Mechanisms, pathophysiology, and diagnostic imaging of left ventricular outflow tract obstruction following mitral valve surgery and transcatheter mitral valve replacement

Abstract

Left ventricular outflow tract obstruction is a serious complication of mitral valve surgery (repair and replacement) and transcatheter mitral valve replacement. An appreciation of the various mechanisms which cause outflow obstruction in these settings is critical to avoiding this complication and to initiating appropriate treatment. This article discusses the mechanisms, pathophysiology, and imaging of left ventricular outflow tract obstruction which can arise following insertion of a variety of mitral valve prosthetics.

Double-layer horizontal cross sutures for intra-atrial mitral valve implantation: An effective surgical method for severe mitral annular calcification

“…The absence of increased LVOT obstruction risk with mitral bioprosthesis implantation in the left atrium could be attributed to 2 factors: (1) the intra-atrial insertion strategy reduces the entry height of the bioprosthetic valve strut into the LVOT; and (2) the choice of an appropriately oversized prosthesis, unrestricted by the calcified mitral annulus' diameter, enhances the aortic-mitral angle and directs the strut away from the LVOT. 29 …”

Bioprosthetic interstrut distance subtending the preserved anterior mitral leaflet mitigates left ventricular outflow tract obstruction

“…15 Individual patient characteristics that predispose to LVOTO, such as aortomitral angulation, septal thickness, and a small LV cavity, should be assessed. 16 Computed tomography software and computer-based models have been developed to predict the risk of LVOTO following transcatheter mitral valve replacement. 17 These models may be helpful in selecting surgical patients for retention of the AML, in association with further research into the methods by which the AML can be safely preserved.…”

Rheology of right ventricular outflow tract obstruction: sub-pulmonary membrane developing months after primary intervention to treat pulmonary atresia with intact interventricular septum

“…11 It has also been reported that minor changes in the left ventricular outflow anatomy, including the aorto-septal angle, 9 can produce significant alterations in the dynamic forces and septal shear stress, and thus influencing the development and the progression of sub-aortic obstruction, which is much faster in infants than in older children. 12,13 These mechanical theories, however, could not explain the increased familial recurrence rate that is also well-identified in cases with sub-aortic membranes; an underlying genetic factors must therefore be coexistent. 8,[14][15][16] A theory that combines both the mechanical and the genetic hypothesis states that the disturbed flow dynamics might induce the expression of a number of genes responsible for endothelial and smooth muscle cell proliferation, similar to the mechanisms involved in atherosclerosis.…”