Author + information
- Yonghoon Rim, PhD,
- Krishnan B. Chandran, DSc,
- Susan T. Laing, MD,
- Patrick Kee, MD,
- David D. McPherson, MD and
- Hyunggun Kim, PhD∗ ()
- ↵∗Division of Cardiovascular Medicine, Department of Internal Medicine, The University of Texas Health Science Center at Houston, 6431 Fannin Street, MSB 1.246, Houston, Texas 77030
Various pathologies of the mitral valve (MV) apparatus include excessive annular dilation, chordal elongation, chordal rupture, and leaflet tissue enlargement, which lead to mitral regurgitation (MR) (1). The recommended treatment for these MV pathologies accompanied by severe MR is MV reconstruction, which has been shown to improve event-free survival (2). Echocardiography is the primary imaging modality to provide MV pathological information and the proper timing for consideration of MV repair (3).
In a recent issue, we demonstrated 4 cases of computational evaluation of MV function (4). Here we extend our patient-specific computational MV evaluation studies to quantitatively determine the biomechanical and physiological characteristics of MV function involving severe annular dilation.
Five patients with normal MV and 5 patients with severe annular dilation accompanied by MR were recruited, and 3-dimensional (3D) transesophageal echocardiography (TEE) was performed. Patient-specific 3D TEE data were converted into computational MV models followed by dynamic simulations to evaluate MV function (5). Stress and contact pressure distributions across the mitral leaflets were determined at peak systole. A ratio of the coapted leaflet area to the entire posterior leaflet area was calculated and compared between the normal and pathological MV groups.
The normal MVs clearly showed 3D cyclic deformation of the saddle-shaped annular morphology across the cardiac cycle. The pathological MVs displaying severe MR revealed larger annular sizes and less elliptical annular morphology compared with the normal MVs. Representative stress distributions across the mitral leaflets at peak systole are demonstrated in Figures 1A and 1B. Symmetrical stress distribution patterns were found over both anterior and posterior leaflets in the normal MVs. In contrast, the pathological MVs with severe annular dilation revealed markedly asymmetrical stress patterns with high stress values spread along the radial direction. The pathological MVs demonstrated higher average maximum stress values (1.3 ± 0.2 MPa; p < 0.01) than the normal MVs (0.8 ± 0.2 MPa). These excessive stress concentrations were found in regions involving incomplete leaflet coaptation. From a biomechanical perspective, this finding implies that severe annular dilation with normal left ventricular function generates high stresses across the leaflet and chordae tissue, causes considerable tissue remodeling in the leaflets and chordae under high stresses (i.e., leaflet enlargement and chordal elongation), and may induce a lack of leaflet coaptation, ultimately leading to significant MR.
Figure 1C demonstrates representative images of contact pressure distributions between the anterior and posterior leaflets at peak systole and the corresponding color Doppler ultrasound images. The normal MVs showed complete coaptation with full leaflet contact. The pathological MVs with severe annular dilation revealed a large lack of leaflet contact, indicating incomplete leaflet closure and a considerable degree of MR. These findings corresponded to the color Doppler ultrasound data. Although there was no regurgitation found in the normal MVs, a severe regurgitant jet was detected in the pathological MVs. The pathological MVs with severe annular dilation revealed markedly reduced leaflet contact ratios (0.19 ± 0.03; p < 0.001) compared with the normal MVs (0.33 ± 0.04) (Figure 1D). These quantitative data indicate that severe annular dilation with normal left ventricular function affects the degree and extent of leaflet coaptation.
A limitation of this study is that patients with complicated pathologies such as severe calcification and chordal rupture were excluded. Our study design allowed us to focus on investigation of the valvular geometric effects on MV dynamics and corresponding clinical observations. A larger number of studies will allow us to determine critical stress values for leaflet and chordal tissue, quantitate the degree of 3D leaflet coaptation, and quantitatively evaluate and predict the degree of MR progression.
In conclusion, computational simulation using patient-specific 3D TEE data provides quantitative information pertaining to biomechanical and physiological abnormalities in MV function. Combining these techniques offers a novel strategy for patient-specific MV evaluation and improved pre-surgical planning.
Please note: This work was supported in part by the National Institutes of Health (R01 HL109597).
- American College of Cardiology Foundation