Importance of shear in prosthetic valve closure dynamics

The results of recent hematological studies have suggested that, under non-physiological flow conditions, circulating procoagulant proteins activate the coagulation cascade. In the present study, in-vitro estimates of flow transients at or near the time of valve closure, including regional backflow velocity (RBV, m/s), flow acceleration (m/s2), and rate of acceleration (jerk, m/s3), have shed new light on the blood-damage potential of prosthetic valves.

Several prosthetic valves were tested in a pulse duplicator under simulated cardiac conditions. A unique prototype subsystem (Leonardo(VSI)) was used to measure the projected dynamic valve areas (PDVAs) from backlit valves. The regional flow velocity was derived by dividing the time-dependent volumetric flow rate by the PDVA. The flow acceleration and jerk were subsequently obtained as time derivatives of the flow velocity.

Current mechanical valves have overt flow transients at valve closure, relating to leaflet nonresponse to flow deceleration and residual PDVA. In contrast, tissue valves initiate closure during the flow deceleration phase, and seal when closed, thus preventing supra-physiological backflow transients. The estimated average RBV transients at or near closure ranged from 45 to 162 m/s for mechanical valves, and from 3 to 10 m/s (i.e., ca. 93% less) for tissue valves. The average derived flow acceleration and jerk transients ranged from +2,235 to -1,786xg and from +10.8 x 106 to -7.5 x 10(6) m/s3 for mechanical valves, respectively, and were substantially lower for tissue valves (ca. 90-99% less).

The study results implicate that RBV transients at or near mechanical valve closure, and not the forward or closed flow phase, as being primary to the shear-induced activation of the coagulation cascade. Results obtained in vitro for an experimental trileaflet mechanical valve (Triflo) were tested only in the aortic site similar to those obtained with tissue valves.