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Load, chamber stiffness, and relaxation are the three established determinants of global diastolic function (DF). Coupling of systolic stiffness and isovolumic relaxation has been hypothesized; however, diastolic stiffness-relaxation coupling (DSRC) remains unknown. The parametrized diastolic filling (PDF) formalism, a validated DF model incorporates DSRC. PDF model-predicted DSRC was validated by analysis of 159 Doppler E-waves from a published data set (22 healthy volunteers undergoing bicycle exercise). E-waves at varying (46-120 bpm) heart rates (HR) demonstrated variation in acceleration time (AT), deceleration time (DT), and E-wave peak velocity. AT, DT, and Epeak were converted into PDF parameters: stiffness (k), relaxation (c), and load (xo) using published numerical methods. Univariate linear regression showed that over a twofold increase in HR, AT, and DT decrease (r = -0.44; P < 0.001 and r = -0.42; P < 0.001, respectively), while, DT/AT remains constant (r = -0.04; P = 0.67). Similarly, k increases with HR (r = 0.55; P < 0.001), while c has no significant correlation with HR (r = 0.08; P = 0.32). However, the dimensionless DSRC parameter ϣ = c²/4k shows no significant correlation with HR (r = -0.03; P = 0.7). Furthermore, ϣ is uniquely determined by DT/AT rather than AT or DT independently. Constancy of w in spite of a twofold increase in HR establishes that stiffness (k) and relaxation (c) are coupled and manifest via a HR-invariant parameter of E-wave asymmetry and should not be considered independent of each other. The manifestation of DSRC through E-wave asymmetry via ϣ underscores the value of DT/AT as a physiological, mechanism-derived index of DF. NEW & NOTEWORTHY: Although diastolic stiffness and relaxation are considered independent chamber properties, the cardiohemic inertial oscillation that generates E-waves obeys Newton's law. E-waves vary with heart rate requiring simultaneous change in stiffness and relaxation. By retrospective analysis of human heart-rate varying transmitral Doppler-data, we show that diastolic stiffness and relaxation are coupled and that the coupling manifests through E-wave asymmetry, quantified through a parametrized diastolic filling model-derived dimensionless parameter, which only depends on deceleration time and acceleration time, readily obtainable via standard echocardiography. [ABSTRACT FROM AUTHOR]

Management of aortic dissections (AD) is still challenging, with no universally approved guideline among possible surgical, endovascular, or medical therapies. Approximately 25% of patients with AD suffer postintervention malperfusion syndrome or hemodynamic instability, with the risk of sudden death if left untreated. Part of the issue is that vascular implants may themselves induce flow disturbances that critically impact vital organs. A multilayer mesh construct might obviate the induced flow disturbances, and it is this concept we investigated. We used preintervention and post-multilayer flow modulator implantation (PM) geometries from clinical cases of type B AD. In-house semiautomatic segmentation routines were applied to computed tomography images to reconstruct the lumen. The device was numerically reconstructed and adapted to the PM geometry concentrically fit to the true lumen centerline. We also numerically designed a pseudohealthy case, where the geometry of the aorta was extracted interpolating geometric features of preintervention, postimplantation, and published representative healthy volunteers. Computational fluid dynamics methods were used to study the time-dependent flow patterns, shear stress metrics, and perfusion to vital organs. A three-element Windkessel lumped parameter module was coupled to a finite-volume solver to assign dynamic outlet boundary conditions. Multilayer flow modulator not only significantly reduced false lumen blood flow, eliminated local flow disturbances, and globally regulated wall shear stress distribution but also maintained physiological perfusion to peripheral vital organs. We propose further investigation to focus the management of AD on both modulation of blood flow and restoration of physiologic end-organ perfusion rather than mere restoration of vascular lamina morphology. [ABSTRACT FROM AUTHOR]