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. 2024 Nov 27;191(6):604-613.
doi: 10.1093/ejendo/lvae145.

Cardiovascular status in endogenous cortisol excess: the prospective CV-CORT-EX study

Caroline Morbach  1   2 , Mario Detomas  3 , Floran Sahiti  1   2 , Kristina Hoffmann  3 , Matthias Kroiss  3   4 , Götz Gelbrich  5   6 , Stefan Frantz  1   2 , Stefanie Hahner  1   3 , Peter Ulrich Heuschmann  4   5   6 , Martin Fassnacht  1   3 , Stefan Störk  1   2 , Timo Deutschbein  3   7
Affiliations

Cardiovascular status in endogenous cortisol excess: the prospective CV-CORT-EX study

Caroline Morbach et al. Eur J Endocrinol. .

Abstract

Objective: Cushing's syndrome (CS) results in increased cardiovascular (CV) morbidity and mortality. Subtype-specific differences and possible reversibility after biochemical cure are not well investigated.

Design: Prospective cohort study evaluating the CV status in different forms of endogenous cortisol excess.

Methods: Patients with overt CS (n = 40, 47 ± 13 years, 75% women; 18 pituitary, 13 adrenal, and 9 ectopic), biochemically cured CS (n = 56, 53 ± 12 years, 79% women; 30 pituitary, 21 adrenal, and 5 ectopic), and adrenal incidentalomas with mild autonomous cortisol secretion (MACS) (n = 18, 62 ± 11 years, 56% women) underwent comprehensive biochemical, metabolic, and CV assessment. Results were compared with a representative sample of the general population of Würzburg (n = 4965, 55 ± 12 years, 52% women).

Results: Overt CS was associated with left ventricular (LV) remodeling along with hypertrophy and impaired longitudinal systolic/diastolic function at echocardiography. In 20 CS patients followed for a median of 8 (quartiles: 6, 11) months after biochemical remission, hypertension, and hyperglycemia were better controlled, while cardiac alterations only partially improved. Patients with previous CS (median time of biochemical remission: 95 [36, 201] months) had worse diastolic function than the general population (LV relaxation velocity e' 0.08 [0.07, 0.10] ms-1 vs 0.10 [0.08, 0.12] ms-1, P < .001). In MACS, cardiac remodeling was even more pronounced than in individuals with metabolic syndrome.

Conclusions: In patients with overt CS, cured CS, and MACS, we found a sizable and significant deviation from the general population mean regarding cardiac structure and function. Even mild cortisol excess is associated with glucocorticoid-induced cardiac alterations, which appear to persist despite long-term biochemical remission.

Keywords: Cushing's syndrome; adrenal incidentaloma; autonomous cortisol secretion; cardiac; echocardiography; glucocorticoid excess; heart; hypercortisolism.

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Conflict of interest statement

Conflict of interest: C.M. reports a research cooperation between the University of Würzburg and Tomtec Imaging Systems (funded by a research grant from the Bavarian Ministry of Economic Affairs, Regional Development and Energy, Germany), honoraria from Alexion, Alnylam, AstraZeneca, Bayer, Boehringer Ingelheim, EBR Systems, Janssen, Novo Nordisk, Pfizer, SOBI, and Tomtec, and her role as principal investigator in clinical trials sponsored by Alnylam, AstraZeneca, Bayer, and Novo Nordisk. G.G. reports a research cooperation between the University of Würzburg and Tomtec Imaging Systems (funded by a research grant from the Bavarian Ministry of Economic Affairs, Regional Development and Energy, Germany). M.K. received advisory fees and speaker honoraria from Advanz Pharma, Bayer, Eisai, HRA Pharma, Lilly, Recordati Rare Diseases, Roche, and Sanofi, reimbursement of travel costs from Lilly, and research support as principal investigator of a clinical trial from Corcept Therapeutics, Ipsen, and Lilly. S.F. received consultancy and lecture fees as well as reimbursement of travel costs from Abbot, Abiomed, Amarin, Amgen, AstraZeneca, Bayer, Berlin-Chemie, Biotronik, Boehringer, Bristol-Myers Squibb, Daiichi Sankyo, Edwards, Lilly, Novartis, Novo Nordisk, Pfizer, sanofi-aventis, Siemens, Vifor, and Zoll. S.H. reports no personal honoraria but consultancy fees from Takeda paid to the institution. All other authors declare no competing interests. P.U.H. reports research grants from the Bavarian State, the European Union, the Federal Joint Committee (G-BA) within the Innovationsfonds, the German Cancer Aid, the German Heart Foundation, the German Ministry of Research and Education, the German Parkinson Society, the German Research Foundation, the University Göttingen (within FIND-AF randomized; supported by an unrestricted research grant to the University Göttingen from Boehringer Ingelheim), the University Hospital Heidelberg (within RASUNOA-prime; supported by an unrestricted research grant to the University Hospital Heidelberg from Bayer, BMS, Boehringer Ingelheim, and Daiichi Sankyo), and the University Hospital Würzburg, all outside the submitted work. S.S. has received consultancy and lecture fees as well as reimbursement of travel costs from AstraZeneca, Bayer, Boehringer Ingelheim, Novartis, Pfizer, and Servier. T.D. received advisory fees and speaker honoraria from HRA Pharma and Novartis, reimbursement of travel costs from Novo Nordisk and Recordati Rare Diseases and research support as principal investigator of a clinical trial from Corcept Therapeutics.

Supplementary concepts