Mitral Annular Disjunction in Advanced Myxomatous Mitral Valve Disease: Echocardiographic Detection and Surgical Correction Maria J. Eriksson, MD, PhD, Catarina Y. Bitkover, MD, PhD, Ahmad S. Omran, MD, Tirone E. David, MD, Joan Ivanov, PhD, Mohamed J. Ali, MD, Anna Woo, MD, Samuel C. Siu, MD, and Harry Rakowski, MD, Toronto, Ontario, Canada Mitral annular disjunction is a structural abnormal- ity of the mitral annulus fibrosus described by pa- thologists in association with mitral leaflet prolapse and defined as a separation between the atrial wall– mitral valve (MV) junction and the left ventricular attachment allowing for hypermobility of the MV apparatus. The transesophageal echocardiographic characteristics of this abnormality have not been previously described. In patients undergoing MV repair for myxomatous MV degeneration and evalu- ated using a standardized transesophageal echocar- diographic protocol, annular disjunction (mean value 10  3 mm) was seen at the base of the posterior leaflet in 98% of patients with advanced, and in 9% of patients with mild/moderate MV de- generation. There was a significant correlation be- tween the magnitude of disjunction and the number of segments with prolapse/flail (r  0.397, P  .001). We found annular disjunction to be a common component of MV apparatus in advanced MV degen- eration. Its recognition on transesophageal echocar- diography is important to facilitate optimal MV re- pair. The modification of the repair technique allows surgical correction of the annular disjunc- tion, which seems to optimize long-term results in these challenging cases. (J Am Soc Echocardiogr 2005;18:1014-1022.) Mitral valve (MV) prolapse is a relatively common disorder and may cause mitral regurgitation (MR) requiring operation. 1 Recent studies have demon- strated excellent long-term outcomes in patients undergoing MV repair, which has gained acceptance as the surgical treatment of choice in patients with severe MR caused by prolapse or flail leaflets. 2-7 Less favorable long-term results of MV repair, with an increased risk for reoperation, have been reported for patients with advanced myxomatous MV degen- eration (MVD). 4,7,8 The purpose of MV repair is to correct leaflet redundancy, elongation, and/or rupture of chordae tendineae, and dilatation of the mitral annulus. Geometric restoration of mitral annulus by annulo- plasty has been shown to be important for the long-term durability of MV repair. 5,6 Although dila- tation is the most common abnormality of the mitral annulus fibrosus, the structure of the annulus itself can vary in different patients. Hutchins et al, 9 in their study of 900 autopsied hearts, observed a disjunction of the mitral annulus in hearts with MV prolapse. They defined disjunction as a separation between atrial wall–MV junction and the left ventric- ular (LV) attachment (Figures 1 and 2). The mitral annulus is an integral part of the MV along with left atrial (LA) and LV coupling. Previous studies have demonstrated that the normal mitral annulus has a complex, nonplanar shape and function, best assessed using 3-dimensional imaging tech- niques. 10-16 In the horizontal plane the normal annulus is elliptic in shape with a long and a short axis. The ratio between these two axes has been previously used as a measure of annular eccentricity. 17 The normal annular function can be characterized by systolic an- nular area reduction, which may improve leaflet coap- tation and normal MV closure. 16,18,19 Because we have observed annular disjunction on direct inspection at operation in some patients with advanced MVD, we sought to describe the mitral annular structure and function in this particular subgroup of patients studied From the Divisions of Cardiology (M. J. E., A. S. O., A. W., S. C. S., and H. R.), and Cardiovascular Surgery (C. Y. B., T. E. D., J. I., and M. J. A.), Toronto General Hospital, University Health Network. Presented as an abstract at the American Heart Association Scien- tific Session in Anaheim, Calif, November 12, 2001. Supported in part by the Hypertrophic Cardiomyopathy Research Fund, University of Toronto, and the Swedish Heart and Lung Foundation (200041256), Stockholm (Dr Eriksson). Reprint requests: Harry Rakowski, MD, Division of Cardiology, Toronto General Hospital, 12EN-212, 200 Elizabeth St, To- ronto, Ontario M5G 2C4, Canada (E-mail: harry.rakowski@ uhn.on.ca). 0894-7317/$30.00 Copyright 2005 by the American Society of Echocardiography. doi:10.1016/j.echo.2005.06.013 1014