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Review
. 2022 Dec;9(6):3768-3784.
doi: 10.1002/ehf2.14089. Epub 2022 Aug 3.

Atrial cardiomyopathy: from cell to bedside

Affiliations
Review

Atrial cardiomyopathy: from cell to bedside

Mengmeng Li et al. ESC Heart Fail. 2022 Dec.

Abstract

Atrial cardiomyopathy refers to structural and electrical remodelling of the atria, which can lead to impaired mechanical function. While historical studies have implicated atrial fibrillation as the leading cause of cardioembolic stroke, atrial cardiomyopathy may be an important, underestimated contributor. To date, the relationship between atrial cardiomyopathy, atrial fibrillation, and cardioembolic stroke remains obscure. This review summarizes the pathogenesis of atrial cardiomyopathy, with a special focus on neurohormonal and inflammatory mechanisms, as well as the role of adipose tissue, especially epicardial fat in atrial remodelling. It reviews the current evidence implicating atrial cardiomyopathy as a cause of embolic stroke, with atrial fibrillation as a lagging marker of an increased thrombogenic atrial substrate. Finally, it discusses the potential of antithrombotic therapy in embolic stroke with undetermined source and appraises the available diagnostic techniques for atrial cardiomyopathy, including imaging techniques such as echocardiography, computed tomography, and magnetic resonance imaging as well as electroanatomic mapping, electrocardiogram, biomarkers, and genetic testing. More prospective studies are needed to define the relationship between atrial cardiomyopathy, atrial fibrillation, and embolic stroke and to establish a prompt diagnosis and specific treatment strategies in these patients with atrial cardiomyopathy for the secondary and even primary prevention of embolic stroke.

Keywords: Atrial cardiomyopathy; Atrial fibrillation; Diagnosis; Embolic stroke; Pathogenesis.

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Conflict of interest statement

A.M.S. received educational grants through his institution from Abbott, Bayer Healthcare, Biosense Webster, Biotronik, Boston Scientific, BMS/Pfizer, and Medtronic and speaker fees/proctoring fees from Bayer Healthcare, Daiichi‐Sankyo, and Medtronic. The other authors report no conflicts of interest.

Figures

Figure 1
Figure 1
The neurohormonal mechanisms involved in atrial remodelling. Ang II, angiotensin II; AT1‐R, angiotensin receptor 1; CTGF, connective tissue growth factor; CTR, calcitonin receptor; DAG, diacylglycerol; IP3, inositol‐1,4,5‐triphosphate; MAPK, mitogen‐activated protein kinase; MMPs, matrix metalloproteinases; MR, mineralocorticoid receptor; NADPH, nicotinamide adenine dinucleotide phosphate; NF‐κB, nuclear factor‐κB; PKC, protein kinase C; PLC, phospholipase C; ROS, reactive oxygen species; TGF‐β, transforming growth factor β.
Figure 2
Figure 2
The possible mechanisms of epicardial adipose tissue promoting atrial remodelling under pathological conditions. AN, autonomic nerve; cirRNA, circular RNA; FABP, fatty acid binding protein; lncRNA, long non‐coding RNA; miRNA, microRNA; MP, membrane protein; mRNA, messenger RNA; P, proteins; ROS, reactive oxygen species; siRNA, small interfering RNA; tRNA, transfer RNA.
Figure 3
Figure 3
The relationship between inflammation and atrial thrombosis in patients with ACM or AF. ACM, atrial cardiomyopathy; AF, atrial fibrillation; eNOS, endothelial nitric oxide synthase; PAR‐1, protease‐activated receptor 1; TF, tissue factor; vWF, von Willebrand factor.

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