Abstract
Both arterial blood pressure (BP) average levels and short-term BP variability (BPV) relate to hypertension-mediated organ damage, in particular increased carotid artery intima-media thickness (IMT) and carotid-femoral pulse wave velocity (PWV). Endothelial dysfunction possibly mediates such damage. The authors aimed at further investigating such role in hypertensive patients. In 189 recently diagnosed, untreated hypertensive patients the authors evaluated, in a cross-sectional design, the relationships of BP average levels and short-term systolic (S) BPV (standard deviation of awake SBP or of 24-hour-weighted SBP) with IMT and PWV, and how much these relationships are explained by endothelial function parameters-brachial artery flow-mediated dilation (FMD) and digital reactive hyperemia index (RHI). Multivariable models assessed the strength of these relationships to derive a plausible pathogenetic sequence. Both average SBP values and our measures of SBPV were significantly related to IMT (24-hour mean SBP: r = .156, P = .034; 24-hour-weighted SBPV: r = .157, P = .033) and to PWV (24-hour mean SBP: r = .179, P = .015; 24-hour-weighted SBPV: r = .175; P = .018), but only poorly related to FMD or RHI (P > .05 for all). At univariable regression analysis, FMD and RHI were both related to IMT, (P < .001), but not to PWV. When FMD and RHI were added to average SBP and SBPV parameters in a multivariable model, both significantly (P < .005) contributed to predict IMT, but not PWV. Thus, endothelial dysfunction relates to IMT independently of BP parameters, but appears to play a minor role in the association between BP variability-related variables and arterial stiffening.