TY - JOUR
T1 - Differentiating Left Ventricular Remodeling in Aortic Stenosis From Systemic Hypertension
AU - Mahmod, Masliza
AU - Chan, Kenneth
AU - Fernandes, Joao F.
AU - Ariga, Rina
AU - Raman, Betty
AU - Zacur, Ernesto
AU - Law, Ho Fon Royce
AU - Rigolli, Marzia
AU - Francis, Jane M.
AU - Dass, Sairia
AU - O’Gallagher, Kevin
AU - Myerson, Saul G.
AU - Karamitsos, Theodoros D.
AU - Neubauer, Stefan
AU - Lamata, Pablo
N1 - Publisher Copyright:
© 2024 The Authors.
PY - 2024/8/1
Y1 - 2024/8/1
N2 - BACKGROUND: Left ventricular (LV) hypertrophy occurs in both aortic stenosis (AS) and systemic hypertension (HTN) in response to wall stress. However, differentiation of hypertrophy due to these 2 etiologies is lacking. The aim was to study the 3-dimensional geometric remodeling pattern in severe AS pre- and postsurgical aortic valve replacement and to compare with HTN and healthy controls. METHODS: Ninety-one subjects (36 severe AS, 19 HTN, and 36 healthy controls) underwent cine cardiac magnetic resonance. Cardiac magnetic resonance was repeated 8 months post-aortic valve replacement (n=18). Principal component analysis was performed on the 3-dimensional meshes reconstructed from 109 cardiac magnetic resonance scans of 91 subjects at end-diastole. Principal component analysis modes were compared across experimental groups together with conventional metrics of shape, strain, and scar. RESULTS: A unique AS signature was identified by wall thickness linked to a LV left-right axis shift and a decrease in short-axis eccentricity. HTN was uniquely linked to increased septal thickness. Combining these 3 features had good discriminative ability between AS and HTN (area under the curve, 0.792). The LV left-right axis shift was not reversible post-aortic valve replacement, did not associate with strain, age, or sex, and was predictive of postoperative LV mass regression (R2=0.339, P=0.014). CONCLUSIONS: Unique remodeling signatures might differentiate the etiology of LV hypertrophy. Preliminary findings suggest that LV axis shift is characteristic in AS, is not reversible post-aortic valve replacement, predicts mass regression, and may be interpreted to be an adaptive mechanism.
AB - BACKGROUND: Left ventricular (LV) hypertrophy occurs in both aortic stenosis (AS) and systemic hypertension (HTN) in response to wall stress. However, differentiation of hypertrophy due to these 2 etiologies is lacking. The aim was to study the 3-dimensional geometric remodeling pattern in severe AS pre- and postsurgical aortic valve replacement and to compare with HTN and healthy controls. METHODS: Ninety-one subjects (36 severe AS, 19 HTN, and 36 healthy controls) underwent cine cardiac magnetic resonance. Cardiac magnetic resonance was repeated 8 months post-aortic valve replacement (n=18). Principal component analysis was performed on the 3-dimensional meshes reconstructed from 109 cardiac magnetic resonance scans of 91 subjects at end-diastole. Principal component analysis modes were compared across experimental groups together with conventional metrics of shape, strain, and scar. RESULTS: A unique AS signature was identified by wall thickness linked to a LV left-right axis shift and a decrease in short-axis eccentricity. HTN was uniquely linked to increased septal thickness. Combining these 3 features had good discriminative ability between AS and HTN (area under the curve, 0.792). The LV left-right axis shift was not reversible post-aortic valve replacement, did not associate with strain, age, or sex, and was predictive of postoperative LV mass regression (R2=0.339, P=0.014). CONCLUSIONS: Unique remodeling signatures might differentiate the etiology of LV hypertrophy. Preliminary findings suggest that LV axis shift is characteristic in AS, is not reversible post-aortic valve replacement, predicts mass regression, and may be interpreted to be an adaptive mechanism.
KW - aortic valve
KW - aortic valve stenosis
KW - hypertension
KW - hypertrophy, left ventricular
KW - principal component analysis
UR - http://www.scopus.com/inward/record.url?scp=85201780594&partnerID=8YFLogxK
U2 - 10.1161/CIRCIMAGING.123.016489
DO - 10.1161/CIRCIMAGING.123.016489
M3 - Article
C2 - 39163368
AN - SCOPUS:85201780594
SN - 1941-9651
VL - 17
SP - e016489
JO - Circulation: Cardiovascular Imaging
JF - Circulation: Cardiovascular Imaging
IS - 8
ER -