Velocities, shear stresses and blood damage potential of the leakage jets of the Medtronic Parallel bileaflet valve.

Even nowadays, the essential problem of mechanical heart valve prostheses is the risk of thromboembolic events mainly caused by unnatural hemodynamics, e.g. just a few years ago the Medtronic Parallel (MP) showed unsatisfactory clinical results caused by thrombi. Therefore, in vitro investigations of the whole leakage jets were performed at the MP in mitral position by means of a pulse duplicator using a two channel laser Doppler anemometer. From the measured data, mean velocity profiles and the distribution of Reynolds shear stresses, as a function of the location within the jet, were calculated. From this data the potential of blood damage is evaluated computing a Blood Damage Index (BDI) of hemolysis and platelet damage. Four regurgitant free jets right above the hinges were observed during systole at the inflow side of the MP. The peak velocities at the origin of the jets were in the order of 1.6-2.1 m/s. Two jets experienced maximum turbulent shear stresses around 100 N/m2 within this area. The BDI for platelets of the MP is around ten times higher than the BDI of the St.-Jude-Medical. The study shows that besides the flow structure within the hinges of a mechanical heart valve, the whole regurgitant jet has a large blood damage potential. This potential is measurable, respectively calculable and seems to be (on account of it's support of the clinical outcome) one piece of the puzzle that explains the negative trials of the MP.

Leakage flow at mechanical heart valve prostheses: improved washout or increased blood damage?

BACKGROUND AND AIMS OF THE STUDY: An essential problem of mechanical heart valve (MHV) prostheses is the risk of thromboembolic events and consequent need of lifetime anticoagulation due to unnatural hemodynamics that results in traumatization of red blood cells and platelets. The precise spatial and tidal localization of blood-damaging events within the flow is poorly understood. The present study addresses the question whether leakage flow at MHV, which is claimed to improve washout in the hinge areas of microthrombi and platelet-activating agents, is responsible for significant blood damage. METHODS: This study investigated leakage flow in vitro, primarily within turbulent leakage jets of currently used mechanical valves. St. Jude Medical, Sorin Bicarbon, Duromedics-Edwards and CarboMedics valves were analyzed in the mitral position of a circulatory mock loop. Jet configuration was determined by echocardiography; velocity and shear stress distributions within jets were measured using laser-Doppler anemometry (LDA). A blood damage index (BDI) was developed in terms of lactate dehydrogenase release by platelets and hemoglobin release by red blood cells (RBC), as a function of exposure time and shear stresses within the flow field. BDIs were validated by direct measurement of hemolysis caused by leakage flow, using porcine blood. RESULTS: All valves showed characteristic and reproducible jet patterns, mainly emerging from the hinge areas. Maximum velocities up to 1.7 m/s were measured. Maximum turbulent shear stresses > 80 Pa were found. The investigated MHV revealed significant differences in calculated BDIs. The Sorin Bicarbon had a significantly lower BDI for RBC damage, as well as for platelet damage; this was validated by direct hemolysis measurements. CONCLUSIONS: The relevance of the leakage-induced blood damage was demonstrated from a literature investigation of hemolysis as a function of valve type and implant position.

Comparison of valvular resistance, stroke work loss, and Gorlin valve area for quantification of aortic stenosis. An in vitro study in a pulsatile aortic flow model.

BACKGROUND: Valvular resistance and stroke work loss have been proposed as alternative measures of stenotic valvular lesions that may be less flow dependent and, thus, superior over valve area calculations for the quantification of aortic stenosis. The present in vitro study was designed to compare the impacts of valvular resistance, stroke work loss, and Gorlin valve area as hemodynamic indexes of aortic stenosis. METHODS AND RESULTS: In a pulsatile aortic flow model, rigid stenotic orifices in varying sizes (0.5, 1.0, 1.5 and 2.0 cm2) and geometry were studied under different hemodynamic conditions. Ventricular and aortic pressures were measured to determine the mean systolic ventricular pressure (LVSPm) and the transstenotic pressure gradient (delta Pm). Transvalvular flow (Fm) was assessed with an electromagnetic flowmeter. Valvular resistance [VR = 1333.(delta Pm/Fm)] and stroke work loss [SWL = 100.(delta Pm/LVSPm)] were calculated and compared with aortic valve area [AVA = Fm/(50 square root of delta Pm)]. The measurements were performed for a large range of transvalvular flows. At low-flow states, flow augmentation (100-->200 mL/s) increased calculated valvular resistance between 21% (2.0 cm2 orifice) and 66% (0.5-cm2 orifice). Stroke work loss demonstrated an increase from 43% (2.0 cm2) to 100% (1.0 cm2). In contrast, Gorlin valve area revealed only a moderate change from 29% (2.0 cm2) to 5% (0.5 cm2). At physiological flow rates, increase in transvalvular flow (200-->300 mL/s) did not alter calculated Gorlin valve area, whereas valvular resistance and stroke work loss demonstrated a continuing increase. Our experimental results were adopted to interpret the results of three clinical studies in aortic stenosis. The flow-dependent increase of Gorlin valve area, which was found in the cited clinical studies, can be elucidated as true further opening of the stenotic valve but not as a calculation error due to the Gorlin formula. CONCLUSIONS: Within the physiological range of flow, calculated aortic valve area was less dependent on hemodynamic conditions than were valvular resistance and stroke work loss, which varied as a function of flow. Thus, for the assessment of the severity of aortic stenosis, the Gorlin valve area is superior over valvular resistance and stroke work loss, which must be indexed for flow to adequately quantify the hemodynamic severity of the obstruction.