title: Can myocardial strain differentiate hypertrophic from infiltrative etiology of a thickened septum?
abstract: OBJECTIVE
  Radial systolic strain (ε) assessed by echocardiography has been shown to identify patterns of normal septal motion brought about by different layers, including left ventricular (LV) subendocardial (LV subendo) and mural (LV mural) layers. We aimed to use myocardial strain in assessing radial and longitudinal myocardial function in normal and thickened septum and to test if myocardial strain can differentiate hypertrophic from infiltrative cause of thickened septum.
  
  
  METHODS
  Forty-five patients (age 61 ± 13 years, 22 males), 13 with hypertrophic cardiomyopathy, 15 with aortic stenosis, and 17 with familial amyloid polyneuropathy, were studied and compared with 29 controls (age 61 ± 12 years, 17 males) using 1D strain and conventional echocardiography.
  
  
  RESULTS
  Patients had normal LV ejection fraction and stroke volume but heart rate was higher (P < 0.05) compared to controls. Septal ɛ was reduced (-7.6 ± 7.0% vs. -14.0 ± 5.5%, for LV mural and -7.9 ± 14.7% vs. -20.3 ±-7.9% for LV subendo, P < 0.001 for both layers) across LV longitudinal axis but not along its radial axis. No difference was found in any of ɛ measurements between patient groups. A decrease in strain length by 50% increased the septal strain by more than 60% in both radial and longitudinal axes.
  
  
  CONCLUSIONS
  Septal systolic strain measurements showed reduced longitudinal function but its localized nature failed to demonstrate radial disturbances in patients with pathologically thickened septum. No difference was found in systolic strain between patients according to the etiology of septal thickness. This limitation might be either technical or is explained by the maintained radial function in all patient groups.
authors.affiliation: Department of Clinical Physiology, Heart Centre, Umeå University Hospital, Umeå, Sweden.
authors.forename: Christer
authors.initials: C
authors.lastname: Engvall
authors.forename: Michael
authors.initials: M
authors.lastname: Henein
authors.forename: Anders
authors.initials: A
authors.lastname: Holmgren
authors.forename: Ole B
authors.initials: OB
authors.lastname: Suhr
authors.forename: Stellan
authors.initials: S
authors.lastname: Mörner
authors.forename: Per
authors.initials: P
authors.lastname: Lindqvist
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D028227:Amyloid Neuropathies, Familial / Q000000981:diagnostic imaging* / Q000503:physiopathology; D000704:Analysis of Variance; D001024:Aortic Valve Stenosis / Q000000981:diagnostic imaging* / Q000503:physiopathology; D002312:Cardiomyopathy, Hypertrophic / Q000000981:diagnostic imaging* / Q000503:physiopathology; D016022:Case-Control Studies; D015150:Echocardiography, Doppler / Q000379:methods*; D004562:Electrocardiography; D005260:Female; D006346:Heart Septum / Q000000981:diagnostic imaging* / Q000503:physiopathology; D006801:Humans; D017379:Hypertrophy, Left Ventricular / Q000000981:diagnostic imaging* / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D013599:Systole