Mounting Evidence That Fibrosis Generates a Major Mechanism for Atrial Fibrillation
| Autor: | Madison S. Spach |
|---|---|
| Rok vydání: | 2007 |
| Předmět: |
medicine.medical_specialty
Physiology business.industry Mechanism (biology) Cardiac arrhythmia Atrial fibrillation medicine.disease Pulmonary vein Left atrial wall Fibrosis Internal medicine Heart failure cardiovascular system Cardiology Medicine Cardiology and Cardiovascular Medicine business Endocardium |
| Zdroj: | Circulation Research. 101:743-745 |
| ISSN: | 1524-4571 0009-7330 |
| DOI: | 10.1161/circresaha.107.163956 |
| Popis: | See related article, pages 839–847 It is widely known that atrial fibrillation (AF) is the most common sustained cardiac arrhythmia, with the problem magnified by the clinical sequelae; eg, thromboembolic events. It is pertinent that the incidence of AF is expected to increase in the future,1 especially in aging patients. Thus, finding preventive measures for this arrhythmia has become an increasingly important goal. In addition to considering clinical risk factors, focusing on prevention necessitates knowledge of the associated pathophysiology of AF,2 which involves the initiation of AF and the wavefront dynamics that sustain it. In recent years considerable new information has appeared concerning AF mechanisms that occur in different regions of the atria in different cardiac states.3 This point is highlighted by the report of Tanaka et al4 in this issue of Circulation Research . These authors used high-resolution electrophysiological and microstructural techniques, along with computer model simulations, to study wavefront dynamics during acetylcholine (ACh)-induced AF in heart failure sheep hearts. The heart failure hearts had developed prominent fibrotic patches in the posterior left atrium near the pulmonary veins, whereas in the control (normal) hearts patches of fibrosis were smaller, diffusely distributed, and more centrally located with respect to the 4 pulmonary vein ostia. In the heart failure hearts, during AF variable wavefront breakthroughs to the endocardium occurred in the area of fibrotic patches adjacent to the pulmonary veins. The authors concluded that scroll waves within the posterior left atrial wall produced a microreentry source for the endocardial breakthroughs in the region of the larger collagen patches, thus providing the underlying mechanism of AF.4 A myriad of reports provide varied information about substrates and mechanisms of AF as a background for the study of Tanaka et al … |
| Databáze: | OpenAIRE |
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