doi: 10.1161/01.CIR.0000153421.88823.C6
(Circulation. 2005;111:e27.)
© 2005 American Heart Association, Inc.
Correspondence |
Letter Regarding Article by Nanthakumar et al, "Electrophysiological Findings in Adolescents With Atrial Fibrillation Who Have Structurally Normal Hearts"
Cardiothoracic and Vascular Department, Vita e Salute University, Milan, Italy
Cardiology Department, Catholic University, Rome, Italy, biocard{at}rm.unicatt.it
We read with interest the recent article by Nanthakumar and colleagues describing electrophysiological findings in 9 adolescents with atrial fibrillation (AF) and structurally normal hearts who failed to respond to antiarrhythmic therapy.1 The authors reported that the electrophysiological substrate of AF was represented by foci in the pulmonary veins, crista terminalis, or left atrium, mainly inducing focal supraventricular tachycardias.
Radiofrequency ablation of these foci was effective in eliminating recurrent AF in 7 of 9 patients. Nevertheless, in treating their patients, the authors failed to consider atrial myocarditis as a possible cause of lone AF. Through the histological analysis of biventricular and atrial biopsy samples, we reported a high prevalence (66%) of isolated atrial myocarditis in young patients with lone AF refractory to antiarrhythmic therapy and apparently normal hearts.2 In addition, in patients treated with corticosteroids because of histological evidence of active myocarditis (25%), we found that the resolution of myocardial inflammation was associated with persisting disappearance of the arrhythmias. In accordance with our findings, isolated atrial myocarditis has been observed in necropsy studies in 50% of young patients with sudden arrhythmic death carrying accessory atrioventricular pathways,3 suggesting that atrial inflammation triggering AF could have precipitated the fatal arrhythmias. Interestingly, in 50% of cases, the inflammatory infiltrates were located mostly around the orifices of the pulmonary veins.
Unfortunately, Nanthakumar and colleagues failed to provide any data on the possible clinical manifestations of viral infections (ie, respiratory or gastrointestinal) preceding the onset of AF, so that the presence of an inflammatory process triggering the arrhythmias cannot be completely excluded, mostly in the 2 patients with recurrences after radiofrequency ablation.
Because myocardial inflammation can resolve spontaneously or after the administration of a specific treatment,4,5 before a practitioner proceeds with invasive and potentially risky therapeutic procedures, isolated atrial myocarditis must be considered as a possible cause of lone AF, particularly in young and adult subjects, with relevant implications for both prognosis and treatment.
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 Top References References |
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1. Nanthakumar K, Lau YR, Plumb VJ, Epstein AE, Kay GN. Electrophysiological findings in adolescents with atrial fibrillation who have structurally normal hearts. Circulation. 2004; 110: 117–123.
2. Frustaci A, Chimenti C, Bellocci F, Morgante E, Russo MA, Maseri A. Histological substrate of atrial biopsies in patients with lone atrial fibrillation. Circulation. 1997; 96: 1180–1184.
3. Basso C, Corrado D, Rossi L, Thiene G. Ventricular preexcitation in children and young adults: atrial myocarditis as a possible trigger of sudden death. Circulation. 2001; 103: 269–275.
4. Frustaci A, Chimenti C, Calabrese F, Pieroni M, Thiene G, Maseri A. Immunosuppressive therapy for active lymphocytic myocarditis: virological and immunologic profile of responders versus nonresponders. Circulation. 2003; 107: 857–863.
5. Kuhl U, Pauschinger M, Schwimmbeck PL, Seeberg B, Lober C, Noutsias M, Poller W, Schultheiss HP. Interferon-beta treatment eliminates cardiotropic viruses and improves left ventricular function in patients with myocardial persistence of viral genomes and left ventricular dysfunction. Circulation. 2003; 107: 2793–2798.
Response
Division of Cardiology, University Health Network, University of Toronto, Toronto, Ontario, Canada, k.nanthakumar{at}whn.on.ca
University of Alabama at Birmingham, Birmingham, Ala
Pieroni et al suggest that atrial myocarditis and local infiltrative processes may be triggers for atrial fibrillation. Frustaci et al, studying 12 patients, showed a high prevalence of biopsy-positive lympho-mononuclear infiltrates with necrosis of adjacent myosites.1 In that series, no mention was made of previous respiratory or gastrointestinal illnesses or clinical manifestations that might be consistent with a viral prodrome. Likewise, in our series,2 no clinical manifestations were suggestive of a viral infection, especially in patients with recurrences.
The treatment of myocarditis (ventricular) with steroids has been disappointing thus far.3 The evidence in favor of treating atrial myocarditis with steroids to manage paroxysmal atrial fibrillation comes from a case series in which 3 patients’ arrhythmias resolved after taking 1 mg · kg–1 · d–1 of prednisone for 1 month.2 The patients in our series had failed antiarrhythmics and had explored all other options, undergoing ablation as a last resort. Given the generally long duration of atrial arrhythmias and the lack of a viral prodrome, treatment with steroids was not considered.
We agree with Pieroni et al that young adults referred for ablation should explore all possible options before considering an invasive approach to their treatment. We are unable to rule out the possibility of atrial myocarditis in our patients. It seems likely that a prospective trial of antiinflammatory medications will be needed to further understand the mechanism of atrial fibrillation in young patients.
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References |
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TopReferencesReferences |
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1. Frustaci A, Chimenti C, Bellocci F, Morgante E, Russo MA, Maseri A. Histological substrate of atrial biopsies in patients with lone atrial fibrillation. Circulation. 1997; 96: 1180–1184.
2. Nanthakumar K, Lau YR, Plumb VJ, Epstein AE, Kay GN. Electrophysiological findings in adolescents with atrial fibrillation who have structurally normal hearts. Circulation. 2004; 110: 117–123.
3. Mason JW, O’Connell JB, Herskowitz A, Rose NR, McManus BM, Billingham ME, Moon TE. A clinical trial of immunosuppressive therapy for myocarditis. The Myocarditis Treatment Trial Investigators. N Engl J Med. 1995; 333: 269–275.
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