title: Myocardial function in aortic stenosis--insights from radial multilayer Doppler strain.
abstract: BACKGROUND
  Left ventricular (LV) radial tissue Doppler imaging (TDI) strain increases gradually from the subepicardial to the subendocardial layer in healthy individuals. A speckle tracking echocardiography study suggested this gradient to be reduced in parallel with increasing aortic stenosis (AS) severity.
  
  
  METHODS
  We used TDI strain in 84 patients with AS (mean age 73 ± 10 years, 56% hypertensive) for superior assessment of layer strain. 38 patients had non-severe and 46 severe AS by aortic valve area corrected for pressure recovery. Peak systolic radial TDI strain was measured in the subendocardial, mid-myocardial and subepicardial layers of the basal inferior LV wall, each within a region of interest of 2 × 6 mm (strain length 2 mm).
  
  
  RESULTS
  Radial strain was lower in the subepicardial layer (33.4 ± 38.6%) compared to the mid-myocardial and subendocardial layers (50.3 ± 37.3% and 53.0 ± 40.0%, respectively, both p < 0.001 vs. subepicardial). In the subendo- and midmyocardium, radial strain was lower in patients with severe AS compared to those with non-severe AS (p < 0.05). In multivariate regression analyses including age, heart rate, inferior wall thickness, hypertension, and AS severity, radial strain in the mid-myocardium was primarily attenuated by presence of hypertension (β = -0.23) and AS severity (β = -0.26, both p < 0.05), while radial strain in the subendocardium was significantly influenced by AS severity only (β = -0.35, p < 0.01).
  
  
  CONCLUSIONS
  In AS, both the AS severity and concomitant hypertension attenuate radial TDI strain in the inferior LV wall. The subendocardial radial strain is mainly influenced by AS severity, while midmyocardial radial strain is attenuated by both hypertension and AS severity.
authors.affiliation: Department of Heart Disease, Haukeland University Hospital, Bergen, Norway. cramariuc_dana@yahoo.com.
authors.forename: Dana
authors.initials: D
authors.lastname: Cramariuc
authors.affiliation: Department of Clinical Science, University of Bergen, Bergen, Norway. Eva.Gerdts@k2.uib.no.
authors.forename: Eva
authors.initials: E
authors.lastname: Gerdts
authors.affiliation: Department of Clinical Science, University of Bergen, Bergen, Norway. johannes@hjertaas.com.
authors.forename: Johannes Just
authors.initials: JJ
authors.lastname: Hjertaas
authors.affiliation: Department of Clinical Science, University of Bergen, Bergen, Norway. crama13@yahoo.com.
authors.forename: Alexandru
authors.initials: A
authors.lastname: Cramariuc
authors.affiliation: Department of Heart Disease, Haukeland University Hospital, Bergen, Norway. esda@helse-bergen.no.
authors.forename: Einar Skulstad
authors.initials: ES
authors.lastname: Davidsen
authors.affiliation: Department of Clinical Science, University of Bergen, Bergen, Norway. knut.matre@k2.uib.no.
authors.forename: Knut
authors.initials: K
authors.lastname: Matre
mesh_terms: D000368:Aged; D016880:Anisotropy; D001024:Aortic Valve Stenosis / Q000150:complications / Q000000981:diagnostic imaging* / Q000503:physiopathology*; D019245:Compressive Strength; D015150:Echocardiography, Doppler / Q000379:methods*; D055119:Elastic Modulus; D005260:Female; D006801:Humans; D008297:Male; D015203:Reproducibility of Results; D012680:Sensitivity and Specificity; D033081:Shear Strength; D013314:Stress, Mechanical; D013718:Tensile Strength; D018487:Ventricular Dysfunction, Left / Q000000981:diagnostic imaging* / Q000209:etiology / Q000503:physiopathology*