EHRA/HRS/APHRS/SOLAECE expert consensus on Atrial cardiomyopathies: Definition, characterisation, and clinical implication

Besides their impact on ventricular filling, they serve as a volume reservoir, host pacemaker cells and important parts of the cardiac conduction system (e.g. sinus node, AV node), and secrete natriuretic peptides like atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) that regulat...

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Published in:Journal of arrhythmia Vol. 32; no. 4; pp. 247 - 278
Main Authors: Goette, Andreas, Kalman, Jonathan M, Aguinaga, Luis, Akar, Joseph, Cabrera, Jose Angel, Chen, Shih Ann, Chugh, Sumeet S, Corradi, Domenico, D׳Avila, Andre, Dobrev, Dobromir, Fenelon, Guilherme, Gonzalez, Mario, Hatem, Stephane N, Helm, Robert, Hindricks, Gerhard, Ho, Siew Yen, Hoit, Brian, Jalife, Jose, Kim, Young-Hoon, Lip, Gregory Y.H, Ma, Chang-Sheng, Marcus, Gregory M, Murray, Katherine, Nogami, Akihiko, Sanders, Prashanthan, Uribe, William, Van Wagoner, David, Nattel, Stanley
Format: Journal Article
Language:English
Published: Japan John Wiley & Sons, Inc 01-08-2016
Elsevier
Wiley
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Abstract Besides their impact on ventricular filling, they serve as a volume reservoir, host pacemaker cells and important parts of the cardiac conduction system (e.g. sinus node, AV node), and secrete natriuretic peptides like atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) that regulate fluid homoeostasis. [...]atrial cells (both cardiomyocytes and non-cardiomyocyte elements like fibroblasts, endothelial cells, and neurons) react briskly and extensively to pathological stimuli [3] and are susceptible to a range of genetic influences [7]. [...]atrial pathologies have a substantial impact on cardiac performance, arrhythmia occurrence, and stroke risk [1,8]. [...]while some pathological processes may affect the atria very selectively (e.g. atrial fibrillation-induced remodelling), most cardiomyopathies that affect the atria also involve the ventricles to a greater or lesser extent. [...]we have proposed here a working histological/ pathopysiological classification scheme for atrial cardiomyopathies ( Table 1; Fig. 1). [...]this classification is purely descriptive and in contrast to other classifications (NYHA class, CCS class etc.), there is no progression in severity from EHRAS class I to EHRAS IV ( Table 2). Unlike ventricular cardiomyocytes, atrial cardiomyocytes do not possess an extensive T-tubule network but they do have prominent sarcoplasmic reticulum (SR) elements known as Z-tubules [33]. [...]the atrial sarcolemma does not protrude into the cell, and voltage-operated Ca2+ channels mainly function at the cell periphery [34].
AbstractList Besides their impact on ventricular filling, they serve as a volume reservoir, host pacemaker cells and important parts of the cardiac conduction system (e.g. sinus node, AV node), and secrete natriuretic peptides like atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) that regulate fluid homoeostasis. [...]atrial cells (both cardiomyocytes and non-cardiomyocyte elements like fibroblasts, endothelial cells, and neurons) react briskly and extensively to pathological stimuli [3] and are susceptible to a range of genetic influences [7]. [...]atrial pathologies have a substantial impact on cardiac performance, arrhythmia occurrence, and stroke risk [1,8]. [...]while some pathological processes may affect the atria very selectively (e.g. atrial fibrillation-induced remodelling), most cardiomyopathies that affect the atria also involve the ventricles to a greater or lesser extent. [...]we have proposed here a working histological/ pathopysiological classification scheme for atrial cardiomyopathies ( Table 1; Fig. 1). [...]this classification is purely descriptive and in contrast to other classifications (NYHA class, CCS class etc.), there is no progression in severity from EHRAS class I to EHRAS IV ( Table 2). Unlike ventricular cardiomyocytes, atrial cardiomyocytes do not possess an extensive T-tubule network but they do have prominent sarcoplasmic reticulum (SR) elements known as Z-tubules [33]. [...]the atrial sarcolemma does not protrude into the cell, and voltage-operated Ca2+ channels mainly function at the cell periphery [34].
