Premium
Epicardial adipose tissue assessed by cardiac magnetic resonance imaging in patients with heart failure due to dilated cardiomyopathy
Author(s) -
Doesch Christina,
Streitner Florian,
Bellm Steven,
Suselbeck Tim,
Haghi Dariusch,
Heggemann Felix,
Schoenberg Stefan O.,
Michaely Henrik,
Borggrefe Martin,
Papavassiliu Theano
Publication year - 2013
Publication title -
obesity
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.438
H-Index - 199
eISSN - 1930-739X
pISSN - 1930-7381
DOI - 10.1002/oby.20149
Subject(s) - medicine , ejection fraction , dilated cardiomyopathy , cardiology , heart failure , diastole , magnetic resonance imaging , cardiac magnetic resonance imaging , mass index , cardiomyopathy , stroke volume , body mass index , blood pressure , radiology
Objective: We sought to investigate the association of the EAT with CMR parameters of ventricular remodelling and left ventricular (LV) dysfunction in patients with non‐ischemic dilated cardiomyopathy (DCM). Design and Methods: One hundred and fifty subjects (112 consecutive patients with DCM and 48 healthy controls) underwent CMR examination. Function, volumes, dimensions, the LV remodelling index (LVRI), the presence of late gadolinium enhancement (LGE) and the amount of EAT were assessed. Results: Compared to healthy controls, patients with DCM revealed a significantly reduced indexed EAT mass (31.7 ± 5.6 g/m 2 vs 24.0 ± 7.5 g/m 2 , p<0.0001). There was no difference in the EAT mass between DCM patients with moderate and severe LV dysfunction (23.5 ± 9.8 g/m 2 vs 24.2 ± 6.6 g/m 2 , P = 0.7). Linear regression analysis in DCM patients showed that with increasing LV end‐diastolic mass index (LV‐EDMI) ( r = 0.417, P < 0.0001), increasing LV end‐diastolic volume index ( r = 0.251, P = 0.01) and increasing LV end‐diastolic diameter ( r = 0.220, P = 0.02), there was also a significantly increased amount of EAT mass. However, there was no correlation between the EAT and the LV ejection fraction ( r = 0.0085, P = 0.37), right ventricular ejection fraction ( r = 0.049, P = 0.6), LVRI ( r = 0.116, P = 0.2) and the extent of LGE % ( r = 0.189, P = 0.1). Among the healthy controls, the amount of EAT only correlated with increasing age ( r = 0.461, P = 0.001), BMI ( r = 0.426, P = 0.003) and LV‐EDMI ( r = 0.346, P = 0.02). Conclusion: In patients with DCM the amount of EAT is decreased compared to healthy controls irrespective of LV function impairment. However, an increase in LV mass and volumes is associated with a significantly increase in EAT in patients with DCM.