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Updated: Aug 25, 2025

Isolation of Atrial Myocytes from Adult Mice
Published on: July 25, 2019
The Complex Relation between Atrial Cardiomyopathy and Thrombogenesis
Elisa D'Alessandro1, Joris Winters1, Frans A van Nieuwenhoven1
1Department of Physiology, Cardiovascular Research Institute Maastricht, Maastricht University Medical Center, 6200 MD Maastricht, The Netherlands.
Insights
Atrial cardiomyopathy, linked to heart disease and metabolic issues, increases stroke risk by promoting blood clots. Activated clotting factors worsen this condition, creating a complex link between atrial issues and stroke.
Area of Science:
- Cardiology
- Pathophysiology
- Biochemistry
Background:
- Heart disease and metabolic disorders cause atrial cardiomyopathy, characterized by structural and functional myocardial changes.
- Fibrosis, hypertrophy, and fatty infiltration in the atria contribute to atrial fibrillation (AF) vulnerability.
- Atrial cardiomyopathy is linked to thromboembolic events, notably stroke.
Purpose of the Study:
- To review mechanisms linking atrial cardiomyopathy to thrombogenesis.
- To explore the impact of activated coagulation factors on atrial remodeling.
- To elucidate the complex relationship between AF, stroke, and atrial cardiomyopathy.
Main Methods:
- Review of existing literature on atrial cardiomyopathy, AF, and stroke.
- Analysis of pathological mechanisms in animal models.
- Examination of the role of coagulation factors in atrial remodeling.
Main Results:
- Atrial cardiomyopathy promotes thrombotic events in the atria and interstitium.
- Activated coagulation factors exert pleiotropic effects, exacerbating atrial cardiomyopathy.
- A multidirectional causal relationship exists between atrial cardiomyopathy, hypercoagulability, and stroke.
Conclusions:
- Atrial cardiomyopathy is a key driver of thrombogenesis, increasing stroke risk.
- Hypercoagulability and atrial remodeling create a vicious cycle.
- Understanding these interactions is crucial for managing AF and stroke risk.
Abstract:
Heart disease, as well as systemic metabolic alterations, can leave a 'fingerprint' of structural and functional changes in the atrial myocardium, leading to the onset of atrial cardiomyopathy. As demonstrated in various animal models, some of these changes, such as fibrosis, cardiomyocyte hypertrophy and fatty infiltration, can increase vulnerability to atrial fibrillation (AF), the most relevant manifestation of atrial cardiomyopathy in clinical practice. Atrial cardiomyopathy accompanying AF is associated with thromboembolic events, such as stroke. The interaction between AF and stroke appears to be far more complicated than initially believed. AF and stroke share many risk factors whose underlying pathological processes can reinforce the development and progression of both cardiovascular conditions. In this review, we summarize the main mechanisms by which atrial cardiomyopathy, preceding AF, supports thrombogenic events within the atrial cavity and myocardial interstitial space. Moreover, we report the pleiotropic effects of activated coagulation factors on atrial remodeling, which may aggravate atrial cardiomyopathy. Finally, we address the complex association between AF and stroke, which can be explained by a multidirectional causal relation between atrial cardiomyopathy and hypercoagulability.
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