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The search for a gold standard to clinically diagnose and monitor atrial cardiomyopathy

  • Giuseppe Boriani
    Correspondence
    Corresponding author: Via del Pozzo, 71, 41124 Modena, Italy.
    Affiliations
    Cardiology Division, Department of Biomedical, Metabolic and Neural Sciences, University of Modena and Reggio Emilia, Policlinico di Modena, Modena, Italy
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  • Marco Vitolo
    Affiliations
    Cardiology Division, Department of Biomedical, Metabolic and Neural Sciences, University of Modena and Reggio Emilia, Policlinico di Modena, Modena, Italy

    Clinical and Experimental Medicine PhD Program, University of Modena and Reggio Emilia, Modena, Italy

    Liverpool Centre for Cardiovascular Science, University of Liverpool and Liverpool Heart & Chest Hospital, Liverpool, UK
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  • Jacopo Francesco Imberti
    Affiliations
    Cardiology Division, Department of Biomedical, Metabolic and Neural Sciences, University of Modena and Reggio Emilia, Policlinico di Modena, Modena, Italy

    Clinical and Experimental Medicine PhD Program, University of Modena and Reggio Emilia, Modena, Italy

    Liverpool Centre for Cardiovascular Science, University of Liverpool and Liverpool Heart & Chest Hospital, Liverpool, UK
    Search for articles by this author
      Atrial cardiomyopathy (AC) is currently defined as “any complex of structural, architectural, contractile or electrophysiological changes affecting the atria with the potential to produce clinically-relevant manifestations” [
      • Goette A.
      • Kalman J.M.
      • Aguinaga L.
      • Akar J.
      • Cabrera J.A.
      • Chen S.A.
      • et al.
      EHRA/HRS/APHRS/SOLAECE expert consensus on atrial cardiomyopathies: definition, characterization, and clinical implication.
      ]. This clinical entity has recently gained relevance for a number of reasons. First, it is well known that AC contributes to atrial fibrillation (AF)-related thromboembolism. Indeed, several AC markers (e.g.: left atrial [LA] size and geometry, LA appendage shape and function, spontaneous echo contrast, LA fibrosis, biomarkers of myocardial stress and injury, epicardial fat, etc.) are associated with an increased risk of stroke in AF patients [
      • Goldberger J.J.
      • Arora R.
      • Green D.
      • Greenland P.
      • Lee D.C.
      • Lloyd-Jones D.M.
      • et al.
      Evaluating the Atrial Myopathy Underlying Atrial Fibrillation: identifying the Arrhythmogenic and Thrombogenic Substrate.
      ,
      • Eren H.
      • Omar M.B.
      • Kaya Ü.
      • Öcal L.
      • Yilmaz M.F.
      • Akkan S.
      Epicardial adipose tissue may predict new-onset atrial fibrillation in patients with ST-segment elevation myocardial infarction.
      ]. Secondly, AC might be responsible for a proportion of strokes occurring in patients without rhythm disturbances. In a secondary analysis of the NAVIGATE ESUS randomized controlled trial, Healey et al. [
      • Healey J.S.
      • Gladstone D.J.
      • Swaminathan B.
      • Eckstein J.
      • Mundl H.
      • Epstein A.E.
      • et al.
      Recurrent Stroke With Rivaroxaban Compared With Aspirin According to Predictors of Atrial Fibrillation: secondary Analysis of the NAVIGATE ESUS Randomized Clinical Trial.
      ] showed that oral anticoagulants (OACs) reduced the risk of recurrent stroke in patients with embolic stroke of undetermined source (ESUS) and moderate or severe LA enlargement. Similarly, other evidences of abnormal atrial substrate (e.g.: LA and LA appendage function, LA fibrosis on cardiac magnetic resonance imaging [MRI], and P-wave terminal force in ECG lead V1) have been found associated with incident stroke [
      • Freedman B.
      • Kamel H.
      • Van Gelder I.C.
      • Schnabel R.B.
      Atrial fibrillation: villain or bystander in vascular brain injury.
      ]. In a EHRA/HRS/APHRS/SOLAECE consensus document [
      • Goette A.
      • Kalman J.M.
      • Aguinaga L.
      • Akar J.
      • Cabrera J.A.
      • Chen S.A.
      • et al.
      EHRA/HRS/APHRS/SOLAECE expert consensus on atrial cardiomyopathies: definition, characterization, and clinical implication.
      ], four classes of AC were identified: (i) principal cardiomyocyte changes; (ii) principally fibrotic changes; (iii) combined cardiomyocyte-pathology/fibrosis; and (iv) primarily non-collagen infiltration (with or without cardiomyocyte changes). Although useful, this classification is based only on histopathologic findings, which is a limit to its large-scale applicability. Several parameters that can more easily assessed, such as echocardiography measurements, MRI findings, ECG findings, biomarkers levels, and invasive electro-anatomic mapping have been proposed for AC diagnosis, but their role needs to be further elucidated.

      Keywords

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