P. Wolf*a (Dr)

a Medical University of Vienna, Division of Endocrinology and Metabolism, Vienna, AUTRICHE

* peter.wolf@meduniwien.ac.at

Cardiovascular disease is the leading cause of death in patients with Cushing’s syndrome. Cortisol excess predisposes to well-established cardiovascular risk factors, including hypertension, visceral obesity, dyslipidemia and glucose intolerance, but also exerts direct effects on cardiac structure and function.

Increased ventricular mass and subclinical ventricular dysfunction, both potentially reversible after treatment, have been reported in patients with Cushing’s syndrome. This increase in ventricular mass contrasts with skeletal muscle atrophy and sarcopenia related to protein wasting induced by hypercortisolism.

Cardiac fat might play an important role in the pathogenesis of Cushing’s syndrome associated cardiomyopathy.

However, in contrast to the general population, in which visceral obesity and diabetes is associated with cardiac steatosis, no increase in intramyocardial lipid content could be found in patients with Cushing’s syndrome. Cortisol excess might stimulate beta oxidation and triglyceride consumption and therefore could “protect” cardiomyocytes from ectopic lipid deposition. On the other hand, an accumulation of epicardial and pericardial fat has been observed in Cushing’s syndrome. Whereas pericardial fat reflects the thoracic visceral adipose tissue, epicardial fat might be highly susceptible to cortisol, as it decreased following biochemical disease remission in short term follow up. Epicardial fat is directly mixed with the myocardium without being separated by any fascia and shares the same blood supply. It therefore directly exerts paracrine actions on the myocardium and is well known to promote inflammation, microvascular dysfunction and fibrosis.

Epicardial fat could play a major role in the pathogenesis of Cushing’s syndrome associated cardiomyopathy.

L’auteur n’a pas transmis de déclaration de conflit d’intérêt.