Towards non-thrombogenic performance of blood recirculating devices

Abstract

Implantable blood recirculating devices have provided life saving solutions to patients with severe cardiovascular diseases. However, common problems of hemolysis and thromboembolism remain an impediment to these devices. In this article, we present a brief review of the work by several groups in the field that has led to the development of new methodologies that may facilitate achieving the daunting goal of optimizing the thrombogenic performance of blood recirculating devices. The aim is to describe work which pertains to the interaction between flow-induced stresses and the blood constituents, and that supports the hypothesis that thromboembolism in prosthetic blood recirculating devices is initiated and maintained primarily by the non-physiological flow patterns and stresses that activate and enhance the aggregation of blood platelets, increasing the risk of thromboembolism and cardioembolic stroke. Such work includes state-of-the-art numerical and experimental tools used to elucidate flow-induced mechanisms leading to thromboembolism in prosthetic devices. Following the review, the paper describes several efforts conducted by some of the groups active in the field, and points to several directions that should be pursued in the future in order to achieve the goal for blood recirculating prosthetic devices becoming more effective as destination therapy in the future.

FIGURE 1

Flow field through St. Jude bileaflet MHV (196 ms after peak systole).

FIGURE 2

FSI simulation comparing SJM and ATS valves. Vector flow fields and wall shear stresses on the leaflets are shown during peak systole (top) and regurgitation (bottom).

FIGURE 3

Platelet dispersion patterns during peak systole (top) and hinges regurgitation (bottom). Different hinge mechanism design translate into higher thrombogenic potential for the SJM valve during regurgitation.

FIGURE 4

DNS simulations of blood flow through St. Jude MHV, showing complex platelet trajectories following helical pattern of counter rotating vortices in the hinges region (zoom in, bottom right).

FIGURE 5

PAS assay: platelets prothrombinase activity, and the effect of prothrombin acetylation-eliminating the feedback loop elimination.

FIGURE 6

In vitro platelet activity measurements in LVAD: the bileaflet MHV generated higher platelet activity than the monoleaflet MHV (p<0.05).

FIGURE 7

The DTE methodology: platelet trajectories and their loading history in MHV flow serve to generate input waveforms to the Hemodynamic Shearing Device (HSD).

FIGURE 8

Plots of (a) stream lines; (b) shear stress contours; and (c) simulated platelet activation parameter for the flow dynamics in the gap width between the leaflet edge and the valve housing for a bi-leaflet mechanical valve at the instant of valve closure.

FIGURE 9

Micro-scale analysis of RBC/platelet interaction in a channel with a width of 42 µm.

FIGURE 10

Experimental fluid dynamics (EFD) and computational fluid dynamics (CFD) at 350 ms into diastole-port and chamber effects for V0 (a) EFD velocity, (b) CFD velocity, (c) CFD wall strain rate and V1 (d) EFD velocity, (e) CFD velocity, and (f) CFD wall strain rate.

FIGURE 11

A comparison between EFD and CFD at 150 ms into diastole focusing on the influence of valve type for (a) V2 EFD with the BSM MHV, (b) V1 CFD with the BSM MHV, (c) V1 CFD with the BSM MHV wall strain rate, (d) V2 EFD with the CM MHV, (e) V1 CFD with the CM MHV, and (f) V1 CFD with the CM MHV wall strain rate.

FIGURE 12

Mean PIV flow maps in the 11 mm plane at (a) 250, (b) 400, (c) 550, and (d) 650 ms for the BSM valve showing the time history of the rotational flow pattern. (From Cooper et al. with permission).

FIGURE 13

Mean PIV flow maps in the 11 mm plane at (a) 300, (b) 400, (c) 550, and (d) 700 ms for the CM valve configuration illustrating the time history of the rotational flow pattern. (From Cooper et al. with permission).

FIGURE 14

Surface locations (S1–S7) used in wall shear calculations for both valve configurations. (From Cooper et al. with permission).

FIGURE 15

Non-dimensionalized wall shear maps for the BSM (left column) and CM (right column) valve configurations in the 11 mm plane for Surface 1 (a, b), Surface 2 (c, d), and Surface 3 (e, f). Areas of interest are highlighted with ovals. Note that the wall locations are defined in a counter-clockwise fashion. (From Cooper et al. with permission).