Chordal geometry determines the shape and extent of systolic anterior mitral motion: In vitro studies

Abstract

In patients with hypertrophic cardiomyopathy, the mitral valve moves anteriorly and assumes a unique shape, with mitral-septal contact centrally and preserved valve orifice area laterally. This shape is not clearly predicted by the Venturi mechanism, which stresses flow above the valve as opposed to changes intrinsic to the valve. On the other hand, it has been suggested that displacement of the papillary muscles anteriorly and toward one another, as observed in this disease, can promote anterior mitral valve motion and produce this unusual shape. The purpose of this in vitro study was to test the hypotheses that anterior motion of a membrane in a flow field can be generated by altering the distribution or effectiveness of chordal tension tethering the membrane, and that the shape achieved by this membrane depends on the geometry of chordal tension. Accordingly, a horizontal leaflet mounted in a flow chamber was attached by chords at its distal end to a series of upstream screws. Chordal tension could be varied by turning the screws or redirected by shifting the screws anteriorly. Anterior leaflet motion having the same unusual configuration seen in patients was reproduced by decreasing central chordal restraint while tension on the leaflet edges was maintained. Directing chordal tension anteriorly caused greater degrees of anterior motion at earlier stages in the release of chordal restraint; increased flow rate had a similar but less marked effect. These studies suggest that primary geometric alterations in the papillary-mitral apparatus can play an important role in determining the presence and geometry of systolic anterior mitral motion. The nature of these alterations suggests a role for anterior and inward papillary muscle displacement in promoting such motion. The geometric factors embodied in this model can explain many observed features of this motion not adequately explained by the Venturi effect, such as early systolic onset and the importance of a distal residual leaflet. Finally, flow visualization studies emphasize the importance in this process of drag forces caused by interposing the leaflet into the flow stream, and of geometric factors that enhance such forces.

Mechanism of Benefit of Negative Inotropes in Obstructive Hypertrophic Cardiomyopathy

“…In addition, delaying the trigger to systolic anterior motion may allow more time for papillary muscle shortening to increase chordal tension; this may provide countertraction to prevent systolic anterior motion, even completely. 32,33 Fig 6 summarizes this hypothesis schematically. After successful treatment, there was no significant reduction in the pulsed Doppler LV peak velocity at the AMV point.…”

Hypertrophic obstructive cardiomyopathy: the Mayo Clinic experience

“…Anomalies of the mitral valve apparatus exist in some patients with obstructive HCM and can lead to persistent LVOT obstruction after septal myectomy (5,6). Anomalous papillary muscle insertion into the body of the anterior mitral leaflet (Figure 2) is a well-recognized entity and its diagnosis may be challenging even for the experienced cardiologist (7).…”

Sustained Improvement After Combined Anterior Mitral Leaflet Extension and Myectomy in Hypertrophic Obstructive Cardiomyopathy

“…5 To counteract these forces, the pericardial patch is grafted in the center portion of the anterior leaflet, where SAM typically reaches a maximum. 5,8,11,23 By extending the patch across the bending point of the mitral valve, we hypothesize that we stiffen the central parts of the buckling anterior leaflet, preventing abnormal mobility. In addition, the patch increases the width of the leaflet, which results in a horizontal extension.…”

“…The most commonly performed intervention is surgical myectomy according to the technique developed by Morrow et al 2 Hypertrophic cardiomyopathy, however, frequently presents with several anatomic alterations of the mitral valve apparatus, including increased mitral leaflet area (MLA), length, and laxity, as well as anterior displacement of the papillary muscles. [3][4][5][6][7][8][9][10][11][12] These structural abnormalities, which are not corrected after a successful myectomy, may predispose to residual SAM and result in a suboptimal outcome with persistence of outflow obstruction and mitral regurgitation. [13][14][15] We therefore performed anterior mitral leaflet extension (MLE), one of several repair techniques originally developed by Carpentier, 16 in combination with myectomy in patients with HOCM and an enlargement of the anterior mitral leaflet.…”