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Strain and mitral regurgitation: is atrial functional mitral regurgitation a ventricular disease?
  1. Francesca Bursi1,
  2. Alex Pui-Wai Lee2
  1. 1 Department of Health Sciences, University of Milan, Milano, Italy
  2. 2 Department of Medicine and Therapeutics, The Chinese University of Hong Kong, Hong Kong, Hong Kong
  1. Correspondence to Professor Alex Pui-Wai Lee, The Chinese University of Hong Kong, Hong Kong, Hong Kong; alexpwlee{at}

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Secondary or functional mitral regurgitation (FMR) is defined as a mitral valve with apparently anatomically normal leaflets that are distorted with consequent malcoaptation and regurgitation due to the interplay of different alterations that can be conducted to two main mechanisms: the increase in tethering forces and reduction in closing forces on the leaflets. FMR has been subclassified into ventricular or ventriculogenic FMR and atrial or atriogenic FMR under the hypothesis that in the first case the disease is in the ventricle, in the second the atrium. In ventricular FMR an abnormality in local or global left ventricular (LV) remodelling determines downward displacement and restriction of the leaflets in the ventricle with or without accompanying decreased systolic closing forces (reduced ejection fraction (EF), reduced annulus contraction, dyssynchrony). In atrial FMR the regurgitation is due to an enlargement of the annulus with pulling and flattening on a horizontal plane of normally moving leaflets accompanied by reduction in annular contraction.

While in ventricular FMR it is clear that the changes occur at the ventricular level, below the annular plane, in atrial FMR the remodelling of the left atrium (LA) is traditionally considered to insist mainly on the annulus. Yet, the annulus does not belong only to the atrium; it is between atrium and ventricle and may dilate due to a disease of the atrium like in atrial fibrillation, but also as an effect of LV dysfunction. Furthermore, the annulus is a fibrous tissue without intrinsic …

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  • Contributors FB drafted the manuscript. AP-WL contributed to concept formation and revision of the manuscript.

  • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

  • Competing interests None declared.

  • Provenance and peer review Commissioned; internally peer reviewed.

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