Atrial Fibrosis: Mechanisms and Clinical Relevance in Atrial Fibrillation
Brett Burstein, BSc and
Stanley Nattel, MD*
Research Center and Department of Medicine, Montreal Heart Institute and Université de Montréal, and Department of Pharmacology and Therapeutics, McGill University, Montreal, Quebec, Canada.
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Figure 1 Mechanisms by Which CHF Leads to AF
In turn, AF causes changes that can impair cardiac function, leading to potentially deleterious positive-feedback systems. Figure illustration by Rob Flewell. AF = atrial fibrillation; CHF = congestive heart failure.
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Figure 2 Schematic Illustrating How Fibrosis Disrupts Myocyte Coupling
Cardiomyocytes in normal myocardial tissue (A) are electrically coupled primarily in an end-to-end fashion by intercellular gap-junctional complexes. Reactive fibrosis results in extracellular matrix expansion between bundles of myocytes (B), while reparative fibrosis replaces degenerating myocytes (C). Both patterns of collagen distribution become exaggerated during structural remodeling. Figure illustration by Rob Flewell.
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Figure 3 Cardiomyocyte–Fibroblast Crosstalk
Autocrine and paracrine mechanisms act to amplify humoral and mechanical stimuli resulting in tissue fibrosis. Figure illustration by Rob Flewell. Ang II = angiotensin II; AT-R = angiotensin receptor; ECM = extracellular matrix; TGF = transforming growth factor; TGFβ-R = trasforming growth factor beta receptor.
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