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Atrial Cardiomyopathy in Valvular Heart Disease: From Molecular Biology to Clinical Perspectives
This review discusses the evolving topic of atrial cardiomyopathy concerning valvular heart disease. The pathogenesis of atrial cardiomyopathy involves multiple factors, such as valvular disease leading to atrial structural and functional remodeling due to pressure and volume overload. Atrial enlarg...
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Published in: | Cells (Basel, Switzerland) Switzerland), 2023-07, Vol.12 (13), p.1796 |
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description | This review discusses the evolving topic of atrial cardiomyopathy concerning valvular heart disease. The pathogenesis of atrial cardiomyopathy involves multiple factors, such as valvular disease leading to atrial structural and functional remodeling due to pressure and volume overload. Atrial enlargement and dysfunction can trigger atrial tachyarrhythmia. The complex interaction between valvular disease and atrial cardiomyopathy creates a vicious cycle of aggravating atrial enlargement, dysfunction, and valvular disease severity. Furthermore, atrial remodeling and arrhythmia can predispose to atrial thrombus formation and stroke. The underlying pathomechanism of atrial myopathy involves molecular, cellular, and subcellular alterations resulting in chronic inflammation, atrial fibrosis, and electrophysiological changes. Atrial dysfunction has emerged as an essential determinant of outcomes in valvular disease and heart failure. Despite its predictive value, the detection of atrial fibrosis and dysfunction is challenging and is not included in the clinical routine. Transthoracic echocardiography and cardiac magnetic resonance imaging are the main diagnostic tools for atrial cardiomyopathy. Recently published data have revealed that both left atrial volumes and functional parameters are independent predictors of cardiovascular events in valvular disease. The integration of atrial function assessment in clinical practice might help in early cardiovascular risk estimation, promoting early therapeutic intervention in valvular disease. |
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The pathogenesis of atrial cardiomyopathy involves multiple factors, such as valvular disease leading to atrial structural and functional remodeling due to pressure and volume overload. Atrial enlargement and dysfunction can trigger atrial tachyarrhythmia. The complex interaction between valvular disease and atrial cardiomyopathy creates a vicious cycle of aggravating atrial enlargement, dysfunction, and valvular disease severity. Furthermore, atrial remodeling and arrhythmia can predispose to atrial thrombus formation and stroke. The underlying pathomechanism of atrial myopathy involves molecular, cellular, and subcellular alterations resulting in chronic inflammation, atrial fibrosis, and electrophysiological changes. Atrial dysfunction has emerged as an essential determinant of outcomes in valvular disease and heart failure. Despite its predictive value, the detection of atrial fibrosis and dysfunction is challenging and is not included in the clinical routine. Transthoracic echocardiography and cardiac magnetic resonance imaging are the main diagnostic tools for atrial cardiomyopathy. Recently published data have revealed that both left atrial volumes and functional parameters are independent predictors of cardiovascular events in valvular disease. The integration of atrial function assessment in clinical practice might help in early cardiovascular risk estimation, promoting early therapeutic intervention in valvular disease.</description><identifier>ISSN: 2073-4409</identifier><identifier>EISSN: 2073-4409</identifier><identifier>DOI: 10.3390/cells12131796</identifier><identifier>PMID: 37443830</identifier><language>eng</language><publisher>Switzerland: MDPI AG</publisher><subject>Analysis ; aortic valve stenosis ; Arrhythmia ; atrial cardiomyopathy ; Atrial Fibrillation ; Biomarkers ; Cardiac arrhythmia ; Cardiomyocytes ; Cardiomyopathies - complications ; Cardiomyopathy ; Cardiovascular disease ; Cardiovascular diseases ; Care and treatment ; Collagen ; Congestive heart failure ; Diagnosis ; Echocardiography ; Electrophysiology ; Enlargement ; Extracellular matrix ; Fibroblasts ; Fibrosis ; Growth factors ; Heart diseases ; Heart failure ; Heart Failure - complications ; Heart valve diseases ; Heart Valve Diseases - complications ; Heart Valve Diseases - drug therapy ; Hemodynamics ; Hormones ; Humans ; Inflammation ; Kinases ; Magnetic resonance imaging ; mitral valve regurgitation ; Molecular Biology ; Myopathy ; Oxidative stress ; Pathophysiology ; Peptides ; Physiology, Pathological ; Review ; Risk factors ; Serology ; Structure-function relationships ; Tachyarrhythmia ; Thrombosis</subject><ispartof>Cells (Basel, Switzerland), 2023-07, Vol.12 (13), p.1796</ispartof><rights>COPYRIGHT 2023 MDPI AG</rights><rights>2023 by the authors. 