Abstract

Ischemic mitral regurgitation is an important consequence of LV remodeling after myocardial infarction. Echocardiographic diagnosis and assessment of ischemic mitral regurgitation are critical to gauge its adverse effects on prognosis and to attempt to tailor rational treatment strategy. There is no single approach to the echocardiographic assessment of ischemic mitral regurgitation: standard echocardiographic measures of mitral regurgitation severity and of LV dysfunction are complemented by assessments of displacement of the papillary muscles and quantitative indices of mitral valve deformation. Development of novel approaches to understand mitral valve geometry by echocardiography may improve understanding of the mechanism, clinical trajectory, and reparability of ischemic mitral regurgitation.Electronic supplementary materialThe online version of this article (doi:10.1186/1476-7120-12-46) contains supplementary material, which is available to authorized users.

Highlights

  • The mitral valve has a specific geometry designed to maintain leaflet coaptation and thereby prevent systolic regurgitation into the left atrium (LA)

  • Mitral valve function must be conceptualized in terms of a holistic relationship with supporting ventricular structures, and derangements of any part of the mitral valve apparatus – including the mitral valve leaflets, and the annulus, chordae tendinae, papillary muscles (PM), and left ventricle (LV) – can disrupt valvular coaptation and cause symptoms, physical examination findings, and echocardiographic manifestations of valvular incompetence

  • Because Chronic ischemic mitral regurgitation (CIMR) may beget CIMR through mechanisms of increased volume loading on the LV and annular dilatation, precise echocardiographic diagnosis and followup are essential

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Summary

Introduction

The mitral valve has a specific geometry designed to maintain leaflet coaptation and thereby prevent systolic regurgitation into the left atrium (LA). This is because the degree of LV dilatation directly relates to apical displacement of the PMs. For asymmetric tethering phenotypes the measures of global LV remodeling do not as robustly correlate with severity of MR because a small infarct can disrupt PM geometry and generate severe MR; the actual measures of mitral valve deformation are better predictors (see below).

Results
Conclusion
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