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Background: The Opening Angle (OA) is widely used as an index of the residual stresses and strains present in the arterial wall not subjected to internal pressure. The aim of this work was to quantify regional variation of the layer-specific OA in the bovine descending thoracic aorta. Methods: Descending thoracic aortae from 7 cows were segmented into 3–4 mm wide rings. Geometrical features (mean internal/external radius Rin and Rout, wall thickness h) were measured. A radial cut was made on the anterior region of each ring, and then the rings were placed in a temperature-controlled water bath (37 °C) for 1.5 h to express the OA. The rings were separated into their three layers and the layer-specific OA was investigated. The separation of the intima from the media is a complex procedure due to its limited thickness. The isolated intima was therefore thicker than values reported in the literature. Results: Except for the most proximal region, h/Rin decreased towards the periphery (table 1). The medial and whole aortic wall OA increased moving towards the periphery, whilst the adventitia showed the opposite behaviour. The intimal OA was significantly higher and relatively constant (figure 1). Conclusions: The present set of experiments indicates that the compressive residual stresses are concentrated mainly in the internal part of the intima-media layer independently from the considered axial region. The other layers exhibit comparable OAs to the whole arterial wall.

An amendment to this paper has been published and can be accessed via the original article.

Brachial cuff blood pressure (BP) is clinically important, but may be an inaccurate substitute for central BP. Many non-invasive devices have been developed that purport to estimate central BP from peripheral artery sites, yet with no standardized guidelines; the accuracy testing of these new devices has not been undertaken in a uniform fashion with comparable protocols. This is an abridged paper describing the recommendations reached by an international task force convened to identify issues that need to be addressed and reach consensus relating to methods for assessing and reporting the accuracy (validation) of central BP devices. The recommendations are endorsed by the Association for Research into Arterial Structure and Physiology (ARTERY) Society, as well as the European Society of Hypertension (ESH) Working Group on Arterial Structure and Function, and the ESH Working Group on Blood Pressure Monitoring and Cardiovascular Variability. Researchers interested in validating central BP monitors should read the full version of the statement.

BackgroundPhysical activity is associated with reduced cardiovascular disease risk, mainly through effects on atherosclerosis. Aortic stiffness may be an alternative mechanism. We examined whether patterns of physical activity and sedentary behavior are associated with rate of aortic stiffening. Methods and ResultsCarotid–femoral pulse wave velocity (PWV) was measured twice using applanation tonometry at mean ages 65 (in 2008/2009) and 70 (in 2012/2013) years in the Whitehall‐II study (N=5196). Physical activity was self‐reported at PWV baseline (2008/2009) and twice before (in 1997/1999 and 2002/2003). Sedentary time was defined as sitting time watching television or at work/commute. Linear mixed models adjusted for metabolic and lifestyle risk factors were used to analyze PWV change. Mean (SD) PWV (m/s) was 8.4 (2.4) at baseline and 9.2 (2.7) at follow‐up, representing a 5‐year increase of 0.76 m/s (95% CI 0.69, 0.83). A smaller 5‐year increase in PWV was observed for each additional hour/week spent in sports activity (−0.02 m/s [95% CI −0.03, −0.001]) or cycling (−0.02 m/s [−0.03, −0.008]). Walking, housework, gardening, or do‐it‐yourself activities were not significantly associated with aortic stiffening. Each additional hour/week spent sitting was associated with faster PWV progression in models adjusted for physical activity (0.007 m/s [95% CI 0.001, 0.013]). Increasing physical activity over time was associated with a smaller subsequent increase in PWV (−0.16 m/s [−0.32, −0.002]) compared with not changing activity levels. ConclusionsHigher levels of moderate‐to‐vigorous physical activity and avoidance of sedentary behavior were each associated with a slower age‐related progression of aortic stiffness independent of conventional vascular risk factors.

BackgroundRheumatoid arthritis is a systemic inflammatory condition associated with increased cardiovascular risk that may be due to underlying endothelial dysfunction and subsequent aortic stiffening. We hypothesized that supplementation with tetrahydrobiopterin (BH4) would recouple endothelial nitric oxide synthase and thus improve endothelial function and consequently reduce aortic stiffness. Methods and ResultsWe conducted 2 randomized, double‐blinded, placebo‐controlled crossover studies examining 2 separate regimens: an acute regimen, with a single dose of BH4 400 mg versus placebo (n=18), and a short‐term regimen, composed of a 1‐week treatment with BH4 400 mg once daily versus placebo (n=15). Flow‐mediated dilatation and aortic pulse wave velocity were studied 4 times, before and after each treatment phase. Acute BH4 supplementation led to an improvement of flow‐mediated dilatation, whereas placebo had no effect (mean±SD of effect difference 2.56±4.79%; P=0.03). Similarly, 1‐week treatment with BH4 improved endothelial function, but there was no change with placebo (mean±SD of effect difference 3.50±5.05%; P=0.02). There was no change in aortic pulse wave velocity following acute or short‐term BH4 supplementation or placebo (mean±SD of effect difference: acute 0.09±0.67 m/s, P=0.6; short‐term 0.03±1.46 m/s, P=0.9). ConclusionBoth acute and short‐term supplementation with oral BH4 improved endothelial function but not aortic stiffness. This result suggests that BH4 supplementation may be beneficial for patients with rheumatoid arthritis by improving endothelial dysfunction and potentially reducing risk of cardiovascular disease. There appears to be no causal relationship between endothelial function and aortic stiffness, suggesting that they occur in parallel, although they may share common risk factors such as inflammation.

