TY - JOUR
T1 - The secret life of the mitral valve
AU - Calafiore, Antonio M.
AU - Totaro, Antonio
AU - Testa, Nicola
AU - Sacra, Cosimo
AU - Castellano, Gaetano
AU - Guarracini, Stefano
AU - Di Marco, Massimo
AU - Prapas, Sotirios
AU - Gaudino, Mario
AU - Lorusso, Roberto
AU - Paparella, Domenico
AU - Di Mauro, Michele
N1 - Publisher Copyright:
© 2020 The Authors. Journal of Cardiac Surgery published by Wiley Periodicals LLC
PY - 2021/1
Y1 - 2021/1
N2 - In secondary mitral regurgitation, the concept that the mitral valve (MV) is an innocent bystander, has been challenged by many studies in the last decades. The MV is a living structure with intrinsic plasticity that reacts to changes in stretch or in mechanical stress activating biohumoral mechanisms that have, as purpose, the adaptation of the valve to the new environment. If the adaptation is balanced, the leaflets increase both surface and length and the chordae tendineae lengthen: the result is a valve with different characteristics, but able to avoid or to limit the regurgitation. However, if the adaptation is unbalanced, the leaflets and the chords do not change their size, but become stiffer and rigid, with moderate or severe regurgitation. These changes are mediated mainly by a cytokine, the transforming growth factor-beta (TGF-beta), which is able to promote the changes that the MV needs to adapt to a new hemodynamic environment. In general, mild TGF-beta activation facilitates leaflet growth, excessive TGF-beta activation, as after myocardial infarction, results in profibrotic changes in the leaflets, with increased thickness and stiffness. The MV is then a plastic organism, that reacts to the external stimuli, trying to maintain its physiologic integrity. This review has the goal to unveil the secret life of the MV, to understand which stimuli can trigger its plasticity, and to explain why the equation "large heart = moderate/severe mitral regurgitation" and "small heart = no/mild mitral regurgitation" does not work into the clinical practice.
AB - In secondary mitral regurgitation, the concept that the mitral valve (MV) is an innocent bystander, has been challenged by many studies in the last decades. The MV is a living structure with intrinsic plasticity that reacts to changes in stretch or in mechanical stress activating biohumoral mechanisms that have, as purpose, the adaptation of the valve to the new environment. If the adaptation is balanced, the leaflets increase both surface and length and the chordae tendineae lengthen: the result is a valve with different characteristics, but able to avoid or to limit the regurgitation. However, if the adaptation is unbalanced, the leaflets and the chords do not change their size, but become stiffer and rigid, with moderate or severe regurgitation. These changes are mediated mainly by a cytokine, the transforming growth factor-beta (TGF-beta), which is able to promote the changes that the MV needs to adapt to a new hemodynamic environment. In general, mild TGF-beta activation facilitates leaflet growth, excessive TGF-beta activation, as after myocardial infarction, results in profibrotic changes in the leaflets, with increased thickness and stiffness. The MV is then a plastic organism, that reacts to the external stimuli, trying to maintain its physiologic integrity. This review has the goal to unveil the secret life of the MV, to understand which stimuli can trigger its plasticity, and to explain why the equation "large heart = moderate/severe mitral regurgitation" and "small heart = no/mild mitral regurgitation" does not work into the clinical practice.
KW - ischemia
KW - ischemic adaptation
KW - left ventricle
KW - mitral regurgitation
KW - mitral valve
KW - GROWTH-FACTOR-BETA
KW - TGF-BETA
KW - COMPENSATORY MECHANISM
KW - MESENCHYMAL TRANSITION
KW - EXTRACELLULAR-MATRIX
KW - HEART-FAILURE
KW - LEAFLET
KW - REGURGITATION
KW - ANGIOTENSIN
KW - ADAPTATION
U2 - 10.1111/jocs.15151
DO - 10.1111/jocs.15151
M3 - (Systematic) Review article
C2 - 33135267
SN - 0886-0440
VL - 36
SP - 247
EP - 259
JO - Journal of Cardiac Surgery
JF - Journal of Cardiac Surgery
IS - 1
ER -