A number of concomitant factors are thought to contribute to an increase in the mean pulmonary arterial pressure (MPAP) of pulmonary arterial hypertension (PAH) patients, such as increased pulmonary vascular resistance (PVR), increased blood flow (due to septal defects), and a decrease in wall distensibility.[1] This is in contrast to the normal pulmonary circuit, which is characterized by compliant artery walls and a low PVR, resulting in a low MPAP with little flow and pressure wave reflection. The influence of pathologic MPAP’s on proximal hemodynamic factors such as artery size, flow pulse waveforms, and wall shear stress (WSS) is unclear. Since these factors are known pathophysiological stimuli in the production of molecules that alter vascular tone and matrix properties,[2] we set out to quantify the geometry, flow, and WSS of the left, right and main pulmonary arteries (LPA, RPA, & MPA) of control and PAH patients using phase-contrast magnetic resonance imaging (PC-MRI).

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