An individual participant data meta-analysis was conducted in the data of 14 673 Japanese participants without a history of cardiovascular disease (CVD) to examine the association of the brachial-ankle pulse wave velocity (baPWV) with the risk of development of CVD. During the average 6.4-year follow-up period, 687 participants died and 735 developed cardiovascular events. A higher baPWV was significantly associated with a higher risk of CVD, even after adjustments for conventional risk factors ( P for trend <0.001). When the baPWV values were classified into quintiles, the multivariable-adjusted hazard ratio for CVD increased significantly as the baPWV quintile increased. The hazard ratio in the subjects with baPWV values in quintile 5 versus that in those with the values in quintile 1 was 3.50 (2.14–5.74; P <0.001). Every 1 SD increase of the baPWV was associated with a 1.19-fold (1.10–1.29; P <0.001) increase in the risk of CVD. Moreover, addition of baPWV to a model incorporating the Framingham risk score significantly increased the C statistics from 0.8026 to 0.8131 ( P <0.001) and also improved the category-free net reclassification (0.247; P <0.001). The present meta-analysis clearly established baPWV as an independent predictor of the risk of development of CVD in Japanese subjects without preexisting CVD. Thus, measurement of the baPWV could enhance the efficacy of prediction of the risk of development of CVD over that of the Framingham risk score, which is based on the traditional cardiovascular risk factors.

The arterial wall has 3 layers (ie, the intima, including the endothelium, the media, and the adventitia); each of these layers has individual roles in systemic circulation. The vascular endothelium regulates the vascular tone, hemostasis and/or vascular permeability, and the media is the major determinant of arterial elasticity, which regulates the conduit function (delivery of blood to tissues) and cushioning effect (for generation of continuous blood flow). Failure of these functions results in organ/vascular damage. Several non-invasive methods are currently used to assess vascular dysfunction, including measurement of flow-mediated vasodilatation of the brachial artery induced by reactive hyperemia (FMD), pulse wave velocity (PWV), the augmentation index (AI), and central blood pressure. Endothelial dysfunction, which is assessed by FMD, contributes to the initiation/progression of atherosclerosis. Increased arterial stiffness, which is assessed by the PWV and/or AI, causes increased cardiac afterload, impaired coronary arterial blood supply, atherogenesis and/or microvascular damage. The combination of risk stratification by assessment of conventional risk factors for cardiovascular disease (CVD) with not only a morphological assessment of vascular damage, such as carotid ultrasound examination, but also vascular function tests, may be a useful strategy for the management of CVD and its related risk factors. (Circ J 2010; 74: 24 - 33).

The brachial-ankle pulse wave velocity (brachial-ankle PWV), which is measured simply by wrapping pressure cuffs around the four extremities, is a simple marker to assess the stiffness of the medium- to large- sized arteries. The accuracy and reproducibility of its measurement have been confirmed to be acceptable. Risk factors for cardiovascular disease, especially advanced age and high blood pressure, are reported to be associated with an increase of the arterial stiffness. Furthermore, arterial stiffness might be involved in a vicious cycle with the development/progression of hypertension, diabetes mellitus and chronic kidney disease. Increase in the arterial stiffness is thought to contribute to the development of cardiovascular disease via pathophysiological abnormalities induced in the heart, brain, kidney, and also the arteries themselves. A recent independent participant data meta-analysis conducted in Japan demonstrated that the brachial-ankle PWV is a useful marker to predict future cardiovascular events in Japanese subjects without a previous history of cardiovascular disease, independent of the conventional model for the risk assessment. The cutoff point may be 16.0 m/s in individuals with a low risk of cardiovascular disease (CVD), and 18.0 m/s in individuals with a high risk of CVD and subjects with hypertension. In addition, the method of measurement of the brachial-ankle PWV can also be used to calculate the inter-arm systolic blood pressure difference and ankle-brachial pressure index, which are also useful markers for cardiovascular risk assessment.

Hypertension Research, official publication of the Japanese Society of Hypertension, publishes papers reporting original clinical and experimental research in the field of hypertension and related cardiovascular diseases.

Background: The mechanisms underlying the possible contribution of chronic inflammation to the development of hypertension remain unclear. We examined the longitudinal association of inflammation with the progression of vascular and/or renal abnormalities in the development of hypertension. Methods and Results: In 3274 middle‐aged Japanese men without hypertension at the study baseline, brachial‐ankle pulse wave velocity, blood pressure, estimated glomerular filtration rate, and serum CRP (C reactive protein) levels were measured annually during a 9‐year period. During this study period, 474 participants (14.5%) developed hypertension. Analysis of the repeated‐measures data revealed that sustained elevation of serum CRP levels was associated with a longitudinal increase of the brachial‐ankle pulse wave velocity. A linear mixed model analysis revealed that higher log‐transformed serum CRP values (log CRP ) at each measurement were associated with a higher annual increase of the brachial‐ankle pulse wave velocity (estimate=32.553±11.635 cm/s per log CRP , P =0.018), and that higher values of the brachial‐ankle pulse wave velocity at each measurement were associated with a higher annual elevation of blood pressure (estimate=0.025±0.002 mm Hg per log CRP , P <0.001). Conclusions: In middle‐aged Japanese men without hypertension at study baseline, long‐term active inflammation appears to be associated with a longitudinal increase of arterial stiffness. In turn, this longitudinal increase of arterial stiffness appears to be associated with longitudinal elevation of blood pressure to the hypertensive range. Thus, systemic inflammation may play a role in the pathogenesis of hypertension by the progression of arterial stiffness.