|
Future Directions In Atrial Fibrillation Surgery: Moving From An Emperic To a Mechanistic Approach
The Maze procedure was developed in the research laboratories of Drs. Cox and Boineau at the Washington University School of Medicine in the early 1980’s. The development of this operation for atrial fibrillation (AF) was a classic example of a stepwise, incremental advance from the laboratory to the operating room. This successful intervention was introduced clinically only after a thorough understanding of the basic electrophysiology, anatomy, and surgical technique in the laboratory [1,2,3].
The theoretical basis of the operation was to create a set of incisions on both the left and right atria that would block all possible potential macroreentrant circuits. This was based on the prevailing theory of the time regarding the electrophysiology of AF. The multiple wavelet hypothesis proposed by Moe, and supported by the animal studies of Allessie, hypothesized that multiple macroreentrant circuits were responsible for the generation and maintenance of AF [4,5]. As such, the Cox-Maze procedure was not designed to address a specific mechanism, but in the true sense was a salvage procedure, designed to treat all possible types of atrial fibrillation. The Cox-Maze procedure has achieved success rates of greater than 90% in long-term followups [6]. The operation is clearly the gold standard against which all interventions for atrial fibrillation are to be judged. Despite its clinical success, the traditional Maze procedure has not gained widespread acceptance because of its invasiveness and the time required to create the complicated set of lesions.
In this issue, Dr. Song and Dr. Puskas beautifully summarized recent advances in the surgical treatment of atrial fibrillation. The development of less extensive lesion sets and new ablation technology have simplified the procedure and allowed for a more widespread application to surgical patients. With this renewed interest in the field, it is more important than ever to take a look into the future and critically examine important avenues for progress.
While the Maze procedure is clearly the gold standard, it is important to remember that it is not the definitive treatment for atrial fibrillation and has significant shortcomings. First of all, it was designed as a salvage operation at a time in which it was difficult, if not impossible, to determine the underlying mechanism of the clinical AF being treated in each patient. While the procedure did undergo rigorous experimental evaluation prior to clinical application, the precise lesion set was developed in an empiric fashion, and it still remains unclear as to the role and importance of each particular lesion or ablation line. As importantly, the underlying theory of AF on which the entire procedure was based has been shown to be simplistic at best and, in some patients, erroneous. Recent mapping data from patients and results from ablation now suggest that atrial fibrillation originates from a single source in many patients [7]. With our improved understanding of the mechanisms of atrial fibrillation, better clinical diagnostic technology, as well as less-invasive ablative techniques, it is clearly time for re-evaluation and for the development of a surgical approach that is guided by the precise mechanisms of the arrhythmia. In order to achieve this goal, it will be necessary to focus our scientific efforts in several important areas.
First of all, we must develop a better understanding of the mechanisms of atrial fibrillation. It has been shown recently that a number of patients do have focal sources for their atrial fibrillation, often originating from the pulmonary veins [7]. It is also important for surgeons to understand that there is a wide clinical spectrum of AF, in which the underlying mechanisms may in fact be quite different. Lone AF may require a different treatment algorithm than AF associated with either ischemic heart disease or mitral valve disease. It is only with a better understanding of the mechanism of arrhythmias that we can develop more limited procedures that seek to either or isolate or ablate the precise source of each arrhythmia.
A second area in need of scientific investigation is in the development and refinement of clinical diagnostic technology. While we may be able to understand the mechanisms of AF in animal models, it will be of little use in the clinical arena unless we can develop tools that can identify the mechanisms responsible for the initiation and maintenance of AF in each particular patient in a quick and rapid fashion. This would allow for tailored surgical therapy. Presently, AF is best described by either epicardial or endocardial mapping systems. Epicardial mapping requires a full sternotomy in order to position the mapping plaques. These epicardial systems are more precise than endocardial ones, but require time-consuming analysis that makes them unsuitable for intraoperative guidance. There is clearly a need for new mapping algorithms that would enable real-time analysis in order to be of clinical utility. Endocardial mapping has the advantage that it can be performed in the catheterization laboratory during an electrophysiology study. Unfortunately, these endocardial systems still require invasive intervention (trans-septal puncture) and yield maps of relatively low resolution that have difficulty defining the precise mechanisms of the arrhythmia. Future advances in endocardial mapping, however, will perhaps allow for preoperative identification of the arrhythmogenic focus and obviate the need for intraoperative mapping.
