The effects on cordal and leaflet stiffness of severe apical, posterior, and outward papillary displacement in advanced ventricular mechanism heart failure and mitral insufficiency.
OBJECTIVE
During the normal opening and closing of the mitral valve there is a finely tuned interaction between the changing ventricular dimensions and fluid pressures, the movement of papillary muscles apically, posteriorly and apart during diastole and in the opposite direction during systole, interactions between leaflets and their controlling cords, and the fluid dynamic forces being exerted on them. The main rough zone cords and the smooth zone of the anterior leaflet are under maximum tension in systole, but retain some tension throughout the cycle. The free edge cords and the rough zone of the leaflets can have no or minimal tension during diastole, and much less tension than the main rough zone cords and the smooth zone in systole. The variability of the form and distribution of rough zone cords influences the flexibility of the rough zone. The net effect of this interaction is a valve that opens rapidly for unobstructed forward flow, and closes at the end of the cycle with minimal leakage. The apical displacement of, usually, the right inferior papillary muscle as a result of ischemic ventricular disease pulls the leaflets into separation because the origins of cords supporting the anterior and posterior leaflets arise specifically from the anterior and posterior sides of each papillary muscle. Myocardial ischemia producing apical papillary displacement can be associated with heart failure and mitral insufficiency. Annuloplasty reducing the annulus to less than the normal systolic dimension can be effective in eliminating both insufficiency and heart failure when the papillary displacement is dominantly apical. In more severe cases of heart failure and mitral insufficiency, the mid-ventricular dimensions increase to a more severe degree, and both papillary muscles are displaced outwards and posteriorly.


RESULTS
Static in vitro experiments performed on three human and nine pig hearts showed that the outward papillary displacements increased the tension on first-order cords, rendering the anterior leaflet and the central scallop of the posterior leaflet stiff. The addition of posterior displacement caused the anterior leaflet to become directed at an angle to the displaced papillary muscles, and the scallops of the posterior leaflet to be perpendicularly splayed around the posterior left ventricular wall, such that the valve no longer opened or closed correctly.


CONCLUSIONS
The valve no longer opens or closes properly, and annuloplasty is no longer of use in restoring valve function.
Albert Einstein College of Medicine, Bronxville, New York 10708, USA. Rwmfglycar@aol.com
Robert W M
RW
Frater
D000818:Animals; D002815:Chordae Tendineae / Q000503:physiopathology*; D006333:Heart Failure / Q000503:physiopathology*; D006801:Humans; D008943:Mitral Valve / Q000502:physiology*; D008944:Mitral Valve Insufficiency / Q000503:physiopathology*; D010210:Papillary Muscles / Q000503:physiopathology*