The History of Atrial Fibrillation: The Last 100 Years

Eric N. Prystowsky, M.D.

Disclosures

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

In This Article

Advances Surrounding Atrial Fibrillation

There have been several key advances in the field of cardiac arrhythmias that are outgrowths of the study and treatment of atrial fibrillation. In 1962, Lown and colleagues[16] performed the first cardioversion on arrhythmias in patients with atrial fibrillation. They applied synchronized cardiac shocks to restore sinus rhythm in these patients, initially in the operating room, but subsequently at the bedside. We consider this routine care for patients with atrial fibrillation and obviously life-saving for patients with ventricular tachycardia and ventricular fibrillation. However, as with all new therapies, there is always the initial patient undergoing such a procedure, and it is never "simple" for that situation.

The concept of functional bundle branch block aberrancy started by a long-short R-R sequence was noted in a patient with atrial fibrillation and reported by Gouaux and Ashman.[17] This is referred to as the Ashman phenomenon, and is well known to be initiated by heart rate changes in refractoriness of the bundle branch (usually the right bundle branch); persistence of aberrancy occurs typically by repetitive retrograde transseptal concealed conduction from one bundle into the other. I find it remarkable that these authors suggested the mechanism merely by observations from the electrocardiogram. They stated that "the reason why the blocking persists… is probably simple. Once an impulse is blocked off from or within the right branch it first enters the left ventricle… passes through the interventricular septum to the right ventricle, and is conducted backward up the right branch…." So "simple" it took many years of study to prove they were correct.

The concept of tachycardia-mediated cardiomyopathy and subsequent heart failure also arose from observations on patients with atrial fibrillation. For example, Phillips and Levine[18] noted that several patients developed congestive heart failure during atrial fibrillation that disappeared after the rhythm was regularized in the presence of quinidine to sinus rhythm. Multiple subsequent studies clearly documented the reversibility of this cardiomyopathy if documented early enough, and have stressed the importance of good rate control to prevent it. I found it particularly interesting that the authors concluded that serious complications with the use of quinidine therapy were practically absent and the therapy could be regarded as safe in patients without any significant heart disease. While this is mostly true, it is now well recognized that even patients with normal hearts who have a propensity to a prolonged QT interval in certain circumstances can develop torsade de pointes ventricular tachycardia. It wasn't until the observations of Selzer and Wray[19] in 1964 that quinidine syncope was documented to be due to episodes of torsade de pointes after restoration of sinus rhythm in patients loaded with quinidine.

Sudden cardiac death is relatively rare in patients with normal ventricular function. However, ventricular fibrillation can occur unexpectedly in patients with Wolff-Parkinson-White Syndrome,[20,21] usually due to degeneration of a rapid preexcited ventricular response during AF to ventricular fibrillation. Thus, this was one of the earlier demonstrations of tachycardia-induced tachycardia, and unfortunately a lethal one. Digitalis was given to the initial patient,[19] and it is now well recognized that digitalis is contraindicated under most circumstances in patients with preexcitation in whom the anterograde conduction properties of the accessory pathway have not been studied. This is certainly true in the presence of atrial fibrillation with preexcited QRS complexes. While atrial fibrillation can be a de novo arrhythmia in patients with Wolff-Parkinson-White (WPW) Syndrome, the usual mechanism is actually another type of tachycardia-induced tachycardia, as demonstrated in Figure 2. Note that during sustained AV reentry there is a sudden degeneration into atrial fibrillation as noted initially on the high right atrial lead. If this patient had a capability of rapid conduction over the accessory pathway, this could lead to a rapid ventricular response and subsequent ventricular fibrillation. In essence, this would be a case of tachycardia-induced tachycardia that repeats itself, leading potentially to sudden death.

Figure 2.

Tachycardia-induced tachycardia causing atrial fibrillation. Simultaneous recorded tracings are from top to bottom: ECG leads I, II, III, aVF, and V1; and intracardiac leads from the high right atrium (HRA-D), His bundle area distal (HBED), and proximal (HBEP), and the right ventricle (RV). Atrioventricular reentry on the left initiates atrial fibrillation on the right.

It has been observed for many years that patients with atrial fibrillation can exhibit at times a pattern on the electrocardiogram that suggests atrial flutter, and these two patterns may come and go in the patient. For this reason, the designation atrial fibrillation/atrial flutter was used to describe such patients. The observations of Waldo and colleagues[22] gave a better understanding of this situation. These investigators analyzed bipolar atrial electrograms from epicardial wire electrodes placed at the time of surgery to study atrial fibrillation and atrial flutter in the postoperative period. They observed that at the same electrode site at different times there appeared to be a very regular but rapid rhythm, while at other times it was clearly more like atrial fibrillation with a grossly irregular rhythm. These and other authors have described parts of atria that are regularized, while at the same time others are in atrial fibrillation. In essence, this is all the same rhythm—atrial fibrillation. Atrial flutter is quite a different arrhythmia, which, like a metronome, has a very regular rate and P-wave morphology, and a distinct macroreentrant mechanism. In so-called atrial flutter/atrial fibrillation, while the electrocardiogram may at times mimic atrial flutter, careful analysis of the P-waves shows inconsistency in morphology and rate.

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