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Key Concepts

  • The normal mitral valve annulus is a saddle-shaped structure with 3:4 ratio of the anterior–posterior to commissure–commissure distance.

  • Mitral stenosis is usually a result of rheumatic fever, and valvular pathology represents antigen cross-reactivity from Group A streptococcus resulting in valvulitis, myocarditis, or pancarditis.

  • Fibroelastic deficiency and Barlow disease are the predominant forms of degenerative mitral valve disease leading to mitral regurgitation. Fibroelastic deficiency is found in older patients whereas congenitally excessive valve tissue seen in younger patients is observed with Barlow valve.

  • Chordal rupture is the most common etiology of mitral regurgitation in degenerative mitral valve disease.

  • Ischemic mitral regurgitation (IMR) is associated with a localized left ventricular infarct with subsequent chamber remodeling and perturbation in the subvalvular apparatus. Functional mitral regurgitation (FMR) is associated with end-stage dilated cardiomyopathy.

  • Both FMR and IMR are characterized by subvalvular remodeling and annular dilation.

  • Leaflet remodeling may contribute to the pathophysiology and severity of both IMR and FMR.

  • Annular dilation and perturbed leaflet coaptation tend to be symmetric in FMR and asymmetric in IMR.


The mitral valve comprises two leaflets with the anterior leaflet being larger and sail-like traversing approximately one-third of the annular circumference. The posterior leaflet is smaller, more rectangular-shaped, and typically has three scallops denoted as P1, P2, and P3 from the anterolateral toward the posteromedial commissure. Corresponding coapting regions of the anterior leaflet are labeled as A1, A2, and A3 according to the Carpentier nomenclature, although no anatomic landmarks, such as distinct interscallop clefts found in the posterior leaflet, separating these regions exist (Fig. 34-1). The free edge of the leaflets is called the bare or membranous zone, with the remainder of the leaflets termed the rough zone. The histologic structure of the leaflets includes the fibrosa, a solid collagenous core that is continuous with the chordae tendineae, and the spongiosa that consists of few collagen fibers but abundant proteoglycans, elastin, and mixed connective tissue cells, which is on the atrial surface and forms the leaflet leading edge. On the atrial aspect of both leaflets, this surface (the atrialis) is rich in elastin whereas the ventricular side (the ventricularis) is much thicker, is confined mostly to the anterior leaflet, and is densely packed with elastin. Nutrients to leaflet tissue are supplied by annular and ascending chordal vessels. The leaflets have long been thought to be passive, inert structures at the hemodynamic mercy of the ebb and flow of ventricular contraction, but recent data refute this view. Leaflet tissue is richly innervated, has intrinsic contractile properties, complex heterogeneous ultrastructure, and may be important in modulating timely and efficient valve closure.1,2

Figure 34-1

Anatomy of the mitral valve complex. LCx, left circumflex coronary artery; RFT, right fibrous trigone; LFT, left fibrous trigone; AC, anterior commissure; PC, posterior commissure.

The mitral annulus ...

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