Hemodynamically Unloading the Distal Pulmonary Circulation in Pulmonary Hypertension: A Modeling Study

Abstract

Pulmonary hypertension (PH) is a progressive disease that is characterized by a gradual increase in both resistive and reactive pulmonary arterial (PA) impedance. Previous studies in a rodent model of PH have shown that reducing the hemodynamic load in the left lung (by banding the left PA) reverses this remodeling phenomenon. However, banding a single side of the pulmonary circulation is not a viable clinical option, so -using in silico modeling- we evaluated if the banding effect can be re-created by replacing the proximal vasculature with a synthetic PA. We developed a computational model of the pulmonary circulation by combining a 1-D model of the proximal vasculature with a 0-D line transmission model to the 12th generation. Using this model, we performed 4 simulations: (1) Control; (2) PH; (3) PH with a stenosis in the left PA; and (4) PH with proximal vessel compliance returned to Control levels. Simulations revealed that vascular changes associated with PH result in an increase in PP and WSS, relative to controls, in the distal circulation. Banding the left PA reduced distal PP and WSS in the left lung. Returning the proximal compliance to Control levels achieved the same effect (as banding the left lung) in both lungs, but also restored the shape of the pressure waveform similar to Control. In conclusion, we present a computational framework to estimate hemodynamic unloading in the distal circulation of rats after LPA banding and show that this can be done by restoring proximal vessel compliance.

Padrões hemodinâmicos pulmonares em pacientes pediátricos com defeitos septais cardíacos congênitos: relação com mediadores inflamatórios e a presença não suspeitada de vírus respiratórios

“…Assim, a hipertrofia vascular pulmonar e a vasoconstrição, são elementos centrais no desencadeamento de transtornos hemodinâmicos graves, além de serem o alvo das intervenções que visam ao remodelamento reverso, já estudado em modelos experimentais (29) após a correção da cardiopatia (14) . Quando considerado o período neonatal, há fatores intrauterinos que podem favorecer a persistência de elevada resistência vascular pulmonar (RVP).…”