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  • Antonio Calafiore,
  • Antonio Totaro,
  • Nicola Testa,
  • Cosimo Sacra,
  • Gaetano Castellano,
  • Stefano Guarracini,
  • Massimo Di Marco,
  • Sotirios Prapas,
  • Mario Gaudino,
  • Roberto Lorusso,
  • Domenico Paparella,
  • Michele Di Mauro
Antonio Calafiore
Gemelli Molise

Corresponding Author:[email protected]

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Antonio Totaro
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Nicola Testa
John Paul II Foundation for Research and Treatment
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Cosimo Sacra
Fondazione di Ricerca e Cura Giovanni Paolo II
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Gaetano Castellano
Gemelli Molise
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Stefano Guarracini
Private Hospital Pierangeli Srl
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Massimo Di Marco
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Sotirios Prapas
Henry Dunant Hospital Center
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Mario Gaudino
NewYork-Presbyterian Hospital/Weill Cornell Medical Center
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Roberto Lorusso
Maastricht University Medical Centre
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Domenico Paparella
University of Bari “Aldo Moro”
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Michele Di Mauro
Maastricht UMC+
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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 an intrinsic plasticity that reacts to changes in stretch or in mechanical stress activating bio-humoral 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 tendinae 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 β (TGF-β), which is able to promote the changes that the MV needs to adapt to a new hemodynamic environment. In general, mild TGF-β activation facilitates leaflet growth, excessive TGF-β activation, as after a 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.
28 Sep 2020Submitted to Journal of Cardiac Surgery
28 Sep 2020Assigned to Editor
28 Sep 2020Submission Checks Completed
28 Sep 2020Reviewer(s) Assigned
13 Oct 2020Review(s) Completed, Editorial Evaluation Pending
13 Oct 2020Editorial Decision: Accept
Nov 2020Published in Journal of Cardiac Surgery. 10.1111/jocs.15151