Characterisation of the fatigue life, dynamic creep and modes of damage accumulation within mitral valve chordae tendineae

Mitral valve prolapse is often caused by either elongated or ruptured chordae tendineae (CT). In many cases, rupture is spontaneous, meaning there is no underlying cause. We hypothesised that spontaneous rupture may be due to mechanical fatigue. To investigate this hypothesis, we tested porcine marginal CT: in uniaxial tension, and in fatigue at a range of peak stresses (n=12 at 15, 10 and 7.5MPa respectively, n=6 at 5MPa). The rupture surfaces of failed CT were observed histologically, under polarised light microscopy, and SEM. The cycles to failure for 15, 10, 7.5 and 5 MPa peak stresses were: (average±SD): 5077±4366, 49513±56414, 99927±108908, 197099±69103. A Weibull plot was constructed and from this, the number of cycles at 50% probability of failure was established in order to approximate the fatigue life, which was found to be 2.43MPa at 10 million cycles. The rate of creep increases exponentially with increasing peak stress. Under histological examination it was observed that CT which have been fatigued at low stress partially lose their organised collagen structure and can sustain micro-cracks that can be linked to increases in the creep rate. Furthermore our SEM images closely matched descriptions from the literature of spontaneous in vivo rupture. In conclusion, we believe that the mechanical test results we present strongly suggest that spontaneous chordal rupture and chordal elongation in vivo can be caused by mechanical fatigue.