Abstract-Aortic stiffness predicts an excess risk of stroke, supposedly via cerebral small-vessel disease. White matter hyperintensities, silent lacunar infarcts, and brain microbleeds, manifestations of cerebral small-vessel disease on neuroimaging, may precede overt cerebrovascular disease. Therefore, we assessed whether aortic stiffness is also related to such lesions. In 167 hypertensive patients (85 men) without a history of cardiovascular or cerebrovascular disease, a mean age of 51.8Ϯ13.1 years, and untreated office blood pressure levels of 169Ϯ25/104Ϯ12 mm Hg, we determined aortic pulse wave velocity and office and ambulatory 24-hour pulse pressure (off medication), as well as the volume of white matter hyperintensities and the presence of lacunar infarcts and microbleeds using brain MRI. Linear and logistic regression analyses were performed to assess the relationships between the arterial stiffness measures and brain lesions. Aortic stiffness and pulse pressure were significantly related to each of the brain lesions in univariate analyses (PϽ0.05). Multivariate analyses, adjusted for age, sex, brain volume, mean arterial pressure, and heart rate, showed that a higher pulse wave velocity was significantly associated with a greater volume of white matter hyperintensities (unstandardized regression coefficient: 0. Key Words: aortic stiffness Ⅲ pulse wave velocity Ⅲ pulse pressure Ⅲ cerebral small-vessel disease Ⅲ brain Ⅲ hypertension T he arterial system gradually stiffens because of the shared effects of ageing, high blood pressure (BP), and other vascular risk factors. 1 Arterial stiffness can be assessed by noninvasive pulse wave velocity (PWV) measurements. 2 In particular, the velocity of the carotidfemoral or aortic pulse wave appears to be of prognostic importance and is considered to be the "gold standard" for arterial stiffness. 3 Several studies, in both population-and patient-based cohorts, have demonstrated a strong association between increased aortic PWV and excess risk of cardiovascular complications, including stroke. 4 -6 Whether the risk of stroke is mediated by large-and/or small-vessel disease is not clear, but the previously reported increased risk of stroke in the presence of preclinical cerebral microvascular disease, ie, white matter hyperintensities (WMHs), silent lacunar infarcts (LACs), and/or brain microbleeds (BMBs), suggests small-vessel disease involvement. 7,8 O'Rourke and Safar 9 hypothesized that cerebral microvascular disease results from the damaging forces of abnormal flow pulsations extending into small cerebral arteries as a consequence of arterial stiffening. However, the relationship between arterial stiffness and manifestations of cerebral small-vessel disease has not been investigated in great detail, and studies have yielded conflicting results. 10 -12 The present study was undertaken to assess the associations between aortic PWV and WMHs, LACs, and BMBs as manifestations of silent cerebral small-vessel disease on MRI of the brain in a cohort of hypertensiv...
The ecNOS Glu298Asp polymorphism is associated with reduced basal NO production and might therefore have functional implications in the development of atherosclerosis or hypertension.
The purpose of this research was to review the literature on home blood pressure measurement (HBPM) and to provide recommendations regarding HBPM assessment. Observational studies on HBPM, published after 1992, as identified by PubMed, EMBASE, and Cochrane literature searches were reviewed. Studies were selected if they met the following criteria: 1) self-measurements had been performed with validated devices; 2) measurement procedures were described in sufficient detail; and 3) papers clearly explained how final HBPM results were calculated upon which conclusions and/or treatment decisions were based. Office blood pressure measurement (OBPM) yields higher blood pressure values than HBPM. For systolic blood pressure, differences between OBPM and HBPM increase with age and the height of office pressure. Differences also tend to be greater in men than in women and greater in patients without than in those with antihypertensive treatment. Furthermore, HBPM can diagnose normotension with almost absolute certainty; it correlates better with target organ damage and cardiovascular mortality than OBPM, it enables prediction of sustained hypertension in patients with borderline hypertension, and it proves to be an appropriate tool for assessing drug efficacy. Despite some limitations and although more data are needed, HBPM is suitable for routine clinical practice.
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