The History of Atrial Fibrillation: The Last 100 Years

Eric N. Prystowsky, M.D.


J Cardiovasc Electrophysiol. 2008;19(6):575-582. 

In This Article

Future Directions

As we sit comfortably in the dawn of the 21st century, reflecting on how much we know today compared with our investigative grandfathers in the early and mid portions of the 20th century, we should surely not get too complacent or too smug; for certain, our investigative great grandchildren 50 to 100 years from now will be surprised at how little we knew regarding the mechanism of atrial fibrillation and approaches to its treatment. Indeed, we still do not know the mechanism of atrial fibrillation in individual patients. The majority of data strongly suggest that automaticity and reentry play a role in the initiation and maintenance of atrial fibrillation, but these mechanisms likely differ depending upon the pathophysiologic conditions present. One observation I have made over time favors triggered activity over abnormal automaticity. Commonly, the initiation of atrial fibrillation, whether after cardioversion or spontaneous, occurs only after a sinus complex (Fig. 5). In my experience, it is rare to see spontaneous atrial fibrillation without preceding atrial activation from another source.

Figure 5.

Spontaneous initiation of atrial fibrillation. Note that spontaneous initiation of atrial fibrillation occurs after a premature atrial complex, followed by a sinus complex (A); and after a short run of atrial fibrillation it starts again only after a sinus complex has occurred (B).

It may be that the clinical presentation of AF gives a clue to the mechanism for that patient. Figure 6 shows schematic representations of clinical presentations that I have observed over decades of treating patients with atrial fibrillation. Triggered activity is postulated as the potential mechanism for patients who have short bursts of paroxysmal atrial fibrillation and never seem to develop persistent atrial fibrillation. It is also possible that microreentry and not triggered activity can sustain AF (Fig. 6, Panel I). Their atria are considered normal. In patients with paroxysmal episodes of atrial fibrillation that can last for minutes to hours, but who never seem to get persistent atrial fibrillation, triggered atrial fibrillation is the postulated primary problem with a likely possibility of some abnormal atrial substrate (Fig. 6, Panel II). There are also patients who typically present in persistent atrial fibrillation and very infrequently have documented paroxysmal episodes of atrial fibrillation (Fig. 6, Panel III). Often, cardioversion may restore sinus rhythm with immediate (IRAF) or early recurrence of atrial fibrillation. I suspect these patients have a combination of triggered activity as well as a major substrate abnormality for atrial fibrillation. The last category is one that is puzzling and infrequently observed. Here, patients have very infrequent episodes of atrial fibrillation, often separated by one or more years, but the episodes are always persistent (Fig. 6, Panel IV). My concept is that there is a clear substrate abnormality, either anatomic or functional, for example, long-lasting heightened vagal tone, but possibly the lack of any common initiating factors such as pulmonary vein ectopy. Thus, I would suspect that a therapeutic ablation or surgical approach aimed solely at isolating pulmonary veins would not be successful in such individuals, which obviously requires more study.

Figure 6.

Schematic representations of clinical presentations of atrial fibrillation and postulated mechanisms.

Seemingly more complicated than the basic mechanism of atrial fibrillation in humans is the answer to the question of why an episode of atrial fibrillation occurs at a given point and time for the patient. Is this due to autonomic nervous system pertubations, the normal ebb and flow of stresses during the day, or other mechanisms such as stretch-activated receptors? None of these answers are available and will clearly dictate directions for therapy in the future. In this regard, it is intriguing that in addition to so-called upstream therapies, there may be opportunities for unique treatments evaluated thus far only in investigational models, for example, a tarantula peptide that inhibits atrial fibrillation induction under certain circumstances.[64] The role of genes in atrial fibrillation also requires more study.[65]

In two recent consensus documents, the participants could not recommend a "standard" ablation approach to cure atrial fibrillation.[66,67] Indeed, we need much more information on mapping, ablation lesions, and new energy sources to cure atrial fibrillation that will undoubtedly become available in the ensuing years. Hopefully, randomized trials will answer a very important question for both investigators and patients; that is, for those individuals with a seemingly ablation cure of atrial fibrillation who are at high risk for stroke, can warfarin therapy safely be discontinued? Many patients at risk for stroke who want to discontinue warfarin have been seeking ablation cures, but investigators do not know whether it is safe to stop warfarin even after what appears to be a successful outcome. This entire area is likely to change with the approval of new types of oral anticoagulation therapy that may be much safer to use and easier for the patients.

This paper was initially presented as the Plenary Lecture for the AFib Summit at the Heart Rhythm Society Annual Scientific Sessions 2007 in Denver, CO.

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