LETTER TO THE EDITOR
Atrial fibrillation and sinus node dysfunction
Maarten P. van den Berg, MD, PhDa and
Isabelle C. van Gelder, MD, PhDa
a Department of Cardiology, Thorax Center, University Hospital Groningen, P.O. Box 30.001, 9700 RB, Groningen, The Netherlands
m.p.van.den.berg{at}thorax.azg.nl
We have read with great interest the article by Lombardi et al. (1), which used analysis of heart rate variability (HRV) to predict recurrence of atrial fibrillation (AF) after electrical cardioversion. Although analysis of HRV in this setting is technically demanding (owing to ectopy) the investigators showed that patients with an early recurrence of AF (within two weeks after cardioversion) are characterized by a high low-frequency/high-frequency ratio compared to patients who maintain sinus rhythm. Based on the implicit assumption that HRV reflects autonomic modulation of the sinus node, Lombardi et al. (1) concluded that sympathetic modulation is increased in these patients. However, it is questionable whether this assumption is valid in the present setting. For the sinus node to reflect autonomic modulation it is required that sinus node function as such is normal. In other words, in case of intrinsic dysfunction, the sinus node is not an adequate "thermometer," and HRV should not be used to assess autonomic modulation. In patients with persistent AF there is reason to doubt whether intrinsic sinus node function is normal.
First, AF is often associated with sick sinus syndrome (2). In fact, histopathological studies demonstrated that persistent AF is associated with significant damage to the sinus node, the perinodal tissue and the sinus node artery (3). Second, and possibly even more important, AF per se causes sinus node dysfunction.
In an experimental pacing-model in dogs, Elvan et al. (4) examined the effect of AF on sinus node function. Intrinsic function was assessed after pharmacological autonomic blockade using propranolol and atropine. No effect was apparent after 1 h of AF, but prolonged AF (two to six weeks) caused a significant increase in intrinsic-corrected sinus node recovery time and a decrease in intrinsic heart rate. Within one week after cessation of AF these measures of sinus node function gradually returned to normal. Comparable data have recently been reported in humans (5). It thus appears that electrical remodeling secondary to AF is not confined to the atrial myocardium but also involves the sinus node.
The clinical data provided by Lombardi et al. (1) on their patients do not indicate intrinsic sinus node dysfunction. Conversely, intrinsic sinus node dysfunction is hard to rule out. Therefore, we believe that the conclusion by Lombardi et al. (1), namely that patients with early recurrence of AF show signs of increased sympathetic modulation, should be toned down.
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References
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1. Lombardi F, Colombo A, Basilico B, et al. Heart rate variability and early recurrence of atrial fibrillation after electrical cardioversion. J Am Coll Cardiol. 2001;37:157–162[Abstract/Free Full Text]
2. Gomes JAC, Kang PS, Matheson M, Gough WB, El-Sherif N. Coexistence of sick sinus rhythm and atrial flutter-fibrillation. Circulation. 1981;63:80–86[Abstract/Free Full Text]
3. Thery C, Gosselin B, Lekieffre J, Warembourg H. Pathology of the sinoatrial node. Correlations with electrocardiographic findings in 111 patients. Am Heart J. 1977;93:735–740[CrossRef][Medline]
4. Elvan A, Wylie K, Zipes DP. Pacing-induced chronic atrial fibrillation impairs sinus node function in dogs. Circulation. 1996;94:2953–2960[Abstract/Free Full Text]
5. Sparks PB, Jayaprakash S, Vohra JK, Kalman JM. Electrical remodeling of the atria associated with paroxysmal and chronic atrial flutter. Circulation 2000;102:1807–13.
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