Epicardial and Pericardial Adiposity Without Myocardial Steatosis in Cushing Syndrome
© The Author(s) 2021. Published by Oxford University Press on behalf of the Endocrine Society. All rights reserved. For permissions, please e-mail: journals.permissionsoup.com..
CONTEXT: Cardiovascular disease is the leading cause of death in patients with Cushing syndrome. Cortisol excess and adverse metabolic profile could increase cardiac fat, which can subsequently impair cardiac structure and function.
OBJECTIVE: We aimed to evaluate cardiac fat mass and distribution in patients with Cushing syndrome.
METHODS: In this prospective, cross-sectional study, 23 patients with Cushing syndrome and 27 control individuals of comparable age, sex, and body mass index were investigated by cardiac magnetic resonance imaging and proton spectroscopy. Patients were explored before and after biochemical disease remission. Myocardial fat measured by the Dixon method was the main outcome measure. The intramyocardial triglyceride/water ratio measured by spectroscopy and epicardial and pericardial fat volumes were secondary outcome measures.
RESULTS: No difference was found between patients and controls in intramyocardial lipid content. Epicardial fat mass was increased in patients compared to controls (30.8 g/m2 [20.4-34.8] vs 17.2 g/m2 [13.1-23.5], P < .001). Similarly, pericardial fat mass was increased in patients compared to controls (28.3 g/m2 [17.9-38.0] vs 11.4 g/m2 [7.5-19.4], P = .003). Sex, glycated hemoglobin A1c, and the presence of hypercortisolism were independent determinants of epicardial fat. Pericardial fat was associated with sex, impaired glucose homeostasis and left ventricular wall thickness. Disease remission decreased epicardial fat mass without affecting pericardial fat.
CONCLUSION: Intramyocardial fat stores are not increased in patients with Cushing syndrome, despite highly prevalent metabolic syndrome, suggesting increased cortisol-mediated lipid consumption. Cushing syndrome is associated with marked accumulation of epicardial and pericardial fat. Epicardial adiposity may exert paracrine proinflammatory effects promoting cardiomyopathy.
| Errataetall: |
CommentIn: J Clin Endocrinol Metab. 2022 Jan 1;107(1):e443-e444. - PMID 34519341 |
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| Medienart: |
E-Artikel |
| Erscheinungsjahr: |
2021 |
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| Erschienen: |
2021 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:106 |
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| Enthalten in: |
The Journal of clinical endocrinology and metabolism - 106(2021), 12 vom: 19. Nov., Seite 3505-3514 |
| Sprache: |
Englisch |
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| Beteiligte Personen: |
Wolf, Peter [VerfasserIn] |
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| Links: |
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| Anmerkungen: |
Date Completed 28.12.2021 Date Revised 07.12.2022 published: Print ClinicalTrials.gov: NCT02202902 CommentIn: J Clin Endocrinol Metab. 2022 Jan 1;107(1):e443-e444. - PMID 34519341 Citation Status MEDLINE |
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| doi: |
10.1210/clinem/dgab556 |
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| funding: |
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| Förderinstitution / Projekttitel: |
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NLM328781592 |
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| 100 | 1 | |a Wolf, Peter |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Epicardial and Pericardial Adiposity Without Myocardial Steatosis in Cushing Syndrome |
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| 500 | |a Date Completed 28.12.2021 | ||
| 500 | |a Date Revised 07.12.2022 | ||
| 500 | |a published: Print | ||
| 500 | |a ClinicalTrials.gov: NCT02202902 | ||
| 500 | |a CommentIn: J Clin Endocrinol Metab. 2022 Jan 1;107(1):e443-e444. - PMID 34519341 | ||
