[Dilated cardiomyopathy in a patient with Cushing's disease - clinical presentation, diagnosis and treatment: a case report].

Cortisol-induced dilated cardiomyopathy (CI-DCM) is a rare manifestation of endogenous hypercortisolism (EH). Optimal management of patients with CI-DCM is a major challenge due to the rarity of the pathology and the lack of expert community guidelines. This article describes a case of successful management of a patient with ACTH-secreting pituitary tumor and CI-DCM.A 44-year-old patient was hospitalized with symptoms of chronic heart failure (CHF) and EH. The diagnosis of non-ischemic myocardial damage with phenotype of DCM was verified by echocardiography and coronary angiography. According to hormonal and imaging tests, and selective blood sampling from the inferior petrosal sinuses, an ACTH-secreting pituitary adenoma was diagnosed. A transnasal transsphenoidal adenomectomy was planned. Due to the symptoms of CHF and systolo-diastolic dysfunction of the left ventricle (LV), significantly increasing the risk of adverse perioperative cardiac events, the intervention was postponed. Stabilization of the patient's condition was achieved after 4-month therapy with use of betaAB, ACEI, MRA, diuretics, and steroidogenesis inhibitors. Stabilization of the patient's condition allowed to perform transnasal transsphenoidal adenomectomy without perioperative complications, with postoperative decrease of ACTH and cortisol levels. Follow-up examinations demonstrated preservation of eucorticism, regression of CHF symptoms. progressive decrease of LV size/volumes with increase of LVEF.Cortisol hypersecretion can damage myocardium with a phenotype of DCM, with symptoms of CHF being the dominant clinical manifestation of EH. The use of betaAB, ACEI, diuretics, MRA, and steroidogenesis inhibitors is reasonable to control symptoms of CHF and prepare a patient with CI-DCM for surgical intervention. After normalization of cortisol level, regression of CHF symptoms and significant reduction of heart chamber size/volumes with increase of LVEF are noted, which allows to conclude about reversibility of pathologic cardiac remodeling.