Affiliations 

  • 1 Department of Biomedical Engineering, Faculty of Engineering, Universiti Malaya, Kuala Lumpur, Malaysia
  • 2 Department of Biomedical Imaging, Faculty of Medicine, Universiti Malaya, Kuala Lumpur, Malaysia
  • 3 Department of Medicine, Faculty of Medicine, Universiti Malaya, Kuala Lumpur, Malaysia
  • 4 Department of Mechanical, Materials and Manufacturing Engineering, Faculty of Science and Engineering, University of Nottingham Malaysia, Semenyih, Malaysia
  • 5 Clinical Oncology Unit, Faculty of Medicine, Universiti Malaya, Kuala Lumpur, Malaysia
  • 6 University Malaya Research Imaging Centre, Department of Biomedical Imaging, Faculty of Medicine, Universiti Malaya, Kuala Lumpur, Malaysia
J Magn Reson Imaging, 2023 Jul 15.
PMID: 37452574 DOI: 10.1002/jmri.28915

Abstract

BACKGROUND: Increased afterload in aortic stenosis (AS) induces left ventricle (LV) remodeling to preserve a normal ejection fraction. This compensatory response can become maladaptive and manifest with motion abnormality. It is a clinical challenge to identify contractile and relaxation dysfunction during early subclinical stage to prevent irreversible deterioration.

PURPOSE: To evaluate the changes of regional wall dynamics in 3D + time domain as remodeling progresses in AS.

STUDY TYPE: Retrospective.

POPULATION: A total of 31 AS patients with reduced and preserved ejection fraction (14 AS_rEF: 7 male, 66.5 [7.8] years old; 17 AS_pEF: 12 male, 67.0 [6.0] years old) and 15 healthy (6 male, 61.0 [7.0] years old).

FIELD STRENGTH/SEQUENCE: 1.5 T Magnetic resonance imaging/steady state free precession and late-gadolinium enhancement sequences.

ASSESSMENT: Individual LV models were reconstructed in 3D + time domain and motion metrics including wall thickening (TI), dyssynchrony index (DI), contraction rate (CR), and relaxation rate (RR) were automatically extracted and associated with the presence of scarring and remodeling.

STATISTICAL TESTS: Shapiro-Wilk: data normality; Kruskal-Wallis: significant difference (P 

* Title and MeSH Headings from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.