When to cut the second-order chordae
There is no specific indication for CC reported in the literature. Borger et al20 divided the second-order chordae to the AL, PL and commissure that arose from the PM(s) affected by the infarcted myocardium. Patients in the CC group had lower ejection fraction and larger hearts. Our group21 included only patients who had an AL banding angle <145° using, as a surgical approach, an aortotomy. However, the revival of the concept of MV remodelling and the surgical implications consequent to this concept25-28, let us think to a different role for the CT in originating and maintaining leaflets tethering, more dynamic than previously supposed.
When MR starts, because of PM displacement and chordal tethering or other causes, a set of adaptations termed ‘mitral plasticity’ is initiated within the MV that serves to reduce the amount of regurgitation. This goal is achieved by an increase of the length and of the area of the leaflets and of the length of the CT. This adaptation to mechanical stress, induced by MR of any origin, is sustained by endothelial-to-mesenchimal transition (EndMT) and matrix remodelling, which facilitates leaflet growth27, mediated by transforming growth factor β (TGF-β). The plasticity is said to be ‘balanced’ if the MV remains competent or with mild regurgitation despite left ventricular dilation and PM displacement, and ‘unbalanced’ if, despite adaptation, significant MR develops27,29. The MV increases its dimensions but histological remodelling is more pronounced than in a balanced response and the valve becomes fibrotic, stiff, less distensible, thick and can shorten later because of the presence of scar-forming cells30,31. CT become stiffer, less extensible, fibrotic and can reduce their length. Of particular interest for MV remodelling is the activation of renin–angiotensin system after MI, as angiotensin II can trigger TGF-β expression32, enhancing the profibrotic effects on the MV. Similar changes at the level of the CT further restrict leaflet movements.
Stress induced mitral plasticity and the resulting MV remodelling is a mechanism present in MR of any aetiology. Experimentally, it was demonstrated that MR, created by making a hole in the PL, was able to induce AL remodelling33. Moreover, tethering of the second-order chordae have been demonstrated in patients with prolapse of the PL34,35 and prolapse or chordal rupture of the AL36.