title: Left Atrial Performance in the Course of Hypertrophic Cardiomyopathy: Relation to Left Ventricular Hypertrophy and Fibrosis.
abstract: Hypertrophic cardiomyopathy (HCM) is associated with left atrial (LA) functional abnormalities. The determinants and the degree of LA dysfunction in the course of HCM are not fully understood. We aimed to characterize LA mechanics in HCM, according to the extent of left ventricular (LV) hypertrophy and fibrosis.
  
  
  
  Seventy-three HCM patients and 23 age- and sex-matched controls underwent cardiovascular magnetic resonance imaging including late gadolinium enhancement (LGE). LA reservoir, conduit, and contractile functions were quantified by fractional volume changes and cardiovascular magnetic resonance feature-tracking-derived strain and strain rate. In multivariable regression, LA mechanics were associated with the extent of LV LGE (P = 0.033 to P < 0.001), but not with the LV mass extent or maximum wall thickness (P = 0.108 to P = 0.964). Left atrial function decreased according to the increase in extent of LV fibrosis (non-LGE; mild LGE ≤ 10%; intermediate LGE 11%-19%; severe LGE ≥ 20%). Compared with healthy controls, LA conduit function was impaired in HCM with no LGE already (LA emptying fraction conduit: 32% ± 7% vs 26 ± 14, P = 0.037). Conversely, LA contractile booster pump function was impaired in HCM with severe LGE only (LA emptying fraction booster: 40% ± 8% vs 20% ± 10%, P < 0.001; for controls vs LGE ≥ 20%, respectively).
  
  
  
  Left atrial functional abnormalities are associated with LV fibrosis, but not with LV hypertrophy. While LA conduit function is impaired in early HCM stages as represented by mild or absent LV fibrosis, LA contractile function is impaired later in the course of disease progression as demonstrated by the presence of severe LV fibrosis only. These novel markers of LA performance may potentially proof useful for disease staging and early detection of cardiac deterioration.
authors.affiliation: From the *Division of Imaging Sciences and Biomedical Engineering, Department of Cardiovascular Imaging, King's College London, St Thomas' Hospital, London, United Kingdom; †Institute for Diagnostic and Interventional Radiology, University Medical Centre Göttingen, Georg-August-University; ‡DZHK (German Centre for Cardiovascular Research), Partner Site Göttingen, Göttingen, Germany; §Children's Hospital and Medical Center, University of Nebraska College of Medicine, Omaha, NE; and ∥Department of Cardiology and Pneumology, University Medical Centre Göttingen, Georg-August-University, Göttingen, Germany.
authors.forename: Johannes T
authors.initials: JT
authors.lastname: Kowallick
authors.forename: Miguel
authors.initials: M
authors.lastname: Silva Vieira
authors.forename: Shelby
authors.initials: S
authors.lastname: Kutty
authors.forename: Joachim
authors.initials: J
authors.lastname: Lotz
authors.forename: Gerd
authors.initials: G
authors.lastname: Hasenfu
authors.forename: Amedeo
authors.initials: A
authors.lastname: Chiribiri
authors.forename: Andreas
authors.initials: A
authors.lastname: Schuster
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D002312:Cardiomyopathy, Hypertrophic / Q000000981:diagnostic imaging / Q000473:pathology* / Q000503:physiopathology*; D003287:Contrast Media; D005260:Female; D005355:Fibrosis; D005682:Gadolinium; D006325:Heart Atria / Q000503:physiopathology; D006352:Heart Ventricles / Q000000981:diagnostic imaging / Q000473:pathology / Q000503:physiopathology; D006801:Humans; D017379:Hypertrophy, Left Ventricular / Q000000981:diagnostic imaging / Q000473:pathology* / Q000503:physiopathology*; D007089:Image Enhancement / Q000379:methods; D008279:Magnetic Resonance Imaging / Q000379:methods*; D008297:Male; D008875:Middle Aged
chemical_list: D003287:Contrast Media; D005682:Gadolinium