In the July 2015 issue of JASE , Pressman et al . report their observations on the effects of mitral annular calcification (MAC) on mitral annular size, shape and dynamics using three-dimensional echocardiographic imaging. It is important to note, however, that using echocardiography to study the annulus is fraught with difficulties. These stem, in large part, from reliance on the identification of hinge points, rather than fiducial markers, to localize the annulus. When MAC is present, hinge points become especially difficult to identify, which may meaningfully compromise data quality. Anteriorly, calcium may conceal hinge points where the anterior mitral leaflet and the aortomitral curtain meet. Posteriorly, calcium frequently extends beyond the annulus into the base of the left ventricular (LV) myocardium as well as into the LV cavity, creating a calcium shelf beneath the ventricular surface of the posterior mitral leaflet (submitral space) ( Figure 1 ). This may prevent visualization of the leaflet as well as its hinge point, precluding accurate localization of the annulus ( Figure 2 ).

Diagram depicting posterior MAC. Note the accumulation of calcium within the base of the left ventricle extending into the LV cavity beneath the posterior mitral leaflet. This calcium precludes adequate visualization of the posterior leaflet as well as its hinge point. The calcium also elevates the leaflet toward the left atrium, placing tension on the chordae tendineae.

Reproduced with permission from Cammack et al .

Zoomed parasternal long-axis echocardiographic image showing posterior MAC forming a calcium shelf ( arrow ), which elevates the posterior mitral leaflet toward the left atrium (LA). Note that the anterior mitral leaflet coapts with the calcium shelf, as indicated by the asterisk , rather than with the posterior leaflet. The posterior leaflet is pinned beneath the calcium shelf and is therefore not visible. Ao , Aorta; LV , left ventricle.

One of the conclusions of this study is that MAC causes a smaller than usual decline in tenting length and volume during systole. The authors suggest that this is “likely linked to reduced annular displacement in systole,” which is presumably insufficient to offset the systolic tethering force imparted by papillary muscle contraction. Reduced systolic displacement of the annulus could conceivably reflect the effects of calcification on basal LV longitudinal fiber function, but this was not addressed in the present study. It should be noted that the smaller than usual decline in systolic tenting observed in this study appears to be counterintuitive. One would have anticipated that superior displacement of the posterior mitral leaflet toward the left atrium by calcium, as depicted in Figure 1 , would bring the coaptation point of the mitral valve leaflets closer to, not farther from, the annular plane, thereby reducing systolic tenting length and volume.

It is important to appreciate that the fibrofatty composition of the annulus precludes contraction. “Contraction” of the annulus is more likely related to shortening of the left ventricular and the left atrial musculature to which it is attached. This is in keeping with the observation that annular contraction is reduced in dilated cardiomyopathy as well as when atrial activity is absent. One of the conclusions of the study by this study is that mitral annular area contraction is reduced in patients with normal LV segmental wall motion and MAC. The authors suggest that this is “likely linked to annular stiffening resulting from calcific deposits.” It seems unlikely, however, that the feeble annular membrane, which is ≤3 mm thick, would be capable of withstanding the contractile forces generated by a normal left ventricle and left atrium, whether or not it is calcified.

This study, as well as a number of others using echocardiography, did not observe any decrement in annular area during diastole in normal (control) hearts. This finding is at odds with a large number of animal studies, summarized by Timek and Miller, which uniformly demonstrate that left atrial systole accounts for an even greater decrease in annular area than LV systole. This inconsistency likely reflects the use of marker fluoroscopy, which, unlike the crude method used with echocardiography, identifies the mitral annulus by direct surgical visualization, unencumbered by limited temporal and spatial resolution, permitting more precise tracking throughout the cardiac cycle.

This article by Pressman et al . represents the first three-dimensional echocardiographic study of annular size, shape, and dynamics in patients with MAC. Although the article suggests a number of novel insights, I believe these must be regarded as speculative given the inherent difficulties encountered in using echocardiography to study the annulus when MAC is present.