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.