BACKGROUND: Sarcoidosis is an inflammatory disease, which may affect vascular function. The study was designed to assess the impact of sarcoidosis on endothelial function and arterial stiffness. METHODS: Eighty-seven sarcoidosis patients and eighty-seven matched healthy subjects (Cl) were included in the study. Sarcoidosis patients were divided into two groups. Group 1 included patients never treated and group 2 included patients receiving cortisone treatment. Endothelial function was evaluated by flow-mediated dilatation (FMD). Carotid-femoral pulse wave velocity (PWV) was measured as an index of aortic stiffness and augmentation index (AI75) as a measure of arterial wave reflections. Serum levels of soluble intercellular adhesion molecule-1 and tumor necrosis factor-α (TNF-α), were measured. RESULTS: In the totality of the population, sarcoidosis patients had significantly lower FMD (P < 0.01) and significantly higher AI75 (P < 0.05). There was also a significant difference, between group 1, and Cl in FMD and AI75, but there was no difference between group 2 and Cl in FMD and AI75. AI75 values were significantly correlated with serum levels of intercellular adhesion molecule-1 (ICAM-1) (r = 0.370, P < 0.01) and TNF-α (r = 0.219, P = 0.049). CONCLUSIONS: In the present study, we have shown that sarcoidosis patients have impaired endothelial function and increased arterial stiffness. Sarcoidosis patients on cortisone treatment had no differences compared to controls on the vascular parameters. Moreover, there was a significant correlation between inflammatory process and vascular function impairment. These findings indicate that sarcoidosis patients have impaired vascular function and increased inflammatory status, which may improve with cortisone treatment.
BACKGROUND:Sarcoidosis is an inflammatory disease, which may affect vascular function. The study was designed to assess the impact of sarcoidosis on endothelial function and arterial stiffness. METHODS: Eighty-seven sarcoidosispatients and eighty-seven matched healthy subjects (Cl) were included in the study. Sarcoidosispatients were divided into two groups. Group 1 included patients never treated and group 2 included patients receiving cortisone treatment. Endothelial function was evaluated by flow-mediated dilatation (FMD). Carotid-femoral pulse wave velocity (PWV) was measured as an index of aortic stiffness and augmentation index (AI75) as a measure of arterial wave reflections. Serum levels of soluble intercellular adhesion molecule-1 and tumor necrosis factor-α (TNF-α), were measured. RESULTS: In the totality of the population, sarcoidosispatients had significantly lower FMD (P < 0.01) and significantly higher AI75 (P < 0.05). There was also a significant difference, between group 1, and Cl in FMD and AI75, but there was no difference between group 2 and Cl in FMD and AI75. AI75 values were significantly correlated with serum levels of intercellular adhesion molecule-1 (ICAM-1) (r = 0.370, P < 0.01) and TNF-α (r = 0.219, P = 0.049). CONCLUSIONS: In the present study, we have shown that sarcoidosispatients have impaired endothelial function and increased arterial stiffness. Sarcoidosispatients on cortisone treatment had no differences compared to controls on the vascular parameters. Moreover, there was a significant correlation between inflammatory process and vascular function impairment. These findings indicate that sarcoidosispatients have impaired vascular function and increased inflammatory status, which may improve with cortisone treatment.