The erythrocyte destruction mechanism in non-physiological shear mechanical hemolysis

Increasingly heart failure patients need to use Ventricular Assist Devices (VADs) to keep themselves alive. During treatment, hemolysis is an inevitable complication of interventional devices. The most common method for evaluating mechanical hemolysis is to calculate Hemolysis Index (HI) by the power-law formula. However, the HI formula still has obvious flaws. With an intention of further understanding the phenomenon of mechanical hemolysis in non-physiological flow, our study developed a coarse-grained erythrocyte destruction model at the cellular scale and explored the mechanism of the single erythrocyte shear destruction utilizing the Dissipative Particle Dynamics, including the erythrocyte stretching destruction process and the erythrocyte non-physiological shearing destruction process. In the process of stretching and shearing, the high-strain distribution areas of erythrocytes are entirely different. The high-strain areas during stretching are concentrated on the central axis. After the stretch failure, the erythrocyte changes from fusiform to shriveled biconcave. In the shear breaking process, the high strain areas are focused on the erythrocyte edge, causing the red blood cells to evolve from an ellipsoid shape to a plate shape. In addition to the flow shear stress, the shear rate acceleration is also an important factor in the erythrocyte shear damage. The erythrocyte placed in low shear stress flow is still unstably destroyed under high shear rate acceleration. Consequently, the inclusion of flow-buffering structures in the design of VADs may improve non-physiological hemolysis. Published under an exclusive license by AIP Publishing.

Automated summary

This study developed a model to investigate the mechanism of mechanical hemolysis in Ventricular Assist Devices (VADs) treatment, revealing the different high-strain areas of erythrocytes during stretching and shearing processes, and highlighting the importance of shear rate acceleration in erythrocyte shear damage.