title: Severe aortic stenosis with preserved ejection fraction and evidence of impairment in structure, myocardial strain and ventricular function: A new contribution to clinical decision making.
abstract: BACKGROUND
  Left ventricular ejection fraction (LVEF) is among the parameters that are usually employed to define surgical timing of severe aortic stenosis (AS). Our hypothesis states that even when their LVEF is preserved, patients with severe symptomatic AS have impaired myocardial structure and function, and such impairment is related to the deleterious progression of left ventricular hypertrophy (LVH) from the compensated to the decompensated stage, as shown by the changes in diastolic function and the increase in left ventricular end-diastolic pressure (LVEDP).
  
  
  RESULTS
  A total of 26 patients with severe AS and LVEF > 50% referred for aortic valve replacement underwent catheterization, echocardiography and an intraoperative biopsy. Patients with severe symptomatic AS were classified as: group 1 (G1; compensated LVH, LVEDP < 15 mm Hg without coronary artery disease [CAD], n = 7), group 2a (G2a, decompensated LVH, without CAD, n = 7), and group 2b (G2b, decompensated LVH with CAD, n = 12). Differences were seen in the following: myocyte area [µm2]: G1: 328 ± 66, G2a: 376 ± 22, G2b: 385 ± 13, p < 0.01; collagen volume [%]: G1: 4.77 ± 1.27, G2a: 8.40 ± 1.27, G2b: 11.05 ± 3.08, p < 0.01; LVEDP normalized by diastolic diameter [mm Hg/mm]: G1: 0.27 ± 0.01, G2a: 0.39 ± 0.06, G2b: 0.44 ± 0.11, p < 0.02; +dP/dtmax/LVEDP [mm Hg/s/mm Hg]: G1: 176 ± 45, G2a: 89.6 ± 20, G2b: 113.1 ± 41, p < 0.01; two-dimensional peak systolic longitudinal strain [%]: G1: –17.7 ± 4.75, G2a: –13.4 ± 3.04, G2b: –13.5 ± 3.13, p < 0.05.
  
  
  CONCLUSIONS
  Patients with severe symptomatic AS and preserved ejection fraction who develop decompensated LVH characterized by increased LVEDP, exhibit an abnormal myocardial structure and diastolic and systolic impairment.
authors.forename: Alejandro
authors.initials: A
authors.lastname: Hita
authors.forename: Sergio
authors.initials: S
authors.lastname: Baratta
authors.forename: Guillermo
authors.initials: G
authors.lastname: Vaccarino
authors.forename: José
authors.initials: J
authors.lastname: Navia
authors.forename: Daniel
authors.initials: D
authors.lastname: Oleno
authors.forename: Juan Manuel
authors.initials: JM
authors.lastname: Telayna
authors.forename: Ricardo
authors.initials: R
authors.lastname: Costantini
authors.forename: Demian
authors.initials: D
authors.lastname: Chejtman
authors.forename: Miriam
authors.initials: M
authors.lastname: Matoso
authors.forename: Ricardo J
authors.initials: RJ
authors.lastname: Gelpi
authors.forename: Martin
authors.initials: M
authors.lastname: Donato
authors.forename: Celina
authors.initials: C
authors.lastname: Morales
mesh_terms: D000368:Aged; D001024:Aortic Valve Stenosis / Q000150:complications / Q000175:diagnosis / Q000503:physiopathology*; D001706:Biopsy; D006328:Cardiac Catheterization; D000066491:Clinical Decision-Making; D004452:Echocardiography; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D017379:Hypertrophy, Left Ventricular / Q000175:diagnosis / Q000209:etiology / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D009206:Myocardium / Q000473:pathology*; D011446:Prospective Studies; D012720:Severity of Illness Index; D013318:Stroke Volume / Q000502:physiology*; D013599:Systole; D016277:Ventricular Function, Left / Q000502:physiology*; D017725:Ventricular Pressure / Q000502:physiology