RESUMEN
Stroke remains a leading cause of complications and mortality in heart failure patients treated with LVAD circulatory support. Hemodynamics plays a central role in affecting risk and etiology of stroke during LVAD support. Yet, detailed quantitative assessment of hemodynamic variables and their relation to stroke outcomes in patients with an implanted LVAD remains a challenge. We present an in silico hemodynamics analysis in a set of 12 patients on LVAD support; 6 with reported stroke outcomes and 6 without. We conducted patient-specific hemodynamics simulations for models with the LVAD outflow graft reconstructed from cardiac-gated CT images. A pre-implantation baseline flow model was virtually generated for each case by removing the LVAD outflow graft and driving flow from the aortic root. Hemodynamics was characterized using quantitative descriptors for helical flow, vortex generation, and wall shear stress. Our analysis showed higher average values for descriptors of positive helical flow, vortex generation, and wall shear stress, across the 6 cases with stroke outcomes on LVAD support, when compared with cases without stroke. When the descriptors for LVAD-driven flow were compared against estimated baseline flow pre-implantation, extent of positive helicity was higher, and vorticity and wall shear were lower in cases with stroke compared to those without. The study suggests that quantitative analysis of hemodynamics after LVAD implantation; and hemodynamic alterations from a pre-implant flow scenario, can potentially reveal hidden information linked to stroke outcomes during LVAD support. This has broad implications on understanding stroke etiology, LVAD treatment planning, surgical optimization, and efficacy assessment.
RESUMEN
In majority of pandemics in human history, respiratory bio-aerosol is the most common route of transmission of diseases. These tiny droplets ejected through mouth and nose from an infected person during exhalation process like coughing, sneezing, speaking, and breathing consist of pathogens and a complex mixture of volatile and nonvolatile substances. A cloud of droplets ejected in such an event gets transmitted in the air, causing a series of coupled thermo-physical processes. Contemplating an individual airborne droplet in the cloud, boundary layers and wakes develop due to relative motion between the droplet and the ambient air. The complex phenomenon of the droplet's dynamics, such as shear-driven internal circulation of the liquid phase and Stefan flow due to vaporization or condensation, comes into effect. In this study, we present a mathematical description of the coupled subprocesses, including droplet aerodynamics, heat, and mass transfer, which were identified and subsequently solved. The presented two-dimensional model gives a complete analysis encompassing the gas phase coupled with the liquid phase responsible for the airborne droplet kinetics in the ambient environment. The transient inhomogeneity of temperature and concentration distribution in the liquid phase caused due to the convective and diffusive transports are captured in the 2D model. The evaporation time and distance traveled by droplets prior to nuclei or aerosol formation are computed for major geographical locations around the globe for nominal-windy conditions. The model presented can be used for determining the evaporation timescale of any viral or bacterial laden respiratory droplets across any geographical location.
RESUMEN
Naturally drying bacterial droplets on inanimate surfaces representing fomites are the most consequential mode for transmitting infection through oro-fecal route. We provide a multiscale holistic approach to understand flow dynamics induced bacterial pattern formation on fomites leading to pathogenesis. The most virulent gut pathogen, Salmonella Typhimurium (STM), typically found in contaminated food and water, is used as model system in the current study. Evaporation-induced flow in sessile droplets facilitates the transport of STM, forming spatio-temporally varying bacterial deposition patterns based on droplet medium's nutrient scale. Mechanical and low moisture stress in the drying process reduced bacterial viability but interestingly induced hyper-proliferation of STM in macrophages, thereby augmenting virulence in fomites. In vivo studies of fomites in mice confirm that STM maintains enhanced virulence. This work demonstrates that stressed bacterial deposit morphologies formed over small timescale (minutes) on organic and inorganic surfaces, plays a significant role in enhancing fomite's pathogenesis over hours and days.
