![]() Median age was 13.5 (9.1, 17) years, and 16 (57%) patients had a single or dominant right ventricle. ![]() Measurements included pulmonary artery, atrial, and systemic arterial pressures, oxygen saturations, and systemic and pulmonary flows and resistances. OBJECTIVE: To describe the acute hemodynamic effect of vasopressin on the Fontan circulation, including systemic and pulmonary pressures and resistances, left atrial pressure, and cardiac index.DESIGN: Prospective, open-label, nonrandomized study (NCT04463394).SETTING: Cardiac catheterization laboratory at Lucile Packard Children's Hospital, Stanford.PATIENTS: Patients 3-50 years old with a Fontan circulation who were referred to the cardiac catheterization laboratory for hemodynamic assessment and/or intervention.INTERVENTIONS: A 0.03 U/kg IV (maximum dose 1 unit) bolus of vasopressin was administered over 5 minutes, followed by a maintenance infusion of 0.3 mU/kg/min (maximum dose 0.03 U/min).MEASUREMENTS AND MAIN RESULTS: Comprehensive cardiac catheterization measurements before and after vasopressin administration. In conclusion, prostacyclins may be safe to use in patients with elevated PVR as part of their VAD and transplant course and may provide a transplant option in those otherwise not candidates. The proportion of patients surviving to transplant in this high-risk cohort is favorable. A significant reduction was observed in vasoactive inotropic scores by 49% in the first 24 hours post-prostacyclin initiation. With continuous intravenous (IV) epoprostenol or treprostinil therapy, there were no bleeding complications or worsening of end-organ function. ![]() Of the 17 patients who met inclusion, 12 survived to transplant and 1 is alive with VAD in situ. ![]() We reviewed our use of prostacyclin therapy in pediatric patients on VAD support with high PVR from 2016 to 2021. We sought to describe our center's experience to show its safety and to present our current protocol for perioperative use. Prostacyclins have been used in adult VAD patients with success, but pediatric data on safety and efficacy in this population are limited. Systemic atrial decompression following ventricular assist device (VAD) implantation may not sufficiently lower pulmonary vascular resistance (PVR) to consider heart transplant candidacy. Pediatric precapillary pulmonary hypertension can develop in response to systemic atrial hypertension. Together, these simulations demonstrate an important step toward predicting changes in metrics of clinical interest for PAH patients and simulating potential treatment approaches. We also employed a series of maladaptive constitutive models, such as smooth muscle hyperproliferation and stiffening, to identify critical contributors to development of PAH phenotypes. We show that non-uniform mechanical behavior is important to establish the homeostatic state of the pulmonary arterial tree, and that hemodynamic feedback is essential for simulating disease time courses. ![]() We coupled a constrained mixture theory-based growth and remodeling framework for the vessel wall with a morphometric tree representation of the pulmonary arterial vasculature. In this work, we develop a framework that models the pulmonary arterial tree through adaptive and maladaptive responses to mechanical and biological perturbations. However, there is a need for new approaches that simulate disease evolution to allow for prediction of long-term outcomes. Computational models have been used to simulate mechanobiological metrics of interest, such as wall shear stress, at single time points for PAH patients. This loading drives changes in mechanobiological stimuli that affect cellular phenotypes and lead to pulmonary vascular remodeling. Hemodynamic loading is known to contribute to the development and progression of pulmonary arterial hypertension (PAH). ![]()
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