Open heart · 2026
Association of epicardial adipose tissue with markers of cardiac remodelling and clinical outcomes in asymptomatic aortic stenosis.
СтатьяМногоцентровое исследованиеНаблюдательное исследованиеНазвание и аннотация: Перевод пока не подготовлен
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Ayton Sarah L, Aslam Saadia, Dattani Abhishek, Yeo Jian L, Gulsin Gaurav S, Slomka Piotr J, Dey Damini, McCann Gerry P, Singh Anvesha
Аннотация
BACKGROUND: Previous studies have suggested an adverse role of epicardial adipose tissue (EAT) in aortic stenosis (AS), potentially mediated by direct effects on the myocardium. This study aimed to assess whether EAT volume and density are associated with cardiac remodelling and clinical outcomes in a well-phenotyped cohort of patients with initially asymptomatic AS.
METHODS: In this post hoc exploratory analysis of a multicentre, prospective longitudinal study, asymptomatic patients with moderate-to-severe AS (n=136; age 68.6 (60.1, 75.3) years, 27% female) and control participants (n=39; age 59.0 (54.0, 67.0) years, 38% female) underwent echocardiography, cardiac CT and MRI. EAT volume and mean CT attenuation were measured from non-contrast cardiac CT using an automated deep learning software. The primary outcome was symptoms necessitating valve replacement, cardiovascular death or major adverse cardiac event.
RESULTS: Participants with AS had significantly higher indexed EAT volumes (56.5 vs 38.8 cm3/m2, p<0.001) and lower EAT attenuation (-76.3 vs -69.9 Hounsfield units, p<0.001). Both measures were correlated with markers of AS severity. Indexed EAT volume was not associated with cardiac remodelling in AS after correcting for confounding variables; however, a higher mean EAT CT attenuation was associated with higher indexed left ventricular mass. There were 42 (31%) primary outcome events over a median of 370 days. Lower indexed EAT volume and higher mean CT attenuation were associated with the outcome, independent of age and sex. Indexed EAT volume remained negatively associated after further adjustment for AS severity.
CONCLUSION: Indexed EAT volume was higher in patients with AS, but not associated with MRI markers of cardiac remodelling. A higher indexed EAT volume was independently associated with a lower occurrence of symptoms and cardiovascular events. Further studies are needed to corroborate these findings and whether EAT has a potentially protective role in symptom progression in AS.
TRIAL REGISTRATION NUMBERS: NCT03518645, NCT03132129.
METHODS: In this post hoc exploratory analysis of a multicentre, prospective longitudinal study, asymptomatic patients with moderate-to-severe AS (n=136; age 68.6 (60.1, 75.3) years, 27% female) and control participants (n=39; age 59.0 (54.0, 67.0) years, 38% female) underwent echocardiography, cardiac CT and MRI. EAT volume and mean CT attenuation were measured from non-contrast cardiac CT using an automated deep learning software. The primary outcome was symptoms necessitating valve replacement, cardiovascular death or major adverse cardiac event.
RESULTS: Participants with AS had significantly higher indexed EAT volumes (56.5 vs 38.8 cm3/m2, p<0.001) and lower EAT attenuation (-76.3 vs -69.9 Hounsfield units, p<0.001). Both measures were correlated with markers of AS severity. Indexed EAT volume was not associated with cardiac remodelling in AS after correcting for confounding variables; however, a higher mean EAT CT attenuation was associated with higher indexed left ventricular mass. There were 42 (31%) primary outcome events over a median of 370 days. Lower indexed EAT volume and higher mean CT attenuation were associated with the outcome, independent of age and sex. Indexed EAT volume remained negatively associated after further adjustment for AS severity.
CONCLUSION: Indexed EAT volume was higher in patients with AS, but not associated with MRI markers of cardiac remodelling. A higher indexed EAT volume was independently associated with a lower occurrence of symptoms and cardiovascular events. Further studies are needed to corroborate these findings and whether EAT has a potentially protective role in symptom progression in AS.
TRIAL REGISTRATION NUMBERS: NCT03518645, NCT03132129.