European Heart Journal Advance Access originally published online on September 1, 2005
European Heart Journal 2005 26(20):2208-2209; doi:10.1093/eurheartj/ehi451
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The emerging role of inflammation in atrial fibrillation and the potential of anti-inflammatory interventions: reply
Department of Cardiology
The Heart Center
University Hospital of Copenhagen
Rigshospitalet
Blegdamsvej 9
2100 Copenhagen
Denmark
Tel: +45 43 45 3848
Fax: +45 43 45 3824
E-mail address: engelmann{at}dadlnet.dk
Department of Cardiology
The Heart Center
University Hospital of Copenhagen
Rigshospitalet
Blegdamsvej 9
2100 Copenhagen
Denmark
The letter by Dr Korantzopoulos and coworkers draw attention to some new studies which were not published when the review ‘Inflammation in the genesis and perpetuation of atrial fibrillation’1 was written. Dr Korantzopoulos mentions four studies on markers of inflammation and AF, studies which are interesting and adds to the body of evidence in favour of an association between AF and inflammation, although it should be emphasized that the observed associations cannot be interpreted as indicating a role for C-reactive protein in the pathogenesis of AF. It is possible that elevated C-reactive protein levels are simply indicative of a generalized inflammatory state antedating AF. Moreover, the majority of studies are limited by the use of C-reactive protein as the only marker of inflammation. C-reactive protein is a non-specific acute-phase protein primarily produced in the liver in response to most forms of tissue damage, infection, inflammation, and malignant neoplasia. Studies in patients with acute myocardial infarction have indicated that cytokines, i.e. interleukin-6 (IL-6) is produced locally in the heart, whereas C-reactive protein is produced mainly in the liver and taken up locally by phagocyting white blood cells.2 Thus, measurement of cytokines (IL-6, TNF-
, etc.) may be more specific than C-reactive protein and may hold important information in AF patients. This is underlined in the study by Psychari et al.3 who measured C-reactive protein and IL-6. Both markers of inflammation were significantly elevated in AF patients and both were independent predictors of left atrial size. In addition, IL-6 levels were positively related to AF duration which may indicate a role for inflammation in the process of atrial remodelling. Interestingly, IL-6 levels were not independently related to the presence of AF, which is in contradiction to our findings in patients with persistent AF,4 where IL-6 was a significant independent predictor of AF. These differences may be due to patient selection, i.e. duration of AF, proportion of persistent and permanent AF, co-morbidities, etc. However, studies on multiple markers of inflammation in AF are scarce and more studies in larger populations should be encouraged.
If one accepts inflammation as being significant in the genesis and perpetuation of AF, a logical step is to clarify the role for anti-inflammatory interventions in the setting of AF. In this regard, we reviewed the impact of glucocorticoides, statins, angiotensin converting enzyme inhibitors, and angiotensin receptor blockers. The list of drugs with anti-inflammatory properties is long and Dr Korantzopoulos and coworkers draw attention to vitamin C, n-3 fatty acids, and aldosterone antagonists as potential and indeed exciting treatment strategies. However, these drugs are only the tip of the iceberg and the need for large randomized, placebo-controlled longitudinal studies should be emphasized. Such studies may herald a new area in the treatment of an arrhythmia, where the effects of pharmacological interventions so far have been disappointing.
Conflict of interest: no conflicts of interest.
References
- Engelmann MDM, Svendsen JH. Inflammation in the genesis and perpetuation of atrial fibrillation. Eur Heart J 2005. Published online ahead of print June 23, 2005; doi:10.1093/eurheartj/ehi350.
- Maier W, Altwegg LA, Corti R, Gay S, Hersberger M, Maly FE, Sutsch G, Roffi M, Neidhart M, Eberli FR, Tanner FC, Gobbi S, von Eckardstein A, Luscher TF. Inflammatory markers at the site of ruptured plaque in acute myocardial infarction: locally increased interleukin-6 and serum amyloid A but decreased C-reactive protein. Circulation 2005;111:1355–1361.
[Abstract/Free Full Text] - Psychari SN, Apostolou TS, Sinos L, Hamodraka E, Liakos G, Kremastinos DT. Relation of elevated C-reactive protein and interleukin-6 levels to left atrial size and duration of episodes in patients with atrial fibrillation. Am J Cardiol 2005;95:764–767.[CrossRef][Web of Science][Medline]
- Engelmann MD, Øgard CG, Niemann L, Skagen K, Kanstrup IL, Godtfredsen J. Increased levels of multiple markers of inflammation in patients with persistent atrial fibrillation. Scan Cardiovasc J 2005;39:36.
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