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Eur J Cardiothorac Surg 2007;32:398-399. doi:10.1016/j.ejcts.2007.04.021
Copyright © 2007, European Association for Cardio-Thoracic Surgery. Published by Elsevier B.V. All rights reserved

Letters to the Editor

Size matters in atrial fibrillation surgery

Emmanuel Villa*, Antonio Messina, Marco Cirillo, Giovanni Troise

Cardiac Surgery Unit, Poliambulanza Foundation Hospital, Brescia, Italy

Received 13 March 2007; accepted 17 April 2007.

* Corresponding author. Address: Cardiac Surgery Unit, Poliambulanza Foundation Hospital, Via Bissolati 57, 25124 Brescia, Italy. Tel.: +39 030 3518534; fax: +39 030 3515244. (Email: emmanuel.villa{at}voila.fr).

Key Words: Atrial fibrillation • Rheumatic valvular disease • Cardiac autotransplantation

We read with interest the paper of Kim et al. [1] reporting their experience in Cox-maze III operation and mitral surgery in the setting of rheumatic valve disease. Studying a 10-year period of surgical cases, the authors added important data to the very fast expanding field of atrial fibrillation (AF) treatment, and they are to be commended. Nevertheless, some issues need further discussion.

Although left atrial size was found to be a predictor of AF recurrence at multivariate analysis and mentioned in the abstract, the issue of surgery for atrial reduction is not discussed in the paper. Since the first observations of the link between atrial dilatation and arrhythmia made by Cushny and Edmunds and recently mentioned by Fye [2], many authors confirmed this pathophysiologic mechanism also in the clinical setting, concluding that the probability to succeed in sinus rhythm restoration is inversely related to atrial size. This is consistent with the Laplace law and it is true for any medical, transcatheter or surgical therapy. Trying to restore the relationship between structure and function, we adopted the cardiac autotransplantation technique to debulk left and right atrial walls, along with plication of left atrial cuff aimed at reducing also the posterior wall, in case of giant atria with permanent AF and mitral valve disease [3]. Other authors implemented their approach with atrial reduction strategies [4]. We deem that return to electrical normalcy requires low wall stress and, although Kim et al. did not record thromboembolic events, a reduced cavity could diminish the thromboembolic risk. Due to the importance of precise measurement for proper comparison, we think also that a three-dimensional structure such as the atrium needs to be characterized by more diameters or by volume estimate and not only by a single diameter. Moreover, the adoption of the Santa Cruz Score to classify atrial contractility after AF treatment, as previously suggested by Melo, is strongly desirable for result analysis [5].

On the contrary, we appreciate the authors’ discussion on the issue of tricuspid valve role and agree with them that the vicious cycle that links tricuspid valve incompetence and AF needs to be directly addressed more often by correction of tricuspid regurgitation.

However, some considerations in the particular setting of rheumatic valve disease are required because these hearts have a very long history of disease; rheumatism is a disease of the whole heart, and the prevalent disturbance in every series is stenosis. These factors may have produced structural changes that sometimes may result in irreversible scars. It could explain the suboptimal results of AF therapy in rheumatic setting in terms of freedom from recurrences and need of antiarrhythmic drugs. Another problematic issue is the capacity of the sinus node to correctly resume its function after many years of disease, as evidenced by the number of sick sinus syndromes and junctional rhythms observed after this kind of surgery.

Nevertheless, we deem that acute size reduction today is the cornerstone to restore sinus rhythm and favour the maintenance of atrial electro-mechanical function.

References

  1. Kim KC, Cho KR, Kim J, Sohn D, Kim K. Long-term results of the Cox-Maze III procedure for persistent atrial fibrillation associated with rheumatic mitral valve disease: 10-year experience. Eur J Cardiothorac Surg 2007;31:261-266.[Abstract/Free Full Text]
  2. Fye WB. Tracing atrial fibrillation — 100 years. N Eng J Med 2006;355:1412-1414.[Free Full Text]
  3. Troise G, Cirillo M, Brunelli F, Tasca G, Amaducci A, Mhagna Z, Dalla Tomba M, Quaini E. Mid-term results of cardiac autotransplantation as method to treat permanent atrial fibrillation and mitral disease. Eur J Cardiothorac Surg 2004;25:1025-1031.[Abstract/Free Full Text]
  4. Badhwar V, Rovin JD, Davenport G, Pruitt JC, Lazzara LL, Ebra G, Dworkin GH. Left atrial reduction enhances outcomes of modified maze procedure for permanent atrial fibrillation during concomitant mitral surgery. Ann Thorac Surg 2006;82:1758-1764.[Abstract/Free Full Text]
  5. Melo JQ, Neves J, Adragao P, Ribeiras R, Ferreira MM, Bruges L, Canada M, Ramos T. When and how to report results of surgery on atrial fibrillation. Eur J Cardiothorac Surg 1997;12:739-744.[Abstract]



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Eur. J. Cardiothorac. Surg., August 1, 2007; 32(2): 399 - 399.
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