Abstract
The ischemic impairment of the left ventricular contractility, followed by an adverse remodeling leading to the displacement of the papillary muscles (PMs), increased tethering forces and loss of valve competence has been the long-term accepted definition of ischemic mitral regurgitation (IMR). Over the years, different approaches of management have attempted to address valve regurgitation, nevertheless failing to achieve satisfactory outcomes. Recent studies have observed some structural and molecular changes of the mitral valve (MV), challenging the concept of a bystander passive to the subvalvular involvement. Indeed, the solely mechanical stretch of the PMs, as in the dilated left ventricle because of the aortic valve regurgitation, is not enough in causing relevant MV regurgitation. This setting triggers a series of structural changes called “mitral plasticity,” leaflets increase in their size among others, ensuring an adequate systolic area closure. In contrast, the ischemic injury not only triggers the mechanical stretch on the subvalvular apparatus but is also a powerful promotor of profibrotic processes, with an upregulation of the transforming growth factor (TGF)-β signaling pathway, leading to a MV with exuberant leaflet thickness and impaired mobility. In this article, we revise the concept of IMR, particularly focusing on the new evidence that supports dynamic changes in the MV apparatus, discussing the consequent clinical insights of “mitral plasticity” and the potential therapeutic implications.
Highlights
INTRODUCTIONIschemic mitral regurgitation (IMR) is a complex syndrome caused by unbalanced closing and tethering forces, that affects 1.6–2.8 million people in the United States and may complicate the 10–20% of patients with the ischemic heart disease [1, 2]
Ischemic mitral regurgitation (IMR) is a complex syndrome caused by unbalanced closing and tethering forces, that affects 1.6–2.8 million people in the United States and may complicate the 10–20% of patients with the ischemic heart disease [1, 2].Several surgical approaches have been described and used over the years to address valve incompetence caused by ischemic injury
Current literature focuses to describe in detail ischemic mitral regurgitation (IMR) phenotypes, differentiating them according to the direction of the tethering forces on mitral valve (MV) leaflets and LV dimensions, in order to offer targeted strategies of approach [5]
Summary
Ischemic mitral regurgitation (IMR) is a complex syndrome caused by unbalanced closing and tethering forces, that affects 1.6–2.8 million people in the United States and may complicate the 10–20% of patients with the ischemic heart disease [1, 2]. Several surgical approaches have been described and used over the years to address valve incompetence caused by ischemic injury. Mitral valve (MV) surgery is still associated with unsatisfactory outcomes; MV replacement and MV repair, including restrictive annuloplasty, were associated with a not negligible in-hospital mortality and mostly a high recurrence rate of MR in long-term follow-up [1, 3]. The target of the medical therapy has been focused on improving LV contractility, following the long-term accepted idea that FMR depended solely on LV impairment, in the absence of a tailored categorization of IMR etiology and subtypes [4]
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