Arnold A. Fontaine

Integrated Mechanism for Functional Mitral Regurgitation Leaflet Restriction Versus Coapting Force: In Vitro Studies

BACKGROUND Functional mitral regurgitation in patients with ischemic or dilated ventricles has been related to competing factors: altered tension on the leaflets due to displacement of their papillary muscle and annular attachments, which restricts leaflet closure, versus global ventricular dysfunction with reduced transmitral pressure to close the leaflets. In vivo, however, geometric changes accompany dysfunction, making it difficult to study these factors independently. Functional mitral regurgitation also paradoxically decreases in midsystole, despite peak transmitral driving pressure, suggesting a change in the force balance acting to create a regurgitant orifice, with rising transmitral pressure counteracting forces that restrict leaflet closure. In vivo, this mechanism cannot be tested independently of annular contraction that could also reduce midsystolic regurgitation. METHODS AND RESULTS An in vitro model was developed that allows independent variation of papillary muscle position, annular size, and transmitral pressure, with direct regurgitant flow rate measurement, to test the hypothesis that functional mitral regurgitation reflects an altered balance of forces acting on the leaflets. Hemodynamic and echocardiographic measurements of excised porcine valves were made under physiological pressures and flows. Apical and posterolateral papillary muscle displacement caused decreased leaflet mobility and apical leaflet tethering or tenting with regurgitation, as seen clinically. It reproduced the clinically observed midsystolic decrease in regurgitant flow and orifice area as transmitral pressure increased. Tethering delayed valve closure, increased the early systolic regurgitant volume before complete coaptation, and decreased the duration of coaptation. Annular dilatation increased regurgitation for any papillary muscle position, creating clinically important regurgitation; conversely, increased transmitral pressure decreased regurgitant orifice area for any geometric configuration. CONCLUSIONS The clinically observed tented-leaflet configuration and dynamic regurgitant orifice area variation can be reproduced in vitro by altering the three-dimensional relationship of the annular and papillary muscle attachments of the valve so as to increase leaflet tension. Increased transmitral pressure acting to close the leaflets decreases the regurgitant orifice area. These results are consistent with a mechanism in which an altered balance of tethering versus coapting forces acting on the leaflets creates the regurgitant orifice.

Integrated Mechanism for Functional Mitral Regurgitation

Background Functional mitral regurgitation in patients with ischemic or dilated ventricles has been related to competing factors: altered tension on the leaflets due to displacement of their papillary muscle and annular attachments, which restricts leaflet closure, versus global ventricular dysfunction with reduced transmitral pressure to close the leaflets. In vivo, however, geometric changes accompany dysfunction, making it difficult to study these factors independently. Functional mitral regurgitation also paradoxically decreases in midsystole, despite peak transmitral driving pressure, suggesting a change in the force balance acting to create a regurgitant orifice, with rising transmitral pressure counteracting forces that restrict leaflet closure. In vivo, this mechanism cannot be tested independently of annular contraction that could also reduce midsystolic regurgitation. Methods and Results An in vitro model was developed that allows independent variation of papillary muscle position, annular size,...

Chordal force distribution determines systolic mitral leaflet configuration and severity of functional mitral regurgitation

