Sophia D Rado1, Roberto Lorbeer2, Sergios Gatidis1, Jürgen Machann3,4,5, Corinna Storz1, Konstantin Nikolaou1, Wolfgang Rathmann5,6, Udo Hoffmann7, Annette Peters8,9,10, Fabian Bamberg1,8,11, Christopher L Schlett11,12. 1. 1 Department of Diagnostic and Interventional Radiology, University Hospital Tuebingen , Tuebingen , Germany. 2. 2 Department of Radiology, Ludwig-Maximilian-University Hospital , Munich , Germany. 3. 3 Department of Diagnostic and Interventional Radiology, Section on Experimental Radiology, University Hospital Tuebingen , Tuebingen , Germany. 4. 4 Institute for Diabetes Research and Metabolic Diseases (IDM) of the Helmholtz Center Munich at the University of Tuebingen , Tuebingen , Germany. 5. 5 German Center for Diabetes Research (DZD) , Neuherberg , Germany. 6. 6 Institute for Biometrics and Epidemiology, German Diabetes Center, Leibniz Center for Diabetes Research at Heinrich Heine University Düsseldorf , Düsseldorf , Germany. 7. 7 Department of Radiology, Massachusetts General Hospital, Harvard Medical School , Boston, MA , USA. 8. 8 German Center for Cardiovascular Disease Research (DZHK e.V.) , Munich , Germany. 9. 9 Institute for Cardiovascular Prevention, Ludwig-Maximilian-University-Hospital , Munich , Germany. 10. 10 Institute of Epidemiology II, Helmholtz Zentrum München, German Research Center for Environmental Health , Neuherberg , Germany. 11. 11 Department of Radiology, University Hospital Freiburg , Freiburg , Germany. 12. 12 Department of Radiology, Diagnostic and Interventional Radiology, University of Heidelberg , Heidelberg , Germany.
Abstract
OBJECTIVE: : To analyze the associations between epicardial and paracardial fat and impaired glucose tolerance as well as left ventricular (LV) alterations. METHODS: : 400 subjects underwent 3 T MRI and fat depots were delineated in the four chamber-view of the steady-state free precession cine sequence (repetition time: 29.97 ms; echo time 1.46 ms). LV parameters were also derived from MRI. Oral glucose tolerance tests were performed. RESULTS: : Epi- and paracardial fat was derived in 372 (93%) subjects (220 healthy controls, 100 persons with prediabetes, 52 with diabetes). Epi- and paracardial fat increased from normal glucose tolerance (NGT) to prediabetes and diabetes (7.7 vs 9.2 vs 10.3 cm2 and 14.3 vs 20.3 vs 27.4 cm2, respectively; all p < 0.001). However, the association between impaired glucose metabolism and cardiac fat attenuated after adjustment, mainly confounded by visceral adipose tissue (VAT). 93 subjects (27%) had LV impairment, defined as late gadolinium enhancement, ejection fraction < 55% or LV concentricity index > 1.3 g ml-1 . Mean epicardial fat was higher in subjects with LV impairment (11.0 vs 8.1 cm2, p < 0.001). This association remained independent after adjustment for traditional risk factors and VAT [β: 1.13 (0.22; 2.03), p = 0.02]. CONCLUSION: : Although epicardial and paracardial fat are increased in prediabetes and diabetes, the association is mostly confounded by VAT. Epicardial fat is independently associated with subclinical LV impairment in subjects without known cardiovascular disease. ADVANCES IN KNOWLEDGE:: This study contributes to the picture of epicardial fat as a pathogenic local fat depot that is independently associated with MR-derived markers of left ventricular alterations.
OBJECTIVE: : To analyze the associations between epicardial and paracardial fat and impaired glucose tolerance as well as left ventricular (LV) alterations. METHODS: : 400 subjects underwent 3 T MRI and fat depots were delineated in the four chamber-view of the steady-state free precession cine sequence (repetition time: 29.97 ms; echo time 1.46 ms). LV parameters were also derived from MRI. Oral glucose tolerance tests were performed. RESULTS: : Epi- and paracardial fat was derived in 372 (93%) subjects (220 healthy controls, 100 persons with prediabetes, 52 with diabetes). Epi- and paracardial fat increased from normal glucose tolerance (NGT) to prediabetes and diabetes (7.7 vs 9.2 vs 10.3 cm2 and 14.3 vs 20.3 vs 27.4 cm2, respectively; all p < 0.001). However, the association between impaired glucose metabolism and cardiac fat attenuated after adjustment, mainly confounded by visceral adipose tissue (VAT). 93 subjects (27%) had LV impairment, defined as late gadolinium enhancement, ejection fraction < 55% or LV concentricity index > 1.3 g ml-1 . Mean epicardial fat was higher in subjects with LV impairment (11.0 vs 8.1 cm2, p < 0.001). This association remained independent after adjustment for traditional risk factors and VAT [β: 1.13 (0.22; 2.03), p = 0.02]. CONCLUSION: : Although epicardial and paracardial fat are increased in prediabetes and diabetes, the association is mostly confounded by VAT. Epicardial fat is independently associated with subclinical LV impairment in subjects without known cardiovascular disease. ADVANCES IN KNOWLEDGE:: This study contributes to the picture of epicardial fat as a pathogenic local fat depot that is independently associated with MR-derived markers of left ventricular alterations.
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