 |
|
More Points on Vagally Mediated Atrial Fibrillation
I just completed reading the brief report by Ringdahl1 on vagally mediated atrial fibrillation in the April 2000 issue of the ARCHIVES. Nice article! I support the author's effort to increase awareness among our colleagues that all atrial fibrillation is not alike and that, on occasion, pure vagal (not just sympathetic) stimuli may induce cardiac arrhythmias. I would like to add a few clinically related points to this relevant article.
Vagally mediated atrial fibrillation may also occur in older patients, especially at night.
When discussing the treatment of supraventricular arrhythmias, I like to specify verapamil or diltiazem rather than use the generic term calcium blockers. Verapamil and diltiazem are the only 2 calcium blockers with utility for treatment of supraventricular tachycardia. All other calcium blockers are dihydropyridines that, if anything, may aggravate supraventricular tachycardia. This is because dihydropyridines are vasodilating medications, without an in vivo atrioventricular nodal-blocking effect; therefore, they may induce reflex tachycardia.
A true "pearl," often cited by Jim Reiffel, MD (author of the article's reference 10), is to consider use of disopyramide for vagally induced atrial fibrillation. This type IA drug differs from others in its class (quinidine and procainamide) in being vagolytic. One need not necessarily prescribe disopyramide continually or long-term if the arrhythmia is primarily related to certain activities. Instead, this drug could be prescribed as a sustained-release nighttime dose for the older patient with nocturnal atrial fibrillation caused by increased vagal tone, or prescribed on an as-needed basis for selected young athletic individuals with vagally induced paroxysmal atrial fibrillation related to specific activities (assuming, of course, that such patients have an otherwise normal heart). I fully share the author's view that fewer drugs are better, and that optimal treatment consists of determining the vagal precipitant and working to alleviate it. However, one might want to keep in mind that disopyramide may be a drug of choice that can help in the treatment of some of these patients.
Finally, I would like to reemphasize Dr Ringdahl's excellent point that use of digoxin is contraindicated for treatment of vagally induced atrial fibrillation (a primary reason for trying to identify this group of atrial fibrillation patients). This is because the principal mechanism through which digoxin slows the rate of atrial fibrillation is by increasing vagal tone, which may worsen this arrhythmia. An interesting aspect about the increase in parasympathetic tone is that this action exerts the opposite effect on atrial tissue than it does on the atrioventricular node. Because digoxin may reduce the refractory period of atrial tissue, it may actually speed up the atrial rate of fibrillation activity and may sometimes even, paradoxically, increase the rate of the ventricular response to atrial fibrillation. For this reason, I would go one step beyond stating that digoxin should be avoided to say that its use should be contraindicated for this entity.
Again, these are minor points intended to complement the fine article of Ringdahl. Keep up the excellent work with your journal!
Ken Grauer, MD
Family Practice Residency Program
University of Florida College of Medicine
PO Box 147001
Gainesville, FL 32614
1. Ringdahl EN. Vagally mediated atrial fibrillation in a young man. Arch Fam Med. 2000;9:389-390.
FREE FULL TEXT
Arch Fam Med. 2000;9:587-588.
|
