Endocrine Abstracts

Myopathy is a common complication of Cushing’s syndrome (CS), which predicts the possibility of heart muscle damage and may be a cause of heart failure. Goal of this study is to evaluate the prevalence of heart failure in patients with active CS and the probability of recovery after achieving a remission.

Materials and methods: We enrolled patients with CS hospitalized in our clinic from October 2018 to December 2022. To confirm the diagnosis of CS we measured: late-night salivary cortisol (LNSC) (reference range 0.5-9.65 nmol/l); 24 hours urine free cortisol (reference range 100-379 nmol/day)., midnight serum cortisol levels (reference range 46.0-270.0 nmol/l). All patients underwent clinical investigation including expert echocardiography with speckle tracking and evaluation of N-terminal pro–B-type natriuretic peptide (NT-proBNP) (reference <125 pg/ml Cobas 6000) and Soluble suppression of tumorigenicity 2 (ST2) (reference <35 ng/ml ; Presage ST2 Assay Kit (Critical Diagnostics, USA) at the baseline and 6 months after surgical treatment. In patients with preserved ejection fraction the H2FPEF and HFA-PEFF heart failure diagnostic algorithms were used.

Results: The study included 70 patients with active CS (n=54 women, 24h urine cortisol = 1193.5 [690.9; 2034.6] nmol/24h, LNSC 21.57 [13.03; 43.89] nmol/l. The causes of CS were Cushing’ disease in 51 patients; Ectopic-ACTH-syndrome in 9 cases and benign cortisol-secreting adrenal adenoma in 10 cases. The diagnosis of heart failure was verified in 46 (65.7%) patients. According to the results of echocardiography, 16 (22%) patients revealed dilation of the left atrium, 3 (4.3%) - left ventricle (LV), 37 (52.9%) patients had LV hypertrophy, 4 patients - decrease of LV ejection fraction (LVEF 40-50%); impaired diastolic function was detected in 37 (52.9%) patients. A decrease in global longitudinal myocardial strain was detected in 28 (39.4%) patients. Remission was confirmed in 52 patients 6 months after surgical treatment. Among 36 re-examined patients with 6 months remission of CS, the heart failure was confirmed in 26 patients, whereas in 16 of them heart failure regressed. The initially elevated NT-proBNP 132.8 [49.2; 444.4] and ST2 31.9 [22.7; 72.6] decreased to 71.8 [13.4; 163.2] P=0.004 and 25.9 [19.9; 33.3] P=0.031 respectively, supporting the reversibility of heart failure.

Conclusion: CS causes heart muscle damage with the development of heart failure in 65.7% of patients. Achieving CS remission led to regression of heart muscle myopathy in 44.4% of the recorded cases after 6 months of observation, which supports the reversibility of this damage.