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The pathogenesis of atrial cardiomyopathy involves multiple factors, such as valvular disease leading to atrial structural and functional remodeling due to pressure and volume overload. Atrial enlargement and dysfunction can trigger atrial tachyarrhythmia. The complex interaction between valvular disease and atrial cardiomyopathy creates a vicious cycle of aggravating atrial enlargement, dysfunction, and valvular disease severity. Furthermore, atrial remodeling and arrhythmia can predispose to atrial thrombus formation and stroke. The underlying pathomechanism of atrial myopathy involves molecular, cellular, and subcellular alterations resulting in chronic inflammation, atrial fibrosis, and electrophysiological changes. Atrial dysfunction has emerged as an essential determinant of outcomes in valvular disease and heart failure. Despite its predictive value, the detection of atrial fibrosis and dysfunction is challenging and is not included in the clinical routine. Transthoracic echocardiography and cardiac magnetic resonance imaging are the main diagnostic tools for atrial cardiomyopathy. Recently published data have revealed that both left atrial volumes and functional parameters are independent predictors of cardiovascular events in valvular disease. The integration of atrial function assessment in clinical practice might help in early cardiovascular risk estimation, promoting early therapeutic intervention in valvular disease.</description><subject>Analysis</subject><subject>aortic valve stenosis</subject><subject>Arrhythmia</subject><subject>atrial cardiomyopathy</subject><subject>Atrial Fibrillation</subject><subject>Biomarkers</subject><subject>Cardiac arrhythmia</subject><subject>Cardiomyocytes</subject><subject>Cardiomyopathies - complications</subject><subject>Cardiomyopathy</subject><subject>Cardiovascular disease</subject><subject>Cardiovascular diseases</subject><subject>Care and treatment</subject><subject>Collagen</subject><subject>Congestive heart failure</subject><subject>Diagnosis</subject><subject>Echocardiography</subject><subject>Electrophysiology</subject><subject>Enlargement</subject><subject>Extracellular matrix</subject><subject>Fibroblasts</subject><subject>Fibrosis</subject><subject>Growth factors</subject><subject>Heart diseases</subject><subject>Heart failure</subject><subject>Heart Failure - complications</subject><subject>Heart valve diseases</subject><subject>Heart Valve Diseases - complications</subject><subject>Heart Valve Diseases - drug therapy</subject><subject>Hemodynamics</subject><subject>Hormones</subject><subject>Humans</subject><subject>Inflammation</subject><subject>Kinases</subject><subject>Magnetic resonance imaging</subject><subject>mitral valve regurgitation</subject><subject>Molecular Biology</subject><subject>Myopathy</subject><subject>Oxidative stress</subject><subject>Pathophysiology</subject><subject>Peptides</subject><subject>Physiology, Pathological</subject><subject>Review</subject><subject>Risk factors</subject><subject>Serology</subject><subject>Structure-function relationships</subject><subject>Tachyarrhythmia</subject><subject>Thrombosis</subject><issn>2073-4409</issn><issn>2073-4409</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid>PIMPY</sourceid><sourceid>DOA</sourceid><recordid>eNptkstvEzEQh1cIRKvSI1e0Ehcu2_r94IJCoA-pCA7A1Uy83tSRd53au5Hy3-M0pTQIW7Ktmd989oynql5jdEapRufWhZAxwRRLLZ5VxwRJ2jCG9PMn56PqNOcVKkNhgRF_WR1RyRhVFB1Xv2Zj8hDqOaTWx34b1zDebms_1D8hbKYAqb5ykMb6k88OsntfX6TY119icPbe-9HHEJfbeoz1PPjB2wL75lJeOzv6jcuvqhcdhOxOH_aT6sfF5-_zq-bm6-X1fHbTWIH52AiuGLKyZIUJXZBOEYmAWEehtRoRTjm1diEoAYH0AlsE2DJqoUVcadUhelJd77lthJVZJ99D2poI3twbYlqakoa3wRmllEVCWKK1YgK1ZdEENHdSOt5JKKwPe9Z6WvSutW4YE4QD6KFn8LdmGTcGI8rKY1khvHsgpHg3uTya3ufdb8Hg4pQNUVQRxhSiRfr2H-kqTmkotdqpBEWcC_5XtYSSgR-6WC62O6iZSS4lZoyTojr7j6rM1vXexsF1vtgPApp9gE0x5-S6xyQxMrsWMwctVvRvnlbmUf2noehveeHJ_Q</recordid><startdate>20230706</startdate><enddate>20230706</enddate><creator>Molnár, Andrea Ágnes</creator><creator>Sánta, Attila</creator><creator>Pásztor, Dorottya Tímea</creator><creator>Merkely, Béla</creator><general>MDPI AG</general><general>MDPI</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>LK8</scope><scope>M7P</scope><scope>P64</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20230706</creationdate><title>Atrial Cardiomyopathy in Valvular Heart Disease: From Molecular Biology to Clinical Perspectives</title><author>Molnár, Andrea Ágnes ; Sánta, Attila ; Pásztor, Dorottya Tímea ; Merkely, Béla</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c615t-65840c7339123b2f8270a2ce3adc9025353ccb632a609b1c0a1c43cad05898f03</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>Analysis</topic><topic>aortic valve stenosis</topic><topic>Arrhythmia</topic><topic>atrial cardiomyopathy</topic><topic>Atrial Fibrillation</topic><topic>Biomarkers</topic><topic>Cardiac arrhythmia</topic><topic>Cardiomyocytes</topic><topic>Cardiomyopathies - complications</topic><topic>Cardiomyopathy</topic><topic>Cardiovascular disease</topic><topic>Cardiovascular diseases</topic><topic>Care