Does the intertrigonal distance dilate? Never say never.

See related article on page 1216. I n an era of dynamic 3-dimensional (3-D) reconstruction using advanced magnetic resonance, echocardiographic, or computed tomographic imaging, a fundamental assumption of mitral valve repair has been challenged by a study based on an old method, anatomic observation and measurement of pathologic specimens. Hueb and colleagues1 from Sao Paulo have updated basic observational techniques by using computer analysis of digital photographs. The authors compared mitral valve and ventricular size in fixed cadaver hearts from normal patients (trauma death) with hearts from patients with advanced heart failure resulting from ischemic or idiopathic (non-Chagas) dilated cardiomyopathy. Some of their findings were not surprising and confirmed prior studies and surgical observations. The left ventricle dilated to a globular shape and the mitral anulus dilated.2-4 However, there was no proportionality of left ventricular to mitral valve dilatation. Therefore, left ventricular remodeling and dilatation itself (increased sphericity) can lead to mitral regurgitation, not necessarily through a proportional amount of mitral valve annular dilatation.5 The majority of the mitral annular dilatation occurred in the muscular portion (primarily along the posterior leaflet) with a mean increase of 78 mm (ischemic) to 164 mm (idiopathic). This also was expected and accounts for the success of mitral valve repair techniques for functional mitral regurgitation that reduce the posterior anulus. The unexpected finding was an increase in the fibrous portion of 72 mm (ischemic) and 84 mm (idiopathic). This corresponds to the intertrigone distance (ITD), commonly used as an aid in sizing mitral repair rings. Furthermore, the ITD change was proportional to the changes in the muscular portions, so that if the anulus became severely dilated, the ITD also changed a large amount. Is it possible that the fibrous skeleton of the heart can stretch? We have been taught that the ITD is part of the fibrous skeleton of the heart and therefore is fixed and does not dilate.6-8 The data to support this conclusion are primarily based on 2-D echocardiographic measurements and surgical observation. However, 2-D reconstruction of the 3-D shape of the anterior anulus may not allow accurate measurement. Furthermore, we know the ITD expands and contracts in systole and diastole.9-11 Scar and ligaments can stretch with enough repetitive pressure; maybe the fibrous portion of the heart can too. The current study has limitations. Are measurements from the excised fixed pathologic specimens accurate representations of in vivo function of the ITD in normal and cardiomyopathic hearts? Kunzelman and colleagues12 documented an increase in mitral anulus dimensions in the excised heart. Therefore, could the measurements in this study partly be explained by the use of pathologic specimens? Can the investigators accurately pinpoint the trigone from digital photographs? Sometimes a surgeon can “feel” the trigone when placing a suture better than one can “see” the trigone. If the fibrous skeleton dilated by 72 to 84 mm, as reported, would there not be associated changes in the adjacent aortic anulus? This is certainly not a hallmark of dilated cardiomyopathy. Since this is a pathologic study, there is no information on premortem mitral regurgitation. When new information is presented, one has to question why it is at odds with the prevailing opinion and previous studies. The answer could be as simple as that the human ITD has not been investigated in a variety of normal and pathologic conditions. Conventional wisdom may have been substituted for hard facts and data. This certainly has been done before with the mitral valve, because it was incorrectly From the Department of Thoracic and Cardiovascular Surgery, Kaufman Center for Heart Failure, Cleveland Clinic Foundation, Cleveland, Ohio.