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Approximately 30 years ago, the first
successful interruption of an accessory pathway associated with the
Wolff-Parkinson-White (WPW) Syndrome was surgically performed by Dr. Will
Sealy at Duke University, resulting in cure of the patient’s recurrent tachycardia.
The operation was the fulfillment of Mines’ prediction at the beginning of the century
that the best test of reentry was to terminate it by interruption of a portion of the
reentry circuit. The procedure was based on careful extrapolation from basic and
clinical research demonstrating the ability to identify the mechanism and location
of the components of the reentry circuit. The syndrome and its surgical cure became
a paradigm for attempts to cure other arrhythmias, as well as becoming the “Rosetta
stone” for understanding the basic mechanism and requirements for reentry.
The methodology was soon extended to accomplish surgical cure of reentry confined
to the AV node and atrial flutter, as well as ischemic and non-ischemic varieties of
ventricular tachycardia.
Earlier in this decade, reproducible cure of preexcitation, reentry in the AV node, and
atrial flutter was achieved by catheter delivery of radiofrequency energy. Currently,
all of these arrhythmias can be cured in 90-95% of cases with minimal risk, suggesting
this approach be used as a first-line treatment modality.
It was only natural that attempts at non-pharmacologic cure would soon be extended
to the ubiquitous problem of atrial fibrillation. With demonstration of surgical cure of
atrial fibrillation by Dr. James Cox using the “Maze” procedure, there has been a rush
to include this in the province of catheter ablation. This final extrapolation however,
has required major leaps not only in technology, but also in our apparent ability to
proceed with minimal understanding of the variety of substrates and mechanisms of
atrial fibrillation not to mention the risk and long-term sequellae of ablative methods.
Heretofore, nonpharmacologic therapies have been developed from an understanding
of the basic and clinical electrophysiologic mechanisms and anatomic/functional
substrate of a given arrhythmia, coupled with a thorough characterization of the
ablation technique used.
In contrast to the original model of the WPW syndrome, the mechanism(s) of atrial
fibrillation are less well characterized, although most investigators agree with the
general outline of Moe’s reentry hypothesis utilizing multiple wavelets. Even here,
there is a resurgence of interest in the role of automaticity in both the induction and
perpetuation of atrial fibrillation in some cases. This has certainly been given
credibility by the work of Haissaguerre and others documenting cure of atrial fibrillation
by abolishing the inciting focal mechanism. Adding to the heterogeneity of mechanism
is the diversity of the anatomic/functional substrate leading to or resulting from atrial
fibrillation. Electrical remodeling, alterations in gene expression of proteins and other
complex interactions have extending macroscopic considerations to a molecular level.
From the outset, it would appear that extrapolation of the comparatively simple
localization and division of accessory pathways cannot and should not be exported
wholesale to the treatment of atrial fibrillation. The ablative modalities under
consideration are not without new unique risks including clot formation, stenosis of
pulmonary veins, and damage to adjacent structures including but not limited to the
coronary arteries, pulmonary artery, and phrenic nerves.
A final reflection concerns the concept of atrial transport function both before and after
ablative procedures, particularly those founded on creation of long linear lines of
block. The topic of multisite atrial pacing to optimize atrial transport and ventricular
filling has become an area for fruitful investigation. It has been shown that alterations
in atrial activation can have significant impact of ventricular function. Should we not
expect the reverse concept to be equally operative – namely that “desynchronizing”
activation in the atria by creation of lines of block will necessarily impair atrial
transport? Further, the importance of the effect will likely relate to the structure and
function of the atrium prior to ablation, as well as the state of ventricular function. The
same considerations apply to the potential of linear lesions to predispose to emboli
because of wall motion change.
The next millennium will undoubtedly lead to further technological advances that will
stratify patients into those likely to benefit from limited focal low-risk procedures, and
those requiring more extensive and risky interventions. In the latter cohort, superiority
of extensive ablation compared to His ablation/pacer implant will have to be
demonstrated with regard to embolic risk and transport function in addition to rate
control.
Finally, in the century that will begin with characterization of the human genome, we
can not exclude the possibility that molecular intervention may someday make our
current approaches seem as archaic as open-heart surgery for cure of the WPW
syndrome. As we go forward, a return to the restrained, stepwise approach to the
diagnosis and treatment of supraventricular arrhythmias that characterized the 20th
century would seem advisable.
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