaging. Although epoprostenol has a strong physiologic rationale in acute PE by reducing pulmonary vascular resistance and unloading the RV, its role remains unclear. These findings underscore the need for prospective studies to identify ideal patient characteristics, optimal timing relative to reperfusion interventions, and dosing strategies that effectively support right heart function without introducing harm. This abstract is funded by: None
Hong et al. (Fri,) conducted a observational in High-risk Pulmonary Embolism (n=46). Inhaled nebulized epoprostenol vs. No epoprostenol was evaluated on In-hospital mortality (p=0.0341). Inhaled nebulized epoprostenol in high-risk pulmonary embolism was associated with higher in-hospital mortality (46.7% vs 16.1%, p=0.0341), likely reflecting its use in the sickest patients.