Endocrine Abstracts

Objectives: Endothelial dysfunction has been described as a predictor of cardiovascular complications. Most important cause for early mortality in acromegaly is cardiovascular involvement, cut-off nadir GH <2.5 ng/ml predicting longer survival The aim of our study was to determine the correlations between endothelial dysfunction and GH oversecretion, associated or not with other cardiovascular risk factors.

Design and method: Cross-sectional study including 31 active acromegalic patients aged 42.8±8.66 years (20 women and 11 men) referred to ‘C.I.Parhon’ National Institute of Endocrinology. All subjects were evaluated for cardiovascular risk factors (BMI, smoking, high blood pressure, dyslipidemia, diabetes mellitus), for nadir GH during 75 g glucose OGTT and IGF1 oversecretion. All the risk factors were used to calculate the cardiovascular risk by Framingham Risk Score. Endothelial dysfunction was calculated by ultrasound assessment of endothelial dependent flow mediated vasodilation of brachial artery (FMD%<10%). Considering GH oversecretion, patients were divided into 2 groups: GH <2.5 ng/ml (eight patients), respectively GH >2.5 ng/ml (23 patients).

Results: There was no statistical difference between men and women regarding the cardiovascular risk score and prevalence for cardiovascular risk factors except smoking for men (P<0.05). Endothelial dysfunction (11 patients) was correlated with the history of hypertension (>5 years) (P<0.05), systolic blood pressure (>160 mmHg) (P<0.05) and diabetes mellitus (P<0.05) and was not correlated with nadir GH (P=0.08). Only high Framingham Risk Score was correlated with endothelial dysfunction (P<0.05).

Conclusions: Endothelial dysfunction, an end point for atherosclerosis, can provide incremental benefit in risk stratification for patients at high cardiovascular risk. This approach could help clinicians to initiate preventive treatment and to evaluate the benefits in a short period of time just retesting endothelial dysfunction by ultrasound flow mediated vasodilation.