and treatment</topic><topic>Collagen</topic><topic>Congestive heart failure</topic><topic>Diagnosis</topic><topic>Echocardiography</topic><topic>Electrophysiology</topic><topic>Enlargement</topic><topic>Extracellular matrix</topic><topic>Fibroblasts</topic><topic>Fibrosis</topic><topic>Growth factors</topic><topic>Heart diseases</topic><topic>Heart failure</topic><topic>Heart Failure - complications</topic><topic>Heart valve diseases</topic><topic>Heart Valve Diseases - complications</topic><topic>Heart Valve Diseases - drug therapy</topic><topic>Hemodynamics</topic><topic>Hormones</topic><topic>Humans</topic><topic>Inflammation</topic><topic>Kinases</topic><topic>Magnetic resonance imaging</topic><topic>mitral valve regurgitation</topic><topic>Molecular Biology</topic><topic>Myopathy</topic><topic>Oxidative stress</topic><topic>Pathophysiology</topic><topic>Peptides</topic><topic>Physiology, Pathological</topic><topic>Review</topic><topic>Risk factors</topic><topic>Serology</topic><topic>Structure-function relationships</topic><topic>Tachyarrhythmia</topic><topic>Thrombosis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Molnár, Andrea Ágnes</creatorcontrib><creatorcontrib>Sánta, Attila</creatorcontrib><creatorcontrib>Pásztor, Dorottya Tímea</creatorcontrib><creatorcontrib>Merkely, Béla</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>AUTh Library subscriptions: ProQuest Central</collection><collection>ProQuest Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</collection><collection>Engineering Research Database</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Biological Science Collection</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>Directory of Open Access Journals</collection><jtitle>Cells (Basel, Switzerland)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Molnár, Andrea Ágnes</au><au>Sánta, Attila</au><au>Pásztor, Dorottya Tímea</au><au>Merkely, Béla</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Atrial Cardiomyopathy in Valvular Heart Disease: From Molecular Biology to Clinical Perspectives</atitle><jtitle>Cells (Basel, Switzerland)</jtitle><addtitle>Cells</addtitle><date>2023-07-06</date><risdate>2023</risdate><volume>12</volume><issue>13</issue><spage>1796</spage><pages>1796-</pages><issn>2073-4409</issn><eissn>2073-4409</eissn><abstract>This review discusses the evolving topic of atrial cardiomyopathy concerning valvular heart disease. The pathogenesis of atrial cardiomyopathy involves multiple factors, such as valvular disease leading to atrial structural and functional remodeling due to pressure and volume overload. Atrial enlargement and dysfunction can trigger atrial tachyarrhythmia. The complex interaction between valvular disease and atrial cardiomyopathy creates a vicious cycle of aggravating atrial enlargement, dysfunction, and valvular disease severity. Furthermore, atrial remodeling and arrhythmia can predispose to atrial thrombus formation and stroke. The underlying pathomechanism of atrial myopathy involves molecular, cellular, and subcellular alterations resulting in chronic inflammation, atrial fibrosis, and electrophysiological changes. Atrial dysfunction has emerged as an essential determinant of outcomes in valvular disease and heart failure. Despite its predictive value, the detection of atrial fibrosis and dysfunction is challenging and is not included in the clinical routine. Transthoracic echocardiography and cardiac magnetic resonance imaging are the main diagnostic tools for atrial cardiomyopathy. Recently published data have revealed that both left atrial volumes and functional parameters are independent predictors of cardiovascular events in valvular disease. The integration of atrial function assessment in clinical practice might help in early cardiovascular risk estimation, promoting early therapeutic intervention in valvular disease.</abstract><cop>Switzerland</cop><pub>MDPI AG</pub><pmid>37443830</pmid><doi>10.3390/cells12131796</doi><oa>free_for_read</oa></addata></record> |
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subjects | Analysis aortic valve stenosis Arrhythmia atrial cardiomyopathy Atrial Fibrillation Biomarkers Cardiac arrhythmia Cardiomyocytes Cardiomyopathies - complications Cardiomyopathy Cardiovascular disease Cardiovascular diseases Care and treatment Collagen Congestive heart failure Diagnosis Echocardiography Electrophysiology Enlargement Extracellular matrix Fibroblasts Fibrosis Growth factors Heart diseases Heart failure Heart Failure - complications Heart valve diseases Heart Valve Diseases - complications Heart Valve Diseases - drug therapy Hemodynamics Hormones Humans Inflammation Kinases Magnetic resonance imaging mitral valve regurgitation Molecular Biology Myopathy Oxidative stress Pathophysiology Peptides Physiology, Pathological Review Risk factors Serology Structure-function relationships Tachyarrhythmia Thrombosis |
title | Atrial Cardiomyopathy in Valvular Heart Disease: From Molecular Biology to Clinical Perspectives |
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