Volume 17 Supplement 1
Turbulent kinetic energy in the ascending aorta is greater in bicuspid than tricuspid aortic valve stenosis
© Loudon et al; licensee BioMed Central Ltd. 2015
Published: 3 February 2015
The main determinant of the haemodynamic significance of aortic stenosis (AS) is the irreversible pressure loss that is created by the stenosis. The majority of the pressure loss is caused by conversion/dissipation of turbulent kinetic energy (TKE) to heat. Recent developments in cardiac magnetic resonance 4D flow imaging have allowed the non-invasive assessment of TKE. Bicuspid aortic valve disease is known to be associated with a larger ascending aorta and disordered flow patterns, and we hypothesised that peak TKE would be higher in bicuspid AS than tricuspid AS.
15 patients with bicuspid AS (mean age 63.6 years; mean aortic valve area 1.4cm2; mean dimension of the ascending aorta at the level of the pulmonary artery 3.9cm) and no more than mild other valve disease were compared with 22 patients with tricuspid AS (mean age 72.9 years; mean aortic valve area 1.2cm2; mean dimension of the ascending aorta at the level of the pulmonary artery 3.2cm) and no more than mild other valve disease.
All subjects underwent time resolved, three dimensional cine magnetic resonance flow imaging at 3 Tesla, for the assessment of peak TKE. The peak TKE was obtained by integrating the TKE per voxel across the ascending aorta at each time frame of the cardiac cycle.
p-value (unpaired t-test)
Peak TKE- valve and ascending aorta
Peak TKE- Ascending aorta alone (sinuses of Valsalva to the arch)
Bicuspid AS is associated with significantly higher peak TKE compared with tricuspid AS of comparable severity. This applies both when including the valve, and when measured in the ascending aorta alone, and may result from the larger aorta and disordered flow patterns typically seen in bicuspid AS. This implies that bicuspid AS may be associated with a greater haemodynamic burden for similar degrees of stenosis.
The research was supported by the National Institute for Health Research (NIHR) Oxford Biomedical Research Centre based at The Oxford University Hospitals Trust at the University of Oxford and the Britsh Heart Foundation, the Swedish Research Council, the Swedish Heart-Lung Foundation.
This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.