Impact of epicardial adipose tissue volume upon left ventricular dysfunction in patients with mild-to-moderate aortic stenosis: A post-hoc analysis.
Adipose Tissue
/ pathology
Adiposity
/ physiology
Aged
Aged, 80 and over
Aortic Valve Stenosis
/ physiopathology
Diastole
/ physiology
Echocardiography
/ methods
Female
Heart Failure
/ physiopathology
Humans
Hypertrophy, Left Ventricular
/ physiopathology
Male
Middle Aged
Pericardium
/ metabolism
Stroke Volume
/ physiology
Tomography, X-Ray Computed
/ methods
Ventricular Dysfunction, Left
/ physiopathology
Ventricular Function, Left
/ physiology
Journal
PloS one
ISSN: 1932-6203
Titre abrégé: PLoS One
Pays: United States
ID NLM: 101285081
Informations de publication
Date de publication:
2020
2020
Historique:
received:
27
04
2018
accepted:
10
02
2020
entrez:
3
3
2020
pubmed:
3
3
2020
medline:
24
6
2020
Statut:
epublish
Résumé
Aortic stenosis (AS) may lead to diastolic dysfunction and later on heart failure (HF) with preserved left ventricular ejection fraction (HFpEF) via increased afterload and left-ventricular (LV) hypertrophy. Since epicardial adipose tissue (EAT) is a metabolically active fat depot that is adjacent to the myocardium and can influence cardiomyocytes and LV function via secretion of proinflammatory cytokines, we hypothesized that high amounts of EAT, as assessed by computed tomography (CT), may aggravate the development and severity of LV hypertrophy and diastolic dysfunction in the context of AS. We studied 50 patients (mean age 71 ± 9 years; 9 women) in this preliminary study with mild or moderate AS and mild to severe LV diastolic dysfunction (LVDD), diagnosed by echocardiography, who underwent non-contrast cardiac CT and echocardiography. EAT parameters were measured on 2nd generation dual source CT. Conventional two-dimensional echocardiography and Tissue Doppler Imaging (TDI) was performed to assess LV function and to derive myocardial straining parameter. All patients had a preserved LV ejection fraction > 50%. Data was analysed using Pearson's correlation. Only weak correlation was found between EAT volume or density and E/é ratio as LVDD marker (r = -.113 p = .433 and r = .260, p = .068 respectively). Also, EAT volume or density were independent from Global Strain Parameters (r = 0.058 p = .688 and r = -0.207 p = .239). E/é ratio was strongly associated with LVDD (r = .761 p≤0.0001) and Strain Parameters were moderately associated with LV Ejection Fraction (r = -.669 p≤0.001 and r = -.454 P≤0.005). In this preliminary study in patients with AS, the EAT volume and density as assessed by CT correlated only weakly with LVDD, as expressed by the commonly used E/é ratio, and with LV strain function. Hence, measuring EAT volume and density may neither contribute to the prediction nor upon the severity of LVDD, respectively.
Sections du résumé
BACKGROUND
Aortic stenosis (AS) may lead to diastolic dysfunction and later on heart failure (HF) with preserved left ventricular ejection fraction (HFpEF) via increased afterload and left-ventricular (LV) hypertrophy. Since epicardial adipose tissue (EAT) is a metabolically active fat depot that is adjacent to the myocardium and can influence cardiomyocytes and LV function via secretion of proinflammatory cytokines, we hypothesized that high amounts of EAT, as assessed by computed tomography (CT), may aggravate the development and severity of LV hypertrophy and diastolic dysfunction in the context of AS.
METHODS
We studied 50 patients (mean age 71 ± 9 years; 9 women) in this preliminary study with mild or moderate AS and mild to severe LV diastolic dysfunction (LVDD), diagnosed by echocardiography, who underwent non-contrast cardiac CT and echocardiography. EAT parameters were measured on 2nd generation dual source CT. Conventional two-dimensional echocardiography and Tissue Doppler Imaging (TDI) was performed to assess LV function and to derive myocardial straining parameter. All patients had a preserved LV ejection fraction > 50%. Data was analysed using Pearson's correlation.
RESULTS
Only weak correlation was found between EAT volume or density and E/é ratio as LVDD marker (r = -.113 p = .433 and r = .260, p = .068 respectively). Also, EAT volume or density were independent from Global Strain Parameters (r = 0.058 p = .688 and r = -0.207 p = .239). E/é ratio was strongly associated with LVDD (r = .761 p≤0.0001) and Strain Parameters were moderately associated with LV Ejection Fraction (r = -.669 p≤0.001 and r = -.454 P≤0.005).
CONCLUSIONS
In this preliminary study in patients with AS, the EAT volume and density as assessed by CT correlated only weakly with LVDD, as expressed by the commonly used E/é ratio, and with LV strain function. Hence, measuring EAT volume and density may neither contribute to the prediction nor upon the severity of LVDD, respectively.
Identifiants
pubmed: 32119694
doi: 10.1371/journal.pone.0229636
pii: PONE-D-18-11688
pmc: PMC7051069
doi:
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
e0229636Déclaration de conflit d'intérêts
The authors have declared that no competing interests exist.
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