There also is a paucity of research on the effect of surgical ablation technology on atrial hemodynamics, function, and electrophysiology. There remain many unanswered basic questions that hamper our appropriate use of this technology. Research is desperately needed in order to define clinically relevant dose-response curves for each of the energy sources, the effect of ablation on vital cardiac structures, and the ability of each particular energy to create transmural epicardial or endocardial lesions. There also is a need to investigate the effect of linear ablation on normal atrial conduction, repolarization, and function. With the improvement of echocardiographic, CT, and MRI techniques, the noninvasive evaluation of atrial function and regional wall motion is now possible, and will allow for a more physiologic assessment of surgical ablation. Further research hopefully will define the advantages and limitations of each energy source and result in the development of a more physiologically sound procedure.
Finally, there is a tremendous amount of information that can be gained from a more careful examination of our clinical results. Because of the critical differences between animal arrhythmia models and actual human tachyarrhythmias, the final development and fine-tuning of all ablative techniques will need to be developed from careful clinical evaluation. It is necessary that investigators throughout the world have careful long-term followup in order to evaluate the true utility of more limited lesions sets over a full Maze III procedure. This requires careful electrocardiographic followup of these patients over longer periods of time. Surgeons also need to report both antiarrhythmic drug use, and the need for further interventional procedures (i.e., flutter ablation).
It is only through a better understanding of the mechanisms of AF, improvement of clinical diagnostic technologies, and a better understanding of the physiology of the ablation technology that we can move from our present empiric approach to mechanistically guided surgery for atrial fibrillation. Without a more precise understanding of clinical AF, it is unlikely that more limited procedures will retain the high effectiveness of the Maze III. If we are to play a significant role in the treatment of lone atrial fibrillation, our procedures will have to exceed the success rates achieved with catheter ablation. Since many groups now are reporting success rates above 70%, our challenge will be to develop a less invasive operation that has success rates of well over 90% [8]. This will require abandoning our present empiric approach and embracing and developing a better scientific understanding of the arrhythmia and our technology. Hopefully, within the next five years, advances will allow for the development of a map-guided approach to atrial fibrillation in which for the first time we can tailor the operation to each patient’s pathophysiology. This is an exciting area that is ripe for future investigation.
References:
1. Cox JL, Schuessler RB, Boineau JP. The surgical treatment of atrial fibrillation. I. Summary of the current concepts of the mechanisms of atrial flutter and atrial fibrillation. J Thorac Cardiovasc Surg 1991;101:402-405.
2. Cox JL, Canavan TE, Schuessler RB, et al. The surgical treatment of atrial fibrillation. II. Intraoperative electrode physiologic mapping and description of the electrophysiologic basis of atrial flutter and atrial fibrillation. J Thorac Cardiovasc Surg 1991;101:406-426.
3. Cox JL, Schuessler RB, D'Agostino HJ Jr, et al. The surgical treatment of atrial fibrillation. III. Development of a definitive surgical procedure. J Thorac Cardiovasc Surg 1991;101:569-583.
4. Moe GK. On the multiple wavelet hypothesis of atrial fibrillation. Arch Int Pharmacodyn Ther 1962;140:183-188.
5. Allesie MA, Lammers WJEP, Bonke FIM, et al. Total mapping of atrial excitation during acetylcholine induced atrial flutter and fibrillation in the isolated canine heart. In Kulbetus HE, Olsson SB, Schlepper M, eds. Atrial Fibrillation. Molndal, Sweden: Lindgren and Soner, 1982.
6. Prasad SM, Maniar HS, Camillo CJ, et al. The Cox maze III procedure for atrial fibrillation: long-term efficacy in patients undergoing lone versus concomitant procedures. J Thorac Cardiovasc Surg 2003;126:1822-8.
7. Haissaguerre M, Jais P, Shah DC, et al. Catheter ablation of chronic atrial fibrillation targeting the reinitiating triggers. J Cardiovasc Electrophysiol 2000;11:2-10.
8. Packer DL, Asirvathan S, Munger TM. Progress in nonpharmacologic therapy of atrial fibrillation. J Cardiovasc Electrophysiol 2003;14:S296-S309.
[Return to Top]
|