Author Nattel, Stanley
Cabrera, Jose Angel
Dobrev, Dobromir
Akar, Joseph
Kim, Young-Hoon
Chugh, Sumeet S
Marcus, Gregory M
Ho, Siew Yen
Uribe, William
Goette, Andreas
Chen, Shih Ann
Ma, Chang-Sheng
Corradi, Domenico
Nogami, Akihiko
Hatem, Stephane N
Hoit, Brian
Jalife, Jose
Lip, Gregory Y.H
Sanders, Prashanthan
D׳Avila, Andre
Fenelon, Guilherme
Helm, Robert
Murray, Katherine
Gonzalez, Mario
Aguinaga, Luis
Van Wagoner, David
Kalman, Jonathan M
Hindricks, Gerhard
AuthorAffiliation q UH Case Medical Center, Cleveland, OH, USA
k Federal University of Sao Paulo, San Paulo, Brazil
t University of Birmingham, Birmingham, UK
c Centro Privado de Cardiología, Tucumán, Argentina
e European University Quiron-Madrid, Madrid, Spain
z Electrophysiology Deparment at Centros Especializados de San Vicente Fundació n and Clínica CES. Universidad CES, Universidad Pontificia Bolivariana (UPB), Medellin, Colombia
y Centre for Heart Rhythm Disorders, South Australian Health and Medical Research Institute, University of Adelaide and Royal Adelaide Hospital, Adelaide, Australia
o University of Leipzig Heart Center, Leipzig, Germany
x University of Tsukuba, Ibaraki, Japan
r University of Michigan, Ann Arbor, MI, USA
f Veterans General Hospital, Taipei, Taiwan
d Yale University, New Haven, CT, USA
b University of Melbourne, Royal Melbourne Hospital, Melbourne, VIC, Australia
u Anzhen Hospital, Beijing, China
w Vanderbilt University, Nashville, TN, USA
p Royal Brompton Hospital and Imperial College Lon
AuthorAffiliation_xml – name: i Mount Sinai School of Medicine, New York, NY, USA
– name: d Yale University, New Haven, CT, USA
– name: h University of Parma, Parma, Italy
– name: s Korea University Medical Center, Seoul, South Korea
– name: k Federal University of Sao Paulo, San Paulo, Brazil
– name: c Centro Privado de Cardiología, Tucumán, Argentina
– name: t University of Birmingham, Birmingham, UK
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– name: p Royal Brompton Hospital and Imperial College London, London, UK
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– name: l Penn State Heart and Vascular Institute, Penn State University, Hershey, PA, USA
– name: w Vanderbilt University, Nashville, TN, USA
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– name: aa Department of Molecular Cardiology, Cleveland Clinic, Cleveland, OH, USA
– name: x University of Tsukuba, Ibaraki, Japan
– name: u Anzhen Hospital, Beijing, China
– name: y Centre for Heart Rhythm Disorders, South Australian Health and Medical Research Institute, University of Adelaide and Royal Adelaide Hospital, Adelaide, Australia
– name: a Departement of Cardiology and Intensive Care Medicine, St. Vincenz-Hospital Paderborn, Working Group: Molecular Electrophysiology, University Hospital Magdeburg, Germany
– name: j Institute of Pharmacology, West German Heart and Vascular Center, University Duisburg-Essen, Essen, Germany
– name: q UH Case Medical Center, Cleveland, OH, USA
– name: o University of Leipzig Heart Center, Leipzig, Germany
– name: g The Heart Institute, Cedars-Sinai Medical Center, Los Angeles, CA, USA
– name: ab Université de Montréal, Montreal Heart Institute Research Center and McGill University, Montreal, Quebec, Canada
– name: n Boston University School of Medicine, Boston Medical Center, Boston, MA, USA
Author_xml – sequence: 1
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/27588148$$D View this record in MEDLINE/PubMed
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Document Reviewers: Osmar A. Centurion (Paraguay), Karl‐Heinz Kuck (Germany), Kristen K. Patton (USA), John L. Sapp (Canada), Martin Stiles (New Zealand), Jesper Hastrup Svendsen (Denmark), and Gaurav A. Upadhyay (USA)
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Notes Developed in partnership with the European Heart Rhythm Association (EHRA), (a registered branch of the European Society of Cardiology (ESC)) the Heart Rhythm Society (HRS), the Asia Pacific Heart Rhythm Society (APHRS), the Sociedad Latino Americana de Estimulación Cardíca y Electrofisiología (SOLAECE), and in collaboration with the American College of Cardiology (ACC), the American Heart Association (AHA). Endorsed by SOLAECE in May 2016, pending endorsement by HRS, APHRS, AHA, and ACC.
Presidente Sociedad de Cardiología de Tucumàn, Ex‐PRESIDENTE DE SOLAECE, Sociedad Latinoamericana de Estimulació nCardíaca y Electrofisiología. Tel.: +54 381 4217676.
Endorsed by EHRA, APHRS, SOLAECE in May 2016, by HRS, AHA, ACC in June 2016.
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Presidente Sociedad de Cardiología de Tucumàn, Ex-PRESIDENTE DE SOLAECE, Sociedad Latinoamericana de Estimulació nCardíaca y Electrofisiología. Tel.: +54 381 4217676.
