Endothelial function affects early carotid atherosclerosis progression in hypertensive postmenopausal women.

摘要

OBJECTIVES: Endothelial dysfunction is known to be associated with atherosclerosis progression and cardiovascular events. Limited information exists regarding the importance of this topic in hypertensive postmenopausal women. In this particular population the influence of endothelial dysfunction on cardio-vascular end cerebro-vascular events is well demonstrated. Therefore, we investigated, in a prospective study, the influence of endothelial-dependent vasodilation on carotid intima-media thickness (IMT) progression in our population of hypertensive postmenopausal women. METHODS: In addition to common risk factors and pharmacological therapy, we measured carotid IMT and flow-mediated dilation (FMD) of the brachial artery at baseline and after 1 year of follow-up. RESULTS: Baseline and follow-up data were available for 618 hypertensive postmenopausal women with an age of 55 +/- 8 years. The mean IMT at baseline was 754 +/- 161 mum [interquartile range (IQR) from 600 to 838 mum]. The mean FMD at baseline was 5.8 +/- 3.9% (IQR from 3.2 to 8.2%). There was a significant correlation between baseline FMD and carotid IMT (r = -0.16; P = 0.003). Mean IMT progression resulted in 103 mum (range from -250 to 567 mum; IQR from 0 to 200 mum) per year. Baseline FMD, FMD change and the amount of SBP reduction during follow-up remained the independent predictors of IMT progression in multivariable analysis. CONCLUSIONS: In this prospective study we observed a significant interaction between baseline FMD, FMD change during follow-up and IMT progression in our population of hypertensive postmenopausal women. These results are in accordance with the suggestion that endothelial dysfunction is associated with enhanced atherosclerosis development. This hypothesis could provide a pathophysiological explanation for the increase in cardio-vascular and cerebro-vascular episodes recorded in hypertensive postmenopausal women with endothelial dysfunction.