Abstract
Vascular pressure differences are established risk markers for a number of cardiovascular diseases. Relative pressures are, however, often driven by turbulence-induced flow fluctuations, where conventional non-invasive methods may yield inaccurate results. Recently, we proposed a novel method for non-turbulent flows, νWERP, utilizing the concept of virtual work-energy to accurately probe relative pressure through complex branching vasculature. Here, we present an extension of this approach for turbulent flows: νWERP-t. We present a theoretical method derivation based on flow covariance, quantifying the impact of flow fluctuations on relative pressure. νWERP-t is tested on a set of in-vitro stenotic flow phantoms with data acquired by 4D flow MRI with six-directional flow encoding, as well as on a patient-specific in-silico model of an acute aortic dissection. Over all tests νWERP-t shows improved accuracy over alternative energy-based approaches, with excellent recovery of estimated relative pressures. In particular, the use of a guaranteed divergence-free virtual field improves accuracy in cases where turbulent flows skew the apparent divergence of the acquired field. With the original νWERP allowing for assessment of relative pressure into previously inaccessible vasculatures, the extended νWERP-t further enlarges the method's clinical scope, underlining its potential as a novel tool for assessing relative pressure in-vivo.
Highlights
Flow abnormalities are typical indicators of cardiovascular disease (CVD)
Utilizing νWERP, we showed that accurate relative pressure estimates could be achieved in arbitrary multibranched vasculatures
We present an extension of the νWERP formulation, νWERP-t, incorporating turbulence-driven energy dissipation and expanding the original method into highly turbulent flow regimes
Summary
Flow abnormalities are typical indicators of cardiovascular disease (CVD). In the presence of valvular stenosis, the development of post-stenotic turbulence is directly related to pathologi-cal changes in cardiac workload (Schöbel et al, 1999; Dyverfeldt et al, 2013), and hemodynamic alterations in heart failure patients have been linked to pathological neurohormonal activation (Schrier and Abraham, 1999). Flow abnormalities are typical indicators of cardiovascular disease (CVD). In the presence of valvular stenosis, the development of post-stenotic turbulence is directly related to pathologi-. Cal changes in cardiac workload (Schöbel et al, 1999; Dyverfeldt et al, 2013), and hemodynamic alterations in heart failure patients have been linked to pathological neurohormonal activation (Schrier and Abraham, 1999). With disease-related flow changes even proposed to occur prior to any detectable morphological change (Pedrizzetti et al, 2014), assessing hemodynamic behaviour is of direct clinical importance. Recent studies have evaluated the production of turbulent flow in patients with aortic stenosis (Dyverfeldt et al, 2013; Bahlmann et al, 2010), indicating links between cardiovascular relative pressure and disease severity
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