Vortex formation of the lvad-assisted left ventricle studied in a cardiac simulator.

摘要

Heart transplantation remains the primary treatment for heart failure (HF), a deadly disease in which the heart fails to pump sufficient blood to meet the body's needs. Unfortunately, of the 600,000 new HF patients per year, only 2200 (0.3%) of them receive heart transplantation. The critical organ shortage presents a need for artificial devices. Left ventricular assist devices (LVADs) are implantable blood pumps that serve as an alternative treatment for HF. Unfortunately, stroke is a devastating complication that occurs in about 17-20% of LVAD patients. Since stroke is the result of blood vessel blockage, we hypothesize that LVADs create flow disturbances such as localized stagnation regions that encourages excessive blood clotting (thrombosis) in the LV, which detach and release into the bloodstream. Experiments were performed using the in vitro SDSU cardiac simulator, which reproduces the flow and hemodynamics of a left ventricle attached to a HeartMate II LVAD. The effect of LVAD support on LV flow patterns was assessed by varying the LVAD speed from low (6500rpm) to high (12500rpm). Particle Image Velocimetry was used to image 2-D fluid structures in the LV model. Briefly, fluorescent tracer particles were seeded into the simulator, the particles were illuminated by a laser plane and their motion captured by a high frame-rate camera. Localized stagnation was measured by the stagnicity (SI), defined as the reciprocal of average velocity within the region of interest. The flow patterns resemble a HF patient as the ventricular inflow jet follows an asymmetric recirculation pattern that redirects the momentum of the fluid stream to the LV outflow tract (LVOT). Once the LVAD is incorporated into the circulation, the fluid stream bifurcates into ventricular outflow and LVAD outflow. As LVAD speed increases further, more fluid is ejected through the LVAD until finally there is a complete series flow. We observe a local stagnation region in the LVOT regardless of LVAD speed. The level of stagnation increases progressively from Pre-LVAD (SI =4.20(m/s)-1), parallel (SI =4.75 (m/s)-1), to series flow (SI =7.75 (m/s)-1). The results suggest that LVAD support alters the cardiac ejection pathways and increases the risk of thrombosis within the left ventricle.