Chordae Rupture Alters Tricuspid Valve Leaflet Biomechanics

Tricuspid valve chordae tendineae rupture is a valvular lesion that is often overlooked, though is postulated to be more prevalent than currently known. We examined the hemodynamics and biomechanical response of the tricuspid valve leaflets following chordae rupture to understand how acute changes in the post-rupture mechanical environment may contribute to long-term remodeling responses.

Porcine valve leaflet deformation was studied in an intact heart in an ex vivo setup using sonomicrometry techniques before and after chordae rupture, which was induced by severing a chordae bundle connected to the septal leaflet.

Following chordae rupture, pulmonary artery pressure dropped approximately 5 mmHg ( $p=0.048$ ), indicating that valvular regurgitation occurred immediately after rupture. Mean maximum principal stretch of the septal leaflet increased 12% after rupture ( $p=0.006$ ).

The immediate changes in post-rupture septal leaflet stretches show that chordae tendineae rupture acutely alters the biomechanical environment of the tricuspid valve, which may result in chronic tissue remodeling responses. The tricuspid valve is one of the four valves in the heart. Rupture of supporting structures of the tricuspid valve leaflet, known as chordae tendineae, may be more common than previously thought. In this study, we used excised pig hearts to examine how chordae rupture affects valvular function. With our experimental beating heart system, we pumped fluid through the hearts under realistic conditions and measured changes in pressure and leaflet motion before and after chordae rupture. After rupture, we observed a change in pressures and leaflet motion, causing the valve to leak and become less efficient. These changes may influence how the valve functions over time.