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Statin use and reduced post-surgery atrial fibrillation. Which are their underlying mechanisms?
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Miguel Ahumada, Medical Doctor Cardiology Department, Hospital General of Alicante, Alicante, Spain, Vanessa Roldán, Domingo A Pascual, José M Arribas, Mariano Valdés, Francisco Marín
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ahumadamiguel{at}yahoo.es Miguel Ahumada, et al.
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To the editor: We read with interest the article by Amar et al (Chest 2005;128:3421- 3427) showing that statins protects against atrial fibrillation (AF) after noncardiac thoracic surgery. In agreement with them, we have published that these drugs protect against AF after coronary artery bypass grafting1. Some studies have reported that there is an inflammatory state in AF and cardiac surgery. Although inflammation has been proposed to have a pivotal role in postoperative AF, our study suggests that others systems are implicated in its development. Unpublished data of our series show the absence of significant influence of C-reactive protein values in the development of AF. We previously found that increased levels of interleukin-6 in non-rheumatic AF appear to be more related to clinical variables of the patients, rather than to the presence of AF2. Atrial remodeling of the extracellular matrix has been associated with the development and maintenance of AF. Interstitial fibrosis in atrial tissue seems to be related to underlying co-morbidities3, so structural changes in the atria could promote postoperative AF. In our study we observed changes in matrix metalloproteinase-1 (MMP-1), the most important enzyme in the extracellular degradation of collagen, and its inhibitor TIMP-1 after surgery. A more attenuated TIMP-1/MMP-1 ratio at 24 hours after surgery was seen in patients who developed postoperative AF1. Statin use was associated with increased TIMP-1 levels and TIMP-1/MMP-1 ratio. Underlying mechanisms for the beneficial effects of statins remain unclear. In an animal model, atorvastatin prevented development of AF by inhibiting inflammation4. However the recent studies by Amar and ours1 suggest that other mechanisms could be implicated in the benefits of statins. Statins are also able to modify extracellular components by regulating the expression of matrix metalloproteinases or their inhibitors. Indeed, statin use may be protective against AF after coronary artery bypass grafting by modulating extracellular remodeling5. References. 1.- Marín F, Pascual DA, Roldán V, et al. Statins and postoperative risk of atrial fibrillation following coronary artery bypass grafting. Am J Cardiol 2006; 97: 55-60. 2.- Roldán V, Marín F, Blann AD, et al. Interleukin-6, endothelial activation and thrombogenesis in chronic atrial fibrillation. Eur Heart J 2003; 24:1373-1380. 3.- Marín F, Roldán V, Climent V, et al. Is thrombogenesis in atrial fibrillation related to matrix metalloproteinase-1 and its inhibitor, TIMP -1? Stroke 2003; 34: 1181-1186. 4.- Kumagai K, Nakashima H, Saku K. The HMG-CoA reductase inhibitior atorvastatin prevents atrial fibrillation by inhibiting inflammation in canine sterile pericarditis model. Cardiovasc Res 2004; 62:105-111. 5.- Hayashidani S, Tsutsui H. Shiomi T, et al. Fluvastatin, a 3-hydroxy-3- methylglutaryl coenzyme A reductase inhibitor, attenuates left ventricular remodelling and failure after experimental myocardial infarction. Circulation 2002; 105: 868-873. |
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