Key result
PVAN repair reduces experimentally induced mitral regurgitant fraction by an absolute ~21% while normalizing chordal forces.
Why the study?
Posterior ventricular anchoring neochordal repair corrects mitral regurgitation, but the stability of the anchoring suture remains a theoretical limitation.
Does posterior ventricular anchoring neochordal (PVAN) repair reduce mitral regurgitation and normalize chordal forces in an ex vivo porcine model?
Does posterior ventricular anchoring neochordal (PVAN) repair reduce mitral regurgitation and normalize chordal forces in an ex vivo porcine model?
PVAN is a biomechanically sound non-resectional repair strategy that fully reverses prolapse-induced mitral regurgitation while subjecting the ventricular anchor point to extremely low forces.
PVAN eliminates MR and normalizes forces in porcine model; leaves open translation to human mitral repair pending clinical trials.
OBJECTIVES: Posterior ventricular anchoring neochordal (PVAN) repair is a non-resectional technique for correcting mitral regurgitation (MR) due to posterior leaflet prolapse, utilizing a single suture anchored in the myocardium behind the leaflet. This technique has demonstrated clinical efficacy, although a theoretical limitation is stability of the anchoring suture. We hypothesize that the PVAN suture positions the leaflet for coaptation, after which forces are distributed evenly with low repair suture forces. METHODS: Porcine mitral valves were mounted in a 3-dimensional-printed heart simulator and chordal forces, haemodynamics and echocardiography were collected at baseline, after inducing MR by severing chordae, and after PVAN repair. Repair suture forces were measured with a force-sensing post positioned to mimic in vivo suture placement. Forces required to pull the myocardial suture free were also determined. RESULTS: Relative primary and secondary chordae forces on both leaflets were elevated during prolapse (P < 0.05). PVAN repair eliminated MR in all valves and normalized chordae forces to baseline levels on anterior primary (0.37 ± 0.23 to 0.22 ± 0.09 N, P < 0.05), posterior primary (0.62 ± 0.37 to 0.14 ± 0.05 N, P = 0.001), anterior secondary (1.48 ± 0.52 to 0.85 ± 0.43 N, P < 0.001) and posterior secondary chordae (1.42 ± 0.69 to 0.59 ± 0.17 N, P = 0.005). Repair suture forces were minimal, even compared to normal primary chordae forces (0.08 ± 0.04 vs 0.19 ± 0.08 N, P = 0.002), and were 90 times smaller than maximum forces tolerated by the myocardium (0.08 ± 0.04 vs 6.9 ± 1.3 N, P < 0.001). DISCUSSION: PVAN repair eliminates MR by positioning the posterior leaflet for coaptation, distributing forces throughout the valve. Given extremely low measured forces, the strength of the repair suture and the myocardium is not a limitation.
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Paulsen et al. (2019) studied Mitral regurgitation (n=8). Posterior ventricular anchoring neochordal (PVAN) repair vs. Induced prolapse condition (severed chordae) was evaluated on Mitral valve regurgitant fraction (p=<0.001). Posterior ventricular anchoring neochordal (PVAN) repair eliminated experimentally induced mitral regurgitation, reducing regurgitant fraction from 30.3% to 9.1% and normalizing chordae forces.
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