Left ventricular assist devices (LVADs) comprise a primary treatment choice for advanced heart failure patients. Treatment with LVAD is commonly associated with complications like stroke and gastro-intestinal (GI) bleeding, which adversely impacts treatment outcomes, and causes fatalities. The etiology and mechanisms of these complications can be linked to the fact that LVAD outflow jet leads to an altered state of hemodynamics in the aorta as compared to baseline flow driven by aortic jet during ventricular systole. Here, we present a systematic quantitative assessment of aortic hemodynamics in LVAD flows within a realistic human aorta model. We consider hemodynamics in the aortic arch proximal to the LVAD outflow graft, as well as in the abdominal aorta away from the LVAD region. We characterize hemodynamics using quantitative descriptors of flow velocity, stasis, helicity, vorticity and mixing, and wall shear stress. These are used on a set of 27 LVAD scenarios obtained by parametrically varying LVAD outflow graft anastomosis angles, and LVAD flow pulse modulation. Computed descriptors for each of these scenarios are compared against the baseline flow, and a detailed quantitative characterization of the altered state of hemodynamics due to LVAD operation (when compared to baseline aortic flow) is compiled. These are interpreted using a conceptual model for LVAD flow that distinguishes between flow originating from the LVAD outflow jet (and its impingement on the aorta wall), and flow originating from aortic jet during aortic valve opening in normal physiological state.
Left ventricular assist devices (LVADs) comprise a primary treatment choice for advanced heart failure patients. Treatment with LVAD is commonly associated with complications like stroke and gastrointestinal (GI) bleeding, which adversely impacts treatment outcomes, and causes fatalities. The etiology and mechanisms of these complications can be linked to the fact that LVAD outflow jet leads to an altered state of hemodynamics in the aorta as compared to baseline flow driven by aortic jet during ventricular systole. Here, we present a systematic quantitative assessment of aortic hemodynamics in LVAD flows within a realistic human aorta model. We consider hemodynamics in the aortic arch proximal to the LVAD outflow graft, as well as in the abdominal aorta away from the LVAD region. We characterize hemodynamics using quantitative descriptors of flow velocity, stasis, helicity, vorticity and mixing, and wall shear stress. These are used on a set of 27 LVAD scenarios obtained by parametrically varying LVAD outflow graft anastomosis angles, and LVAD flow pulse modulation. Computed descriptors for each of these scenarios are compared against the baseline flow, and a detailed quantitative characterization of the altered state of hemodynamics due to LVAD operation (when compared to baseline aortic flow) is compiled. These are interpreted using a conceptual model for LVAD flow that distinguishes between flow originating from the LVAD outflow jet (and its impingement on the aorta wall), and flow originating from aortic jet during aortic valve opening in normal physiological state.
Left ventricular assist device (LVAD) provides mechanical circulatory support for patients with advanced heart failure. Treatment using LVAD is commonly associated with complications such as stroke and gastro-intestinal bleeding. These complications are intimately related to the state of hemodynamics in the aorta, driven by a jet flow from the LVAD outflow graft that impinges into the aorta wall. Here we conduct a systematic analyses of hemodynamics driven by an LVAD with a specific focus on viscous energy transport and dissipation. We conduct a complementary set of analysis using idealized cylindrical tubes with diameter equivalent to common carotid artery and aorta, and a patient-specific model of 27 different LVAD configurations. Results from our analysis demonstrate how energy dissipation is governed by key parameters such as frequency and pulsation, wall elasticity, and LVAD outflow graft surgical anastomosis. We find that frequency, pulsation, and surgical angles have a dominant effect, while wall elasticity has a weaker effect, in determining the state of energy dissipation. For the patient-specific scenario, we also find that energy dissipation is higher in the aortic arch and lower in the abdominal aorta, when compared to the baseline flow without an LVAD. This further illustrates the key hemodynamic role played by the LVAD outflow jet impingement, and subsequent aortic hemodynamics during LVAD operation.
Introduction: Stroke is a leading cause of death and disability and a significant complication for heart failure patients on Left Ventricular Assist Device (LVAD) support. Most of these stroke cases are embolic in nature. Yet, specifics of embolus transport to the brain by the flow driven by an LVAD are poorly understood; precluding a clear understanding of post-implant stroke risks in these patients. Here we demonstrate an innovative stroke risk descriptor using in silico embolus transport analysis. Methods: Cardiac gated CTA images with LVAD graft were obtained for 6 patients. 3 patients reported post-LVAD stroke and the other 3 did not. 3D computer models of the LVAD graft, aortic arch, and branch vessels to the head were created using SimVascular. Blood flow from LVAD was computed for each model using LVAD flow rate and mean blood pressure as inputs. A custom fluid-particle interaction model for embolus transport was used to obtain the distribution of emboli entering the arch from the LVAD. A combination of normalized embolus distribution was used to create a stroke risk descriptor and compared across the stroke and non-stroke cases. Two sets of descriptors were defined using: (a) embolus distribution to the head; and (b) distribution to the head as well as accumulation at aortic root near the dysfunctional aortic valve. Results: We present results from 5,000 different embolism scenarios using representative thromboembolic particles of 1 mm diameter. For descriptor category (a) defined in Methods, the computed average for post-LVAD stroke cases was 0.35 as compared to 0.24 for those without post-LVAD stroke. For risk of embolic events in the brain including embolus accumulation in aortic root (i.e. descriptor category (b) in Methods) the reported averages were 0.38 and 0.27 for stroke vs no-stroke cases. Conclusions: The results indicate that our descriptor is a good surrogate for identifying stroke risks post-LVAD implantation, with stroke cases correlated with high values of the descriptor. The results also indicate that emboli traveling from LVAD graft into the arch, as well as emboli accumulating in regions of stasis at the aortic root may both contribute to stroke risks in patients with an LVAD. Continued investigations with bigger patient cohorts are needed.
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