Impaired endothelium mediated vascular reactivity in endogenous Cushing's syndrome.

Endogenous Cushing's syndrome (CS) is associated with a high incidence of cardiovascular morbidity and mortality resulting from the co-existence of multiple cardiovascular risk factors which probably induce a state of endothelial dysfunction. Recently, studies conducted in vitro as well as in normal human subjects suggest a direct role of cortisol in the causation of vascular dysfunction in this disorder. We non-invasively assessed the vascular reactivity and its potential association with elevated cortisol levels in patients of CS. A single time point observational study was conducted in 18 patients of CS and 15 age and gender matched healthy subjects. Vascular reactivity was assessed non-invasively by measuring the peripheral pulse wave form changes during reactive hyperemia (RH) using digital photoplethysmography (PPG). Parameters measured were pulse wave form amplitude (PWA), slope and pulse transit time (PTT). Maximal percentage changes in PWA during RH with reference to baseline were significantly lower in the patients as compared to controls [23.19% (13.19-53.54) vs 61.71% (38.21-95.36); p=0.0079]. Normalized PTT responses during the 1(st) minute of RH were blunted in the patients as compared to controls (1.036 ± 0.026 vs 1.056 ± 0.029; p=0.0425). Percentage changes in PTT during the 2(nd) minute of RH were negatively correlated to the morning cortisol levels in patients (r = -0.6328; p=0.0064). The present study showed that endothelium mediated vascular reactivity along with myogenic regulation of vascular tone is impaired in CS. Hypercortisolism possibly plays an important role in the causation of impaired vascular reactivity and endothelial dysfunction in CS.