Successful mitral valve repair is dependent upon a full understanding of normal and abnormal mitral valve anatomy and function. Computational analysis is one such method that can be applied to simulate mitral valve function in order to analyse the roles of individual components and evaluate proposed surgical repair. We developed the first three-dimensional finite element computer model of the mitral valve including leaflets and chordae tendineae; however, one critical aspect that has been missing until the last few years was the evaluation of fluid flow, as coupled to the function of the mitral valve structure. We present here our latest results for normal function and specific pathological changes using a fluid-structure interaction model. Normal valve function was first assessed, followed by pathological material changes in collagen fibre volume fraction, fibre stiffness, fibre splay and isotropic stiffness. Leaflet and chordal stress and strain and papillary muscle force were determined. In addition, transmitral flow, time to leaflet closure and heart valve sound were assessed. Model predictions in the normal state agreed well with a wide range of available in vivo and in vitro data. Further, pathological material changes that preserved the anisotropy of the valve leaflets were found to preserve valve function. By contrast, material changes that altered the anisotropy of the valve were found to profoundly alter valve function. The addition of blood flow and an experimentally driven microstructural description of mitral tissue represent significant advances in computational studies of the mitral valve, which allow further insight to be gained. This work is another building block in the foundation of a computational framework to aid in the refinement and development of a truly non-invasive diagnostic evaluation of the mitral valve. Ultimately, it represents the basis for simulation of surgical repair of pathological valves in a clinical and educational setting.

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Fluid–structure interaction models of the mitral valve: function in normal and pathological states

Although it has been proposed that incomplete relaxation explains certain increases in left ventricular end diastolic pressure relative to volume, there has been no clear demonstration that incomplete relaxation occurs in the intact working ventricle. To identify incomplete relaxation, left ventricular pressure-dimension relationships were studied in 10 canine right heart bypass preparations during ventricular pacing. The fully relaxed, exponential diastolic pressure-dimension line for each ventricle was first determined from pressure and dimension values at the end of prolonged diastoles after interruption of pacing. For 167 beats during pacing under widely varying hemodynamic conditions, diastolic pressure-dimension values encountered this line defining the fully relaxed state during the filling period indicating that relaxation was complete before end diastole. The time constant for isovolumic exponential pressure fall (T) was determined for all beats. For this exponential function, if no diastolic filling occurred, 97% of pressure fall would be complete by 3.5 T after maximal negative dP/dt. For the 167 beats the fully relaxed pressure-dimension line was always encountered before 3.5 T.

With very rapid pacing rates (170-200 beats/min) and(or) with pharmacologic prolongation of relaxation, incomplete relaxation occurred as evidenced by the fact that the line defining the fully relaxed state was never reached during diastole (n = 15). This evidence of incomplete relaxation occurred only when the subsequent beat began before 3.5 T but did not always occur under these conditions. Thus, an increase in end diastolic pressure relative to diastolic volume may result from incomplete relaxation under conditions of sufficiently rapid heart rate or sufficiently prolonged ventricular relaxation. Incomplete relaxation does not occur when the next beat begins more than 3.5 T after maximum negative dP/dt.

/pdf/evidence-of-incomplete-left-ventricular-relaxation-in-the-q9wumekojv.pdf

Evidence of incomplete left ventricular relaxation in the dog: prediction from the time constant for isovolumic pressure fall.

Fluid mechanics of the natural mitral valve

Diastolic mitral regurgitation in patients with atrioventricular conduction abnormalities: A common finding by doppler echocardiography

In 64 patients requiring cardiac catheterization for chest pain, echocardiograms showing anterior mitral leaflet and left ventricular cavity simultaneously were recorded. These were digitized and their first derivatives computed in order to study time relations between mitral valve and left ventricular wall movement in early distole. In 10 patients with normal left ventricular angiograms and coronary arteriograms, mitral valve opening began 1-1 +/- 9-3 ms (mean +/- SD) before the onset of outward wall movement, and reached peak opening velocity 2-0 +/- 13 ms after maximum rate of change of dimension. Virtually identical time relations were seen in 15 patients with normal left ventricular angiograms but with obstructive coronary artery disease (3-6 +/- 9-3 ms and 0-7 +/- 7-3 ms, respectively). These close relations were lost in patients with segmental abnormalities of contraction on left ventricular angiogram. In 19 such patients with normal septal motion, outward wall movement began 53 +/- 31 ms before the onset of anterior movement of the mitral valve leaflet, and this isovolumic wall movement accounted for 31 per cent of the total diastolic excursion. In 9 patients with reversed septal movement, these abnormalities were greater, 92 +/- 39 ms and 33 per cent, respectively, while in 11 patients with diffuse left ventricular involvement they were small, 5-5 +/- 13 ms and 3 per cent. Frame-by-frame digitization of cineangiograms was used to confirm these findings which appear to reflect an abnormal change in left ventricular cavity shape during isovolumic relaxation.

https://heart.bmj.com/content/heartjnl/38/10/1001.full.pdf

Echocardiographic assessment of abnormal left ventricular relaxation in man.

The echocardiogram of the anterior leaflet of the mitral valve (ECHO) was compared to hemodynamic and cineroentgenographic data to evaluate its accuracy in timing mitral valve (MV) opening and closure, and to validate it as an indicator of MV motion. The ECHO, high speed cineroentgenography at 250 frames/sec, and/or measurement of intracardiac pressures allowed accurate timing of the events of MV motion in dogs on right heart bypass. The intersection of left ventricular and left atrial pressures in early diastole preceded the onset of rapid anterior motion of ECHO (D' point) by 17 to 33 plus or minus 7.6 msec; r equals 0.98. The onset of left ventricular systole occurred before the termination of final rapid posterior motion of the ECHO in end diastole (Co point) by 25 plus or minus 10 msec; r equals 0.96. Radiopaque clips were attached to the free edges of both leaflets of the MV. Cineroentgenographically determined plots of clip distance from the ultrasound transducer were morphologically similar to the simultaneously recorded ECHO. A delay of 23 plus or minus 3 (0 to 40) msec was observed in the ECHO peaks of diastolic anterior excursion compared to clip motion. Contrast medium advances beyond the free edges of MV leaflets mixing with left ventricular blood 43 plus or minus 3 msec after initial separation. These cineroentgenographic studies elucidate nonuniformity of leaflet motion responsible for ECHO delays. Thus, ECHO D' and Co correlate well with hemodynamic indicators of MV opening and closure. However, ECHO motion, although qualitatively similar, is unpredictably delayed compared to cineroentgenography of clips on the MV free edge. Since the ECHO correlates well with hemodynamic indices of MV opening and closure, this noninvasive technique can be used as a reference in the timing of intracardiac events and in the determination of systolic and diastolic time intervals.

H E Scully

Papers

The echocardiogram of the anterior leaflet of the mitral valve. Correlation with hemodynamic and cineroentgenographic studies in dogs.