TY - JOUR
T1 - The Complex Relation between Atrial Cardiomyopathy and Thrombogenesis
AU - D'Alessandro, E.
AU - Winters, J.
AU - van Nieuwenhoven, F.A.
AU - Schotten, U.
AU - Verheule, S.
N1 - Funding Information:
This work was supported by grants from the Netherlands Heart Foundation (CVON2014-09, RACE V Reappraisal of Atrial Fibrillation: Interaction between hyper Coagulability, Electrical remodeling, and Vascular Destabilisation in the Progression of AF) and the European Union (ITN Network Personalize AF: Personalized Therapies for Atrial Fibrillation: a translational network, grant number 860974; CATCH ME: Characterizing Atrial fibrillation by Translating its Causes into Health Modifiers in the Elderly, grant number 633196; MAESTRIA: Machine Learning Artificial Intelligence Early Detection Stroke Atrial Fibrillation, grant number 965286; REPAIR: Restoring cardiac mechanical function by polymeric artificial muscular tissue, grant number 952166).
Publisher Copyright:
© 2022 by the authors.
PY - 2022/10/1
Y1 - 2022/10/1
N2 - 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.
AB - 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.
KW - BLOOD-FLOW
KW - CANINE MODELS
KW - CARDIAC FIBROBLASTS
KW - EPICARDIAL ADIPOSE-TISSUE
KW - FACTOR XA
KW - FIBRILLATION
KW - RISK-FACTORS
KW - SEX-DIFFERENCES
KW - STRUCTURAL HEART-DISEASE
KW - VON-WILLEBRAND-FACTOR
KW - atrial cardiomyopathy
KW - atrial fibrillation
KW - cardiac remodeling
KW - thrombogenesis
U2 - 10.3390/cells11192963
DO - 10.3390/cells11192963
M3 - (Systematic) Review article
C2 - 36230924
SN - 2073-4409
VL - 11
JO - Cells
JF - Cells
IS - 19
M1 - 2963
ER -