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2008; 31
2012; 14
2012; 13
1972; 45
2005; 66
2005; 67
2011; 124
2006; 449
1986; 8
1995; 25
2008; 29
2007; 297
2002; 89
2002; 88
2013; 112
2008; 117
2008; 359
2008; 358
2008; 21
2012; 29
2002; 90
2010; 3
2010; 2
2012; 23
2011; 123
2012; 21
2010; 7
2001; 52
1992; 3
2011; 121
2004; 43
2004; 44
2007; 18
2006; 119
1992; 262
2013; 106
1996; 94
2008; 128
1964; 26
2008; 126
1999; 100
2008; 52
1977; 89
2011; 4
2008; 51
2012; 35
2016; 17
2012; 33
1996; 98
2014; 311
2011; 9
2006; 113
2006; 109
1987; 60
2009; 71
2005; 95
2005; 96
1999; 34
1999; 31
2001; 37
1999; 30
2010; 170
2005; 2
2006; 105
1959; 58
1996; 87
2016; 9
1998; 9
2010; 56
2010; 55
1990; 11
2013; 28
1997; 81
2002; 53
1990; 16
2013; 24
2002; 54
2015; 187
2004; 68
2011; 97
2014; 68
2008; 5
1995; 333
2014; 63
2008; 1
2008; 72
2014; 175
2001; 104
2003; 98
2014; 64
2007; 38
2013; 19
2007; 28
2013; 18
2013; 14
2003; 90
2014; 3
2003; 91
2003; 92
2001
2013; 11
2013; 10
1993; 72
1947; 34
1997; 96
2002; 40
2003; 7
2005; 149
2002; 43
1999; 15
1987; 317
2007; 131
2004; 79
2002; 106
2013; 310
2003; 4
2002; 105
2001; 12
1981; 30
2014; 7
2003; 89
2015; 1
2000; 279
2006; 17
2007; 243
2006; 15
2015; 165
2010; 121
2006; 151
2006; 19
2004; 90
2008; 94
2015; 8
2012; 303
2016; 120
2007; 114
2007; 115
2004; 94
2011; 108
2007; 116
2004; 93
1997; 77
2013; 34
2002; 23
2007; 232
1995; 108
1995; 346
2009; 7
2015
2009; 6
2009; 2
1989; 13
2010; 96
2014; 76
2007; 49
2010; 12
1997; 157
2007; 104
2010; 11
1993; 24
2013; 3
2010; 16
2013; 2
2010; 19
1997; 151
1997; 272
2010; 106
2000; 139
1993; 22
2006; 37
2014; 27
2014; 25
1970; 32
2011; 57
2007; 71
2006; 291
1998; 83
2011; 58
2012; 125
2012; 126
2013; 8
2009; 119
2014; 130
2013; 6
2014; 23
2011; 197
2014; 129
2009; 11
2010; 21
2010; 20
1990; 45
2009; 10
1991; 100
2010; 29
2006; 27
2004; 292
2014; 16
2014; 15
2011; 65
2003; 41
1994; 74
2014; 12
2003; 42
2014; 11
2010; 33
2006; 56
2005; 111
1997; 20
2005; 112
1994; 89
1997; 29
2007; 93
2014; 2014
2012; 109
1995; 8
2003; 34
2010; 45
2011; 301
1990; 21
2003; 108
2012; 110
1983; 244
2010; 48
2003; 107
1991; 69
2011; 91
2011; 92
2015; 66
2006; 47
2015; 65
2006; 48
2000; 75
2014; 35
2011; 89
2000; 101
2014; 39
1988; 20
2005; 18
2009; 103
2009; 104
2009; 105
2006; 70
2012; 60
1995; 73
2015; 36
2004; 126
2015; 104
1987; 148
2000; 46
2015; 101
2012; 160
1995; 76
2015; 32
1994; 23
2013; 167
2003; 14
2005; 20
2011; 13
1983; 50
2011; 12
1999; 84
1999; 83
2012; 59
2005; 26
2001; 88
2001; 89
1993; 2
2003; 111
1987; 153
2009; 58
2013; 718
2006; 63
1966; 28
2009; 54
2009; 53
2013; 99
2013; 159
1997; 14
2011; 20
2011; 22
2011; 24
2011; 25
2005; 37
2008; 155
2005; 36
2006; 92
2015; 12
2009; 22
2012; 141
2009; 25
1984; 86
1995; 92
2006; 97
2006; 98
2008; 19
2015; 10
2008; 17
2011; 31
2009; 132
2011; 32
2008; 10
2006; 3
2011; 34
2009; 373
2004; 109
2014; 111
2014; 114
2005; 45
2009; 26
1990; 82
2009; 29
2015; 24
2015; 26
1997; 248
2004; 351
1998; 39
2009; 30
2012; 154
2015; 28
2009; 32
2009; 31
2000; 35
2004; 17
2000; 32
1984; 79
2004; 13
1999; 78
1994; 58
1972; 34
2011; 183
2012; 5
2004; 117
1998; 31
2005; 55
2014; 588
2012; 9
2001; 76
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e_1_2_11_339_2
e_1_2_11_270_2
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e_1_2_11_293_2
e_1_2_11_108_2
e_1_2_11_15_2
e_1_2_11_38_2
e_1_2_11_414_2
e_1_2_11_380_2
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SubjectTerms Autopsies
Biopsy
Cardiac arrhythmia
Cardiomyocytes
Cardiomyopathy
Cardiovascular
Classification
Collagen
Disease
Guideline
Heart
Morphology
Myocarditis
Pathology
Peptides
Veins & arteries
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Title EHRA/HRS/APHRS/SOLAECE expert consensus on Atrial cardiomyopathies: Definition, characterisation, and clinical implication
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