We read with interest the letter by Dr Silbiger regarding our article “Mitral Annular Dynamics in Mitral Annular Calcification: A Three-Dimensional Imaging Study” and offer the following response.
The mitral annulus is generally easily identified on echocardiography. The presence of calcification can make identification more difficult if the calcification extends beyond the bounds of the normal annulus. However, by carefully following the line of the mitral leaflet, we were able to identify where it intersected the line of the left atrium and left ventricle. In addition, we compared the spatial relationship of each new point with already placed points. In this way we could be quite confident that the final annular tracing tracked the true annulus closely.
With regard to the observed smaller than usual decrease in systolic tenting, we believe this is for two reasons: (1) There is decreased motion of the annulus in systole (i.e., reduced folding along the intercommissural axis), with the result that the leaflets are not brought together in normal fashion early in systole.(2) Mitral annular calcium often extends onto the leaflets, stiffening them and making them less pliable and thus less able to squeeze together in systole. In fact, in an earlier publication, we observed reduced motion of leaflet segments subtended by a calcified annular segment. We note as well that calcified aortic valve leaflets show restricted mobility, even in the face of markedly increased left ventricular pressure.
We would also question Dr Silbiger’s assertion that mitral annular calcification always pushes the posterior leaflet superiorly. It is our observation that annular calcium can accumulate on the ventricular side of the leaflet attachment or the atrial side of leaflet attachment or can encase the affected leaflet (usually the posterior leaflet); it does not always occur in a predictable pattern.
With regard to annular contraction, we concur that contraction of the adjacent left atrium and left ventricle plays a contributory role. However, we respectfully disagree with the assertion that the calcified mitral annulus is incapable of withstanding the force of normal atrial and ventricular contraction. Although the normal annular circumstance may indeed be one of a “feeble annular membrane, which is ≤3 mm thick,” the calcified annulus is, for all practical purposes, much thicker. Indeed, one of the common definitions of severe mitral annular calcification is a bar of calcium >5 mm thick. It should be kept in mind that calcium deposits do not respect the annular boundaries and often extend onto the mitral leaflets, into the ventricular myocardium, or toward the left atrium. For this reason, mitral annular calcification presents the surgeon with additional challenges when replacing or repairing the mitral valve.
Finally, with regard to annular motion in diastole, we did not find any systematic changes and thus reported none. We did find systematic changes in systole, as described in our report.
In closing, we would also point out that three-dimensional echocardiography, although it has limitations in temporal resolution, holds great promise for gaining new knowledge of mitral annular structure and function, both in the normal situation and in various disease states. This technology allows detailed observation in living humans without the confounders of surgery or anesthesia, both required for animal experimentation. It is also more suited to serial studies than other three-dimensional techniques such as computed tomography and magnetic resonance imaging and can potentially be applied to a wide range of subjects.