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Ann Thorac Surg 1996;61:1678-1679
© 1996 The Society of Thoracic Surgeons
DR JAMES J. MORRIS (Charleston, SC): Doctor Gandhi, along with Dr Cox, Dr Huddleston, and their colleagues, has presented a very well conceived and elegant investigation.
Over the past several decades with improvements in the treatment of congenital heart disease and with the availability of long-term follow-up, the late occurrence of atrial tachydysrhythmias after a variety of corrective operations has been increasingly recognized to be a significant source of subsequent morbidity and mortality. Attempts to more clearly understand the relationship between atrial anatomy and the electrophysiologic basis of these dysrhythmias to modify old operations and to tailor new operations to prevent problematic late atrial flutter and fibrillation seems to represent an important new frontier in cardiac surgery.
In this light, Dr Gandhi and his colleagues have demonstrated several points. First, the combination of a longitudinal atriotomy and an incision in the right atrial appendage, as would be performed with the classic Fontan atriopulmonary connection, results in a reproducible macroreentrant substrate for the induction of sustained reentrant atrial tachycardia. They have shown characteristic propagation of the reentrant wavefront is through the bridge of atrial myocardium between the two atrial incisions.
Second, and importantly, the investigators have shown that placement of an additional incision to transect the bridging segment of atrial myocardium can disrupt the reentry circuit and prevent reinduction of atrial flutter. Together these two findings would suggest the minimal addition of an atrial incision at the time of a Fontan operation may prevent subsequent development of problematic atrial dysrhythmias.
A third point not framed as a major conclusion, but still noteworthy, is that anatomically guided approaches to ablate this type of reentrant tachycardia have a much higher likelihood of success than does an electrophysiology-guided approach, such as a catheter ablation, because it is critical to identify the anatomic location of the atrial pathway between the two nonconducting regions rather than just identify the site of slowest conduction.
This is an important study that would seem to have immediate potential clinical applications or at least questions of applications. Doctor Gandhi and his colleagues, both in the presentation this morning and in their manuscript, have been prudent and cautious in interpreting their findings and in their recommendations for clinical applications. It is in this area that I would like to question them and press them a bit farther.
In their acute canine model, two atrial incisions are shown to be permissive for the establishment of atrial reentry. Clearly, though, a number of other factors such as atrial size and three-dimensional geometry, atrial stretch, fibrosis, and other variables that may alter the spatial distribution of refractoriness, including perhaps cellular and subcellular mechanisms of microreentry, may also be permissive or in fact triggering events for the establishment of sustained reentry. Late after a Fontan operation, or other reconstructive operations, chronic hemodynamic alterations, the atrial myocardial response to those alterations, and the nonconducting atrial incision scars together would constitute the potential arrhythmogenic substrate.
Do you believe the addition of a single atrial incision will uniformly curtail the development of late dysrhythmias after the classic Fontan operation?
Should a classic maze operation or at least a right atrial maze operation instead be offered to these patients if the procedure could be tailored to the abnormal anatomy?
Future investigative work will hopefully clarify triggering sites for atrial reentry and ways to tailor atrial incisions in individual patients and with specific disease states to disrupt discrete reentrant circuits or to construct an effective localized regional maze rather than a global atrial maze.
In the meantime, Dr Gandhi, have you and your colleagues begun to develop a perception as to what would be the minimal operation needed for maximal effectiveness in uniformly preventing reentrant tachycardia in Fontan patients? Similar questions are now also being asked in certain patients undergoing atrial septal defect repair and in the larger group of patients with degenerative mitral valve disease with preexistent reentrant tachycardia.
Again, congratulations on good work and thank you for the opportunity to discuss this paper.
DR GANDHI: Thank you, Dr Morris, for your kind comments.
The principal substrate for atrial flutter is an anatomic abnormality in atrial myocardium. Based on our animal model of the classic Fontan operation and our previous animal model of the total cavopulmonary connection, it seems apparent that surgically created barriers to conduction are the fundamental anatomic substrates for reentrant tachyarrhythmias after a Fontan operation. Therefore, eliminating postoperative atrial flutter should focus on removing these substrates. Creating a line of conduction block between two nonconducting barriers that border a reentrant circuit will terminate circus movement. In the present model, an incision from the atriotomy to the atriopulmonary connection accomplished this goal without producing any novel reentrant circuits. Doctor Cox has done much pioneering work in surgically treating human atrial fibrillation and atrial flutter. The maze procedure is based on the premise of interrupting all potential microreentrant circuits within the atria to effectively cure atrial fibrillation. Because, in our model, atrial flutter appears to result from a single consistent macroreentrant loop, such a complex procedure is not required.
With respect to the prevention of postoperative atrial flutter, much work remains to be done. To date, operative strategies designed to reduce the incidence of atrial flutter after the Fontan operation have focused on methods by which to alleviate the degree of right atrial enlargement and hypertension. In fact, Dr Hanley's group from San Francisco regards recalcitrant arrhythmias after atriopulmonary connection to be an indication for conversion to either an intraatrial tunnel or an extracardiac conduit. The spontaneous initiation of atrial flutter depends on functional substrates, namely a nonuniform duration of repolarization of myocardium within or adjacent to the potential reentrant pathway, and triggering agents, represented by atrial premature depolarizations. Operations that reduce the hemodynamic consequences of the Fontan circulation should theoretically decrease dispersion of refractoriness and atrial premature depolarizations; however, the anatomic substrate may still remain. Further research is required to elucidate the consequences of prophylactic atrial incisions on the occurrence of postoperative atrial flutter after a Fontan operation. Thank you.
Related Article
Ann. Thorac. Surg. 1996 61: 1666-1678.
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