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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
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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).
Methods and 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.
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).
Methods and 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.
Keywords
aortic stenosis, hypertrophy, function
About this articleTitle
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
Journal
Issue
Pages
613-621
Published online
2015-06-19
Page views
1642
Article views/downloads
2328
DOI
10.5603/CJ.a2015.0034
Pubmed
Bibliographic record
Cardiol J 2015;22(6):613-621.
Keywords
aortic stenosis
hypertrophy
function
Authors
Alejandro Hita
Sergio Baratta
Guillermo Vaccarino
José Navia
Daniel Olano
Juan Manuel Telayna
Ricardo Costantini
Demian Chejtman
Miriam Matoso
Ricardo J. Gelpi
Martin Donato
Celina Morales