| 500 | |a Citation Status MEDLINE | ||
| 520 | |a © The Author(s) 2021. Published by Oxford University Press on behalf of the Endocrine Society. All rights reserved. For permissions, please e-mail: journals.permissionsoup.com. | ||
| 520 | |a CONTEXT: Cardiovascular disease is the leading cause of death in patients with Cushing syndrome. Cortisol excess and adverse metabolic profile could increase cardiac fat, which can subsequently impair cardiac structure and function | ||
| 520 | |a OBJECTIVE: We aimed to evaluate cardiac fat mass and distribution in patients with Cushing syndrome | ||
| 520 | |a METHODS: In this prospective, cross-sectional study, 23 patients with Cushing syndrome and 27 control individuals of comparable age, sex, and body mass index were investigated by cardiac magnetic resonance imaging and proton spectroscopy. Patients were explored before and after biochemical disease remission. Myocardial fat measured by the Dixon method was the main outcome measure. The intramyocardial triglyceride/water ratio measured by spectroscopy and epicardial and pericardial fat volumes were secondary outcome measures | ||
| 520 | |a RESULTS: No difference was found between patients and controls in intramyocardial lipid content. Epicardial fat mass was increased in patients compared to controls (30.8 g/m2 [20.4-34.8] vs 17.2 g/m2 [13.1-23.5], P < .001). Similarly, pericardial fat mass was increased in patients compared to controls (28.3 g/m2 [17.9-38.0] vs 11.4 g/m2 [7.5-19.4], P = .003). Sex, glycated hemoglobin A1c, and the presence of hypercortisolism were independent determinants of epicardial fat. Pericardial fat was associated with sex, impaired glucose homeostasis and left ventricular wall thickness. Disease remission decreased epicardial fat mass without affecting pericardial fat | ||
| 520 | |a CONCLUSION: Intramyocardial fat stores are not increased in patients with Cushing syndrome, despite highly prevalent metabolic syndrome, suggesting increased cortisol-mediated lipid consumption. Cushing syndrome is associated with marked accumulation of epicardial and pericardial fat. Epicardial adiposity may exert paracrine proinflammatory effects promoting cardiomyopathy | ||
| 650 | 4 | |a Journal Article | |
| 650 | 4 | |a Research Support, Non-U.S. Gov't | |
| 650 | 4 | |a Cushing syndrome | |
| 650 | 4 | |a cardiac magnetic resonance imaging | |
| 650 | 4 | |a cardiac steatosis | |
| 650 | 4 | |a cardiomyopathy | |
| 650 | 4 | |a pericardial and epicardial fat | |
| 650 | 4 | |a proton magnetic resonance spectroscopy | |
| 650 | 7 | |a Biomarkers |2 NLM | |
| 650 | 7 | |a Blood Glucose |2 NLM | |
| 650 | 7 | |a Glycated Hemoglobin A |2 NLM | |
| 650 | 7 | |a hemoglobin A1c protein, human |2 NLM | |
| 700 | 1 | |a Marty, Benjamin |e verfasserin |4 aut | |
| 700 | 1 | |a Bouazizi, Khaoula |e verfasserin |4 aut | |
| 700 | 1 | |a Kachenoura, Nadjia |e verfasserin |4 aut | |
| 700 | 1 | |a Piedvache, Céline |e verfasserin |4 aut | |
| 700 | 1 | |a Blanchard, Anne |e verfasserin |4 aut | |
| 700 | 1 | |a Salenave, Sylvie |e verfasserin |4 aut | |
| 700 | 1 | |a Prigent, Mikaël |e verfasserin |4 aut | |
| 700 | 1 | |a Jublanc, Christel |e verfasserin |4 aut | |
| 700 | 1 | |a Ajzenberg, Christiane |e verfasserin |4 aut | |
| 700 | 1 | |a Droumaguet, Céline |e verfasserin |4 aut | |
| 700 | 1 | |a Young, Jacques |e verfasserin |4 aut | |
| 700 | 1 | |a Lecoq, Anne-Lise |e verfasserin |4 aut | |
| 700 | 1 | |a Kuhn, Emmanuelle |e verfasserin |4 aut | |
| 700 | 1 | |a Agostini, Helene |e verfasserin |4 aut | |
| 700 | 1 | |a Trabado, Severine |e verfasserin |4 aut | |
| 700 | 1 | |a Carlier, Pierre G |e verfasserin |4 aut | |
| 700 | 1 | |a Fève, Bruno |e verfasserin |4 aut | |
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| 700 | 1 | |a Chanson, Philippe |e verfasserin |4 aut | |
| 700 | 1 | |a Kamenický, Peter |e verfasserin |4 aut | |
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