Abstract
The normal mitral valve is a dynamic structure that permits blood to flow from the left atrial (LA) to left ventricle (LV) during diastole and sealing of the LA from the LV during systole. The main components of the mitral apparatus are the mitral annulus (MA), the mitral leaflets, the chordae tendineae, and the papillary muscles (PM) (Figure 1). Normal valve function is dependent on the integrity and normal interplay of these components. Abnormal function of any one of the components, or their interplay can result in mitral regurgitation (MR). Understanding the anatomy and physiology of all the component of the mitral valve is important for the diagnosis, and for optimal planning of repair procedures. In this review we will focus first on normal anatomy and physiology of the different parts of the mitral valve (MA, leaflets, chordae tendineae, and PM). In the second part we will focus on the pathologic anatomic and physiologic derangements associated with different types of MR.
Highlights
Movie 2 | (A,B) Schematic representation of a 3D reconstructed mitral annulus and leaflets in motion in a patient with Type II mitral regurgitation (MR) compared to normal valve
Many unresolved questions remain in this type of MR: Is it associated with excess mortality despite normal left ventricle (LV) systolic function?: Will it l improve with simple annuloplasty or mitral replacement?: What is the reason for left atrial (LA) dilatation in patients in sinus rhythm?; And should we treat moderate MR when the patients require tricuspid surgery for severe regurgitation due to right-sided annular enlargement secondary to chronic atrial fibrillation
MR is affected by a complex dynamic change of the annulus, leaflets, chords, papillary muscles, and atrial and ventricular interaction
Summary
Movie 2 | (A,B) Schematic representation of a 3D reconstructed mitral annulus and leaflets (oblique view A; En face B) in motion in a patient with Type II MR compared to normal valve. This contraction leads to very early-systolic annular area contraction, accentuation of saddle shape, and approximation of anterior and posterior leaflets. Many unresolved questions remain in this type of MR: Is it associated with excess mortality despite normal LV systolic function?: Will it l improve with simple annuloplasty or mitral replacement?: What is the reason for LA dilatation in patients in sinus rhythm?; And should we treat moderate MR when the patients require tricuspid surgery for severe regurgitation due to right-sided annular enlargement secondary to chronic atrial fibrillation.
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