Atrial fibrosis: mechanisms and clinical relevance in atrial fibrillation.

By B. Burstein, Stanley Nattel. Journal of the American College of Cardiology, 2008

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Atrial fibrillation: profile and burden of an evolving epidemic in the 21st century. (2013, background): “Pooled AF prevalence estimates overall (A) and for men (B) and women (C) separ age-adjusted (and sex-adjusted for overall data only) prevalence proportions (red boxes) w associated pathological changes (including myocardial fibrosis [73,74]).”
Cardiovascular Risks Associated with Gender and Aging (2019, background): “Fibrosis, due to impaired ECM turnover, has been shown to develop in the atria of aging patients, which also results in atrial fibrillation in many of these patients [12].”
The clinical profile and pathophysiology of atrial fibrillation: relationships among clinical features, epidemiology, and mechanisms. (2014, background): “For a full discussion of the complex signaling mechanisms that lead to atrial fibrosis, please see detailed reviews.(167,185,188)”
Pathophysiological mechanisms of atrial fibrillation: a translational appraisal. (2011, background): “models that atrial fibrosis can be proarrhythmic (80, 169),”
Atrial remodeling and atrial fibrillation: recent advances and translational perspectives. (2014, background): “Angiotensin II (AT-II) and other profibrotic mediators can enhance production of diacylglycerol, which activates protein kinase C. Conventional protein kinase C is stimulated by an increase in levels of intracellular Ca2þ and induces downstream signaling cascades such as mitogen-activated protein ki”