OBJECTIVES The purpose of this study was to investigate the impact of the chordae tendineae force distribution on systolic mitral leaflet geometry and mitral valve competence in vitro. BACKGROUND Functional mitral regurgitation is caused by changes in several elements of the valve apparatus. Interaction among these have to comply with the chordal force distribution defined by the chordal coapting forces (F(c)) created by the transmitral pressure difference, which close the leaflets and the chordal tethering forces (FT) pulling the leaflets apart. METHODS Porcine mitral valves (n = 5) were mounted in a left ventricular model where leading edge chordal forces measured by dedicated miniature force transducers were controlled by changing left ventricular pressure and papillary muscle position. Chordae geometry and occlusional leaflet area (OLA) needed to cover the leaflet orifice for a given leaflet configuration were determined by two-dimensional echo and reconstructed three-dimensionally. Occlusional leaflet area was used as expression for incomplete leaflet coaptation. Regurgitant fraction (RF) was measured with an electromagnetic flowmeter. RESULTS Mixed procedure statistics revealed a linear correlation between the sum of the chordal net forces, sigma[Fc - FT]S, and OLA with regression coefficient (minimum - maximum) beta = -115 to -65 [mm2/N]; p < 0.001 and RF (beta = -0.06 to -0.01 [%/N]; p < 0.001). Increasing FT by papillary muscle malalignment restricted leaflet mobility, resulting in a tented leaflet configuration due to an apical and posterior shift of the coaptation line. Anterior leaflet coapting forces increased due to mitral leaflet remodeling, which generated a nonuniform regurgitant orifice area. CONCLUSIONS Altered chordal force distribution caused functional mitral regurgitation based on tented leaflet configuration as observed clinically.

Experimental analysis of fluid mechanical energy losses in aortic valve stenosis: Importance of pressure recovery

Current methods for assessing the severity of aortic stenosis depend primarily on measures of maximum systolic pressure drop at the aortic valve orifice and related calculations such as valve area. It is becoming increasingly obvious, however, that the impact of the obstruction on the left ventricle is equally important in assessing its severity and could potentially be influenced by geometric factors of the valve, causing variable degrees of downstream pressure recovery. The goal of this study was to develop a method for measuring fluid mechanical energy losses in aortic stenosis that could then be directly related to the hemodynamic load placed on the left ventricle. A control volume form of conservation of energy was theoretically analyzed and modified for application to aortic valve stenosis measurements.In vitro physiological pulsatile flow experiments were conducted with different types of aortic stenosis models, including a venturi meter, a nozzle, and 21-mm Medtronic-Hall tilting disc and St. Jude bileaflet mechanical valves. The energy loss created by each model was measured for a wide range of experimental conditions, simulating physiological variation. In all cases, there was more energy lost for the nozzle (mean=0.27 J) than for any other model for a given stroke volume. The two prosthetic valves generated approximately the same energy losses (mean=0.18 J), which were not statistically different, whereas the venturi meter had the lowest energy loss for all conditions (mean=0.037 J). Energy loss correlated poorly with orifice pressure drop (r2=0.34) but correlated well with recovered pressure drop (r2=0.94). However, when the valves were considered separately, orifice and recovered pressure drop were both strongly correlated with energy loss (r2=0.99, 0.96). The results show that recovered pressure drop, not orfice pressure drop, is directly related to the energy loss that determines pump work and therefore is a more accurate measure of the hemodynamic significance of aortic stenosis.

identification of Peak Stresses in Cardiac Prostheses : a Comparison of Two-dimensional versus three-dimensional Principal Stress Analyses

&NA; This study assessed the accuracy of using a two‐dimensional principal stress analysis compared to a three‐dimensional analysis in estimating peak turbulent stresses in complex three‐dimensional flows associated with cardiac prostheses. Three‐component, coincident laser Doppler anemometer measurements were obtained in steady flow downstream of three prosthetic valves: a St. Jude bileaflet, Bjork‐Shiley monostrut tilting disc, and Starr‐Edwards ball and cage. Two‐dimensional and three‐dimensional principal stress analyses were performed to identify local peak stresses. Valves with locally two‐dimensional flows exhibited a 10‐15% underestimation of the largest measured normal stresses compared to the three‐dimensional principal stresses. In nearly all flows, measured shear stresses underestimated peak principal shear stresses by 10‐100%. Differences between the two‐dimensional and three‐dimensional principal stress analysis were less than 10% in locally two‐dimensional flows. In three‐dimensional flows, the two‐dimensional principal stresses typically underestimated three‐dimensional values by nearly 20%. However, the agreement of the two‐dimensional principal stress with the three‐dimensional principal stresses was dependent upon the two velocity‐components used in the two‐dimensional analysis, and was observed to vary across the valve flow field because of flow structure variation. The use of a two‐dimensional principal stress analysis with two‐component velocity data obtained from measurements misaligned with the plane of maximum mean flow shear can underpredict maximum shear stresses by as much as 100%. ASAIO Journal 1996;42:154‐163.

