Atrial ~brillation (AF) is the most common sustained arrhythmia in clinical practice. It affects approximately 2,000,000 Americans with 160,000 new cases per year. Drug therapy can be associated with a number of untoward effects such as proarrhythmia, long term inef~cacy and even an increase in mortality, especially in those with impaired ventricular function [1,2]. Catheter ablation of the atrioventricular node with pacemaker implantation [3,4], or modi~cation of the AV node without pacer implantation [5,6] can be useful to facilitate ventricular rate control, but thromboembolic risk is unchanged and atrial systole is not restored. Given the limitations of medical therapy, repeated cardioversions and atrioventricular conduction ablation, an approach that cures atrial ~brillation would be highly desirable. At the present time, catheter-based cure of atrial ~brillation must be considered highly investigational. Nevertheless, because the clinical need for better therapy of atrial ~brillation is so vast, there are a number of on-going efforts to develop devices and techniques for atrial ablation in order to effectively restore sinus rhythm and atrial mechanical contraction. Do we need a cure for atrial ~brillation? Certainly, given the problems with drug treatment and the impact on quality of life, a cure would be highly desirable, and efforts to create such a cure well rewarded. In the history of electrophysiologic intervention, there are many examples in which a cycle of clinical science and new interventional techniques has been demonstrated. That is, we start with a given hypothesis of arrhythmia mechanism or substrate, we intervene to alter what we believe to be the substrate (with surgery, or with catheter-based techniques), in the process of intervention we have an opportunity to garner further, more accurate insights into mechanism and substrate and to develop subsets of what we has thought was a single disorder, and this in turn allows us to develop better interventional tools and techniques. For example, all regular narrow complex tachycardias used to go by the moniker of “PAT.” First with surgery, and then with catheter-based techniques, we came to be able to discern that “PAT” may actually be one of several speci~c arrhythmia substrates such as WPW, AV nodal reentry, etc. In the era of catheter ablation, we can now even describe three or more types of AV nodal reentry. So, too, our ability to intervene on patients with atrial ~brillation has just begun to allow us to develop more detailed descriptions of mechanism. “Atrial ~brillation” as such may come to be recognized as the common surface manifestation of multiple potential mechanisms. This will allow us to develop tools and techniques that are more directly targeted to a given mechanism. In the case of atrial ~brillation this will be particularly important, since if one considers the current “gold standard” for curative intervention to be the extensive lesions produced during the Cox surgical maze operation, then recognition of AF mechanisms that require a less extensive lesion set would be highly desirable. Recently, it has come to be understood that the initiating event in many cases of AF is a “focal trigger” arising in the vast majority of cases from within one of the pulmonary veins [7]. The purpose of the present paper is to brie_y describe early progress towards the development of a novel technology addressing this particular class of AF mechanism.
Search from 250 M+ research papersSearch from 250 M+ research papers
Open Access
Oct 12, 2022
Nicolette C Mininni + 4
