Johannes T Kowallick1, Miguel Silva Vieira, Shelby Kutty, Joachim Lotz, Gerd Hasenfu, Amedeo Chiribiri, Andreas Schuster. 1. 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.
Abstract
OBJECTIVES: 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. METHODS AND RESULTS: 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). CONCLUSIONS: 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.
OBJECTIVES: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. METHODS AND RESULTS: 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). CONCLUSIONS: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: Laura Kristin Wandelt; Johannes Tammo Kowallick; Andreas Schuster; Rolf Wachter; Thomas Stümpfig; Christina Unterberg-Buchwald; Michael Steinmetz; Christian Oliver Ritter; Joachim Lotz; Wieland Staab Journal: Int J Cardiovasc Imaging Date: 2017-05-18 Impact factor: 2.357
Authors: Mariya Kuk; Simon Newsome; Francisco Alpendurada; Marc Dweck; Dudley J Pennell; Vassilios S Vassiliou; Sanjay K Prasad Journal: JRSM Cardiovasc Dis Date: 2020-04-27
Authors: Johannes T Kowallick; Geraint Morton; Pablo Lamata; Roy Jogiya; Shelby Kutty; Gerd Hasenfuß; Joachim Lotz; Amedeo Chiribiri; Eike Nagel; Andreas Schuster Journal: JRSM Cardiovasc Dis Date: 2017-05-15
Authors: Andreas Schuster; Sören J Backhaus; Thomas Stiermaier; Jenny-Lou Navarra; Johannes Uhlig; Karl-Philipp Rommel; Alexander Koschalka; Johannes T Kowallick; Boris Bigalke; Shelby Kutty; Matthias Gutberlet; Gerd Hasenfuß; Holger Thiele; Ingo Eitel Journal: J Clin Med Date: 2020-01-12 Impact factor: 4.241