Computer simulations of transapical mitral valve repair with neochordae implantation: Clinical implications

Abstract

Objectives: Transapical beating heart neochordae implantation is an innovative mitral valve repair technique that has demonstrated promising clinical results in patients with primary mitral regurgitation. However, as clinical experience continues to increase, neochordae implantation criteria have not been fully standardized. The aim of this study was to investigate the biomechanical effects of selecting an antero-lateral apical access site compared with a postero-lateral site, and suboptimal neochordae length compared with optimal suture length, on restoring physiologic left heart dynamics.

Methods: Transapical neochordae implantation using 3 and 4 sutures was computer simulated under 3 posterior mitral leaflet prolapse conditions: isolated P2, multiscallop P2/P3 and multiscallop P2/P1. Physiologic, pre- and postrepair left heart dynamics were evaluated using a fluid-structure interaction modeling framework.

Results: Despite the absence of residual mitral regurgitation in all postrepair models with optimal neochordae length, selecting an antero-lateral apical entry site for the treatment of P2/P3 prolapse generated a significant increase (>80%) in neochordae tension and P2 peak stress, with respect to a postero-lateral entry site. During isolated P2 prolapse repair, although neochordae overtension by 5% led to minimal hemodynamic changes in the regurgitant volume compared with using an optimal suture length, a significant increase in systolic and diastolic neochordae tension (>300%) and posterior leaflet average stress (70%-460%) was quantified. On the other hand, neochordae undertension by 5% led to worsening of regurgitation severity.

Conclusions: This parametric computer study represents a further step toward an improved understanding of the biomechanical outcomes of transapical neochordae technologies.

Keywords: AL-NC, antero-lateral neochordae; AML, anterior mitral leaflet; AV, aortic valve; FSI, fluid-structure interaction; LV, left ventricle; MR, mitral regurgitation; MV, mitral valve; NC, neochordae; PL-NC, postero-lateral neochordae; PM, papillary muscle; PML, posterior mitral leaflet; beating heart mitral valve repair; ePTFE suture; ePTFE, expanded polytetrafluoroethylene; fluid-structure interaction FSI; primary mitral regurgitation; transapical neochord.

Graphical abstract

Physiologic, pre- and postrepair simulations of transapical neochordae repair.

Figure 1

A, Representative isolated P2 prolapse left heart model showing antero-lateral apical access site with NC3. B, Neochordae number and leaflet attachment location for the 6 postrepair models. C, Epicardial and endocardial wall motion between peak diastole (green) and peak systole (yellow). AV, Aortic valve; MV, mitral valve; LV, left ventricle; LA, left atrium; APM, antero-lateral papillary muscle; PPM, postero-medial papillary muscle; AML, anterior mitral leaflet; PML, posterior mitral leaflet divided into P1, P2, and P3 scallops; NC3, 3 neochordae; NC4, 4 neochordae.

Figure 2

Flow rate (mL/sec) curves across the mitral valve (MV) throughout the cardiac cycle. The negative systolic mitral flow indicates backflow of blood into the left atrium due to valve closing and regurgitation. APM, Antero-lateral papillary muscle; PPM, postero-medial papillary muscle; NC3, 3 neochordae, NC4, 4 neochordae.

Figure 3

Papillary muscle (PM) and neochordae tension (N) curves for the antero-lateral (AL-NC) and postero-lateral (PL-NC) neochordae implantation configurations throughout the cardiac cycle. NC3, 3 Neochordae, NC4, 4 neochordae.

Figure 4

Average stress (kPa) in the mitral leaflets at peak systole. Circles highlight a marked increase (>50%) in leaflet stress with respect to the physiologic left heart model (blue). NC3, 3 Neochordae; NC4, 4 neochordae; AML, anterior mitral leaflet.

Figure 5

Stress (MPa) distribution in the mitral leaflets at peak systole. A stress value threshold of 0.5 MPa was applied such that relatively large stress values were displayed in grey, facilitating comparison between models. Native chordae and neochordae not shown for clarity. PML, Posterior mitral leaflet; AML, anterior mitral leaflet; NC3, 3 neochordae; NC4, 4 neochordae.

Figure 6

Isolated P2 NC4 postrepair left heart models with optimal and suboptimal neochordae lengths. A, Mitral valve (MV) flow rate (mL/sec) curves throughout the cardiac cycle. The negative systolic flow indicates the backflow into the left atrium due to valve closing and mitral regurgitation (MR). B, Neochordae tension (N) curves throughout the cardiac cycle. C, Average mitral leaflet stress (kPa) at peak systole. D, Velocity (mm/sec) vectors showing MR jet at peak systole with neochordae undertension. Circles highlight a marked reduction/increase (>50%) with respect to the left heart model with optimal neochordae length (orange). Video 1, Video 2, Video 3, Video 4, Video 5 linked to this figure show the left heart dynamics for the physiologic, pre- and postrepair LH models with optimal and suboptimal neochordae lengths when treating isolated P2 prolapse. MV, Mitral valve; MR, mitral regurgitation; AML, anterior mitral leaflet.

Figure 7

Graphical abstract summarizing study methodology, main findings and clinical implications.

Figure 8

Aortic and left atrium (LA) pressure (mm Hg) boundary conditions.

Figure 9

Native mitral chordae tension (N) at peak systole. Circles highlight a marked reduction/increase (>50%) in chordae tension with respect to the physiologic left heart model (blue). NC3, 3 neochordae, NC4, 4 neochordae; AML, anterior mitral leaflet; PML, posterior mitral leaflet.