title: Reduced global longitudinal strain in association to increased left ventricular mass in patients with aortic valve stenosis and normal ejection fraction: a hybrid study combining echocardiography and magnetic resonance imaging.
abstract: BACKGROUND
  Increased muscle mass index of the left ventricle (LVMi) is an independent predictor for the development of symptoms in patients with asymptomatic aortic stenosis (AS). While the onset of clinical symptoms and left ventricular systolic dysfunction determines a poor prognosis, the standard echocardiographic evaluation of LV dysfunction, only based on measurements of the LV ejection fraction (EF), may be insufficient for an early assessment of imminent heart failure. Contrary, 2-dimensional speckle tracking (2DS) seems to be superior in detecting subtle changes in myocardial function. The aim of the study was to assess these LV function deteriorations with global longitudinal strain (GLS) analysis and the relations to LVMi in patients with AS and normal EF.
  
  
  METHODS
  50 patients with moderate to severe AS and 31 controls were enrolled. All patients underwent echocardiography, including 2DS imaging. LVMi measures were performed with magnetic resonance imaging in 38 patients with AS and indexed for body surface area.
  
  
  RESULTS
  The total group of patients with AST showed a GLS of -15,2 +/- 3,6% while the control group reached -19,5 +/- 2,7% (p < 0,001). By splitting the group with AS in normal, moderate and severe increased LVMi, the GLS was -17,0 +/- 2,6%, -13,2 +/- 3,8% and -12,4 +/- 2,9%, respectively (p = 0,001), where LVMi and GLS showed a significant correlation (r = 0,6, p < 0,001).
  
  
  CONCLUSIONS
  In conclusion, increased LVMi is reflected in abnormalities of GLS and the proportion of GLS impairment depends on the extent of LV hypertrophy. Therefore, simultaneous measurement of LVMi and GLS might be useful to identify patients at high risk for transition into heart failure who would benefit from aortic valve replacement irrespectively of LV EF.
authors.affiliation: Institute for Heart and Circulation Research, University Witten/Herdecke, Germany. wilfried.dinh@helios-kliniken.de
authors.forename: Wilfried
authors.initials: W
authors.lastname: Dinh
authors.forename: Werner
authors.initials: W
authors.lastname: Nickl
authors.forename: Jan
authors.initials: J
authors.lastname: Smettan
authors.forename: Frank
authors.initials: F
authors.lastname: Kramer
authors.forename: Thomas
authors.initials: T
authors.lastname: Krahn
authors.forename: Thomas
authors.initials: T
authors.lastname: Scheffold
authors.forename: Michael Coll
authors.initials: MC
authors.lastname: Barroso
authors.forename: Hilmar
authors.initials: H
authors.lastname: Brinkmann
authors.forename: Till
authors.initials: T
authors.lastname: Koehler
authors.forename: Mark
authors.initials: M
authors.lastname: Lankisch
authors.forename: Reiner
authors.initials: R
authors.lastname: Füth
mesh_terms: D000368:Aged; D001024:Aortic Valve Stenosis / Q000150:complications / Q000175:diagnosis* / Q000503:physiopathology; D015150:Echocardiography, Doppler / Q000379:methods*; D005260:Female; D006352:Heart Ventricles / Q000000981:diagnostic imaging / Q000473:pathology* / Q000503:physiopathology; D006801:Humans; D008279:Magnetic Resonance Imaging / Q000379:methods*; D008297:Male; D015203:Reproducibility of Results; D012720:Severity of Illness Index; D013318:Stroke Volume / Q000502:physiology*; D018487:Ventricular Dysfunction, Left / Q000175:diagnosis* / Q000209:etiology / Q000503:physiopathology