Pulmonary arterial hypertension (PAH)

In pulmonary arterial hypertension (PAH), there are two changes to the pulmonary vasculature that significantly affect hemodynamics: the vessel walls are abnormally stiff and the resistance to blood flow is high. Both of these changes result in excess afterload on the right ventricle (RV), ultimately resulting in right heart failure.

Healthy pulmonary arteries (PA) have highly elastic walls that easily stretch to accept the incoming stroke volume of blood with minimal pressure increases. In PAH the walls of these vessels become stiff due to a combination of cellular proliferation and remodeling driven by elastin breakdown and collagen deposition. The stiff vessel walls result in a reduction in pulmonary vascular compliance (stroke volume/pulse pressure or SV/PP) which leads to an increase in pulmonary arterial pulse pressure (PP) and systolic pulmonary artery pressure (sPAP). Collectively these are representative of an increase in the pulsatile component of afterload (pulsatile load) on the right ventricle.

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In PAH, the resistance to blood flow is increased due to vasoconstriction and cellular proliferation in the distal PA vessels. The proliferation is stimulated, at least in part, by the increased pulse pressure. The increase in pulmonary vascular resistance (PVR) results in increased mean pulmonary artery blood pressure and the steady state component of afterload (steady state load) on the RV.

Historically, the increase in PVR formed the basis of our understanding of PAH and is the target for drug therapy. Currently approved pharmacotherapy primarily functions to dilate the distal PA vessels to lower PVR and lessen the steady state load. But current drug therapy does not directly address the pulsatile load that is imposed on the RV by the stiffening of the PA vessels.

The Aria CV Pulmonary Hypertension System

The Aria CV Pulmonary Hypertension System is designed to mimic the function of healthy pulmonary artery walls and restore compliance to the pulmonary vasculature. By doing so, it may decrease pulse and systolic pressures as well as the pulsatile load on the RV. The system includes an implantable gas-filled Balloon that is introduced percutaneously and anchored in the main PA and an implantable gas Reservoir connected to the Balloon. The Balloon collapses (in systole) and expands (in diastole) with the cardiac cycle, potentially restoring compliance to the PA vasculature.

The Balloon is delivered via a catheter system and secured in the main PA by a nitinol frame (Anchor). The Reservoir is implanted in a subcutaneous pocket created in the underarm or abdominal position. A subcutaneous access port connected to the Reservoir allows for controlled filling and adjustment of gas in the reservoir and balloon to achieve the desired compliance.


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Clinical Study Information

The ASPIRE PH Study will be enrolling patients with severe PAH. To learn more about this study and find a study center near you, go to: