We are working on a chronic implant that would be placed at the junction of the TCPC, and would provide the necessary pressure augmentation to re-establish a circulation that recapitulates a normal two-ventricle circulation.
Importantly, however, it provides a novel mechanistic insight into the factors responsible for the shape of the aortic pressure waveform in humans by demonstrating that while the onset of pressure augmentation (the shoulder) is determined by the arrival of the backward-traveling (reflected) wave, the degree of augmentation is principally determined by the arterial reservoir.
Only the central pressure augmentation index (AIx) was considered for the analysis of arterial stiffness in this study.
In this secondary analysis, the outcomes were central and peripheral hemodynamics: aPWV, central systolic and diastolic blood pressure, pulse pressure, augmented pressure, augmentation index, brachial systolic and diastolic blood pressure, and brachial pulse pressure.
The timescales of permeability reduction and strength recovery presented in this study may aid our understanding of the permeability evolution of conduit margin fractures, magma fracture-healing cycles, surface outgassing cycles, and the timescales required for pore pressure augmentation and the initiation of explosive eruptions.
Indeed, a metaanalysis of the published literature has failed to identify the changes in reflection timing on which the current hypotheses for pressure augmentation are based (1).
At odds with those studies, ours did not rely on the direct measure of pulse wave velocity (PWV) by applanation tonometry (the real gold standard of arterial stiffness evaluation) but on the measure of central pressure augmentation (i.e. a proxy of PWV) using a more convenient and less operator-dependent oscillometric method.
In the present study, the stronger association with mortality of SOFA-defined cardiovascular failure suggests this SOFA cardiovascular component score does not merely reflect therapeutic intervention in the form of blood pressure augmentation to maintain cerebral blood flow.
Loss of arterial distensibility results in a more rigid aorta that is less able to accommodate the volume of blood ejected by the left ventricle, resulting in greater pressure augmentation in systole and higher pulse pressures [ 89].
Accordingly, central systolic and diastolic blood pressure, pulse pressure, augmentation pressure and the augmentation index (AiX@HR75) are computed as described elsewhere [ 65].
