In recent years, a number of novel percutaneous therapies have been developed for the treatment of mitral regurgitation (MR). The MitraClip device (Abbot Vascular, Abbot Park, IL), an adaptation of the Alfieri stitch, approximates the leaflets of the mitral valve, creating a characteristic double-orifice configuration ( Figure 1 ). The MitraClip has been evaluated in a number of recent clinical trials, and its role in the treatment of MR continues to be defined. In a recent issue of JASE , Scandura et al. described significant left ventricular (LV) reverse remodeling after MitraClip implantation. In their study, echocardiographic follow-up examinations performed 6 months after clip insertion revealed significant reductions in LV dimensions and sphericity and improved LV ejection fraction. Here, I propose a novel mechanism by which MitraClip implantation may favorably alter the natural history of the remodeling process.
Severe chronic MR increases systolic wall stress and through the Laplace relationship increases the distending forces acting on the LV walls. At a molecular level, increased wall stress up-regulates metalloproteinase activity, which disrupts the integrity of the myocardium’s extracellular matrix, causing adverse LV remodeling and increased chamber volume. Conventional surgical methods, which unload the left ventricle by eliminating MR, reverse the molecular and cellular stigmata of adverse LV remodeling and restore chamber volumes toward normal. I suggest that MitraClip implantation retards adverse remodeling not only by eliminating MR but by a novel mechanism (described below) involving the so-called ventricular-valvular loop (VVL).
The epicardial fibers inserted at the aortic annulus may be arbitrarily designated as the starting point of the VVL ( Figure 2 ). As these fibers descend obliquely toward the LV apex, they gradually assume a subendocardial location, where they give rise to the vertically oriented fibers of the papillary muscles. The strut chords emerging from the papillary muscles ( Figure 3 ) attach to a highly ordered collagen network within the anterior mitral leaflet ( Figure 4 ) that provides further fibrous continuity that terminates at the right and left fibrous trigones, thereby closing the VVL. The strut chords can be likened to stretched rubber bands that remain under tension throughout systole. This tension is produced by contraction of the papillary muscles at one end and by the pressure the left ventricle exerts on the closing mitral valve at the other end ( Figure 2 ). Transmission of this tension throughout the fibromuscular syncytium of the VVL generates an (inward) restoring force that helps maintain the geometric integrity of the left ventricle by opposing (outward) distending wall stress forces. This is supported by the observation that the left ventricle dilates when mitral valve replacement is performed without adequate chordal preservation.