Mechanism of Incomplete Mitral Leaflet Coaptation—Interaction of Chordal Restraint and Changes in Mitral Leaflet Coaptation Geometry: Insight from In Vitro Validation of the Premise of Force Equilibrium

Clinically observed incomplete mitral leaflet coaptation was reproduced in vitro by altering the balance of the chordal tethering and chordal coapting force components. Mitral leaflet coaptation geometry was distorted by changes of the spatial relations between the papillary muscles and the mitral valve as well as hemodynamics. Mitral leaflet malalignment was accentuated by a redistribution of the chordal tethering and coapting force components. For the overall assessment of systolic mitral leaflet configuration in functional mitral regurgitation it is important to consider the interaction between chordal restraint and an altered mitral leaflet coaptation geometry.

An automated method for analysis and visualization of laser doppler velocimetry data

The analysis and visualization of large data sets collected by use of laser Doppler velocimetry has presented a challenge to researchers using this technique to investigate complex flow fields. This paper describes an automated procedure for analysis and animation of two- and three-dimensional laser Doppler velocimetry data. The procedure consists of a suite of FORTRAN programs for calculating phase window averages of velocity and the Reynolds stress tensor, calculating the principal normal stresses, maximum shear stresses, and preparation of data files for input into Plot-3D compatible data visualization software. An example application of these techniques to data collected from anin vitro investigation of the retrograde flow field associated with a bileaflet mechanical heart valve is also presented.

A three-component force vector cell for in vitro quantification of the force exerted by the papillary muscle on the left ventricular wall

Recent clinical studies indicate that functional mitral regurgitation, which is a common complication in patients who suffer from ischemic heart disease, is related to an increase in the tethering forces acting on the mitral valve leaflets. Alterations in the valvular assembly, displacement of the papillary muscles or dilatation of the mitral valve annulus can disrupt the normal force balance on the mitral leaflets and result in an abnormal coaptation geometry with incomplete mitral leaflet closure. The force balance imposed on the mitral leaflets is created by the coapting forces generated by the transmitral pressure difference and the tethering forces at the leaflet attachments. A unique force vector cell capable of accurately measuring the three-component force vector applied by the papillary muscle on the left-ventricular wall was designed and manufactured to permit quantification of the alteration in the force balance acting on the mitral leaflets, and to allow for the study of the influence of papillary muscle displacement on mitral regurgitation.

A model based on dimensional analysis for noninvasive quantification of valvular regurgitation under confined and impinging conditions: in vitro pulsatile flow validation.

A technique is proposed for the noninvasive quantification of regurgitant flows under confined and impinging conditions. Its use requires only the knowledge of the jet orifice velocity, receiving chamber diameter, orifice-to-end wall distance and any downstream jet centerline velocity at a known distance from the orifice. The technique is based on dimensional analysis and provides a prediction of peak regurgitant flow rates. To validate the technique, known physiologic pulsatile flows were pumped through 2- and 4-mm circular orifices at 70 to 150 beats/min, into two different receiving chambers of 51 and 88 mm in diameter. At each heart rate, the peak orifice velocity was varied from 2 to 5 m/s, and the orifice-to-end wall distance was varied from 30 to 93 mm. Centerline velocities were recorded by pulsed Doppler ultrasound and averaged over multiple beats. A dimensional analysis of the parameters of the study provided an equation relating normalized centerline velocity to orifice-to-end wall distance, chamber diameter and downstream location. Statistical modeling of the experimental data was performed to compute the constants involved in this equation. The estimated (i.e., predicted by the technique) peak regurgitant flow rates were found to fall within 10% of the actual values, when centerline velocities were measured over a range of centerline distances from six orifice diameters to 85% of the chamber length. Therefore, the proposed technique provides, for the first time, a quantitative method for calculating valvular regurgitant flow rates under confined and impinging conditions.