Background: COPD is independently associated with increased cardiovascular events. Arterial stiffening and systemic inflammation are postulated aetiological factors. We hypothesised that vascular inflammation links systemic inflammation with vascular stiffening and sought to test this in a cohort of COPD subjects undergoing baseline FDG PET/CT either as part of the EVOLVE observational study or EVOLUTION trial (NCT 01541852). Methods: 85 COPD subjects underwent assessments including spirometry, arterial stiffness (aortic pulse wave velocity (aPWV)), inflammatory biomarkers (fibrinogen and hsCRP) and FDG PET/CT imaging (lungs, aorta and carotids) to evaluate inflammation and aortic calcification. Results: 66% of the cohort were male, median age was 68 (IQR 63–73) years, 87% were ex-smokers. Mean aPWV was 9.9 (SEM 0.2) m/s, aortic calcification volume 7156 (1461) mm3, hsCRP 5.2 (0.8) mg/dl, fibrinogen 3.4 (0.08) g/l. Log hsCRP correlated only with carotid FDG uptake (R=0.23, p=0.04) and log fibrinogen did not correlate with FDG uptake in any vascular region. Systemic inflammatory markers were positively associated with aortic inflammation but only weakly. The estimated change in FDG uptake was 0.2 (95% CI 0.11–0.29) and 0.07 (0.06–0.08), for each log unit change in fibrinogen and hsCRP respectively. Aortic inflammation was not a significant determinant of aPWV, but aortic calcification was, adjusted for age, supine HR, MAP and years smoked (p=0.02, β=0.26). Conclusion: HsCRP and fibrinogen are weak predictors of vascular inflammation and therefore likely unsuitable stratification biomarkers of vascular inflammation in COPD. Calcification rather than inflammation appears to be the dominant pathophysiological mechanism underlying arterial stiffness in COPD.

Introduction: COPD is associated with increased cardiovascular risk, independent of established risk factors. Arterial stiffness is a surrogate of cardiovascular risk and we sought to determine its relationship with COPD severity and prognosis in the ERICA (Evaluation of role of inflammation in airways disease) multi-site UK study: the largest cohort study focusing on cardiovascular manifestations in COPD. Methods: Spirometry and haemodynamic measures (aortic pulse wave velocity (aPWV), augmentation index (AIx)) were performed in 729 COPD subjects aged ≥40 years. COPD severity was classified by BODE Index [BMI (low BMI worse prognosis), Obstruction (FEV1), Dyspnoea (mMRC score), Exercise tolerance (6-minute walk distance) high BODE index: worse outcome], a validated score based on clinical variables and an independent predictor of mortality in COPD. Results: Mean aPWV was 10.3 (SD 2.6) m/s, AIx 27 (10)%. BODE correlated with aPWV (R = 0.2, p = 0.0001) and this was maintained when adjusted for study site, age, supine HR and MAP, years smoked and cardiovascular comorbidities (MI, stroke, diabetes, peripheral vascular disease), (β = 0.2, p = 0.0001). BODE was also a determinant of AIx when adjusted for site, age, seated HR and MAP, years smoked and cardiovascular comorbidities (β = 0.1, p = 0.02). Conclusions: BODE is associated with arterial stiffness in COPD, independent of traditional risk factors. Its composite variables are not on the causal pathway for vascular stiffness, so its association likely reflects patient susceptibility to smoke injury in the lungs and vasculature. BODE may also enhance cardiovascular risk stratification in COPD, since its relationship with stiffness was independent of self-reported cardiovascular comorbidities.

Background: Central systolic blood pressure (cSBP) may be more predictive of cardiovascular events than brachial BP. Therefore, non-invasive methods of determining central BP, which are suitable for routine clinical use, are required. The aim of this study was to compare estimates of cSBP provided by the Centron cBP301 with those obtained with the widely used SphygmoCor system. Methods: In 60 subjects (30 females), age range 22–90 years, brachial BP was measured using the Centron device and then cSBP estimated using the Centron, and then SphygmoCor. In a subset of 16 subjects (8 females), measurements were repeated at rest and following the administration of glyceryl trinitrate (GTN). Results: There was a strong correlation (r = 0.98; P < 0.001) between the estimates of cSBP obtained with each device. There was also good agreement between devices, with a mean difference (±SD) of 0.2 ± 3.5 mmHg (P = 0.5). Similarly, the devices were highly correlated and in good agreement following the administration of GTN, with the mean difference in cSBP ranging from 0.5 ± 3.9 mmHg to 2.3 ± 3.7 mmHg, across the measurement period. Conclusion: The Centron cBP301 and SphygmoCor devices produce similar estimates of cSBP, both at rest and in response to a pharmacological challenge. The Centron device is potentially suitable for routine clinical monitoring of central BP.

Systemic inflammatory conditions are associated with an increased risk of cardiovascular disease (CVD). How exactly inflammation leads to this is not fully understood, but it has been suggested that arterial stiffening, could provide potential mechanisms to explain it. Chronic, systemic inflammatory conditions, as well as acute-models of inflammation are associated with arterial stiffening. Moreover, aortic stiffness can be reversed with successful immunomodulatory therapy. Although it seems evident that inflammation is involved in the process of aortic stiffening, the precise mechanism responsible for this remains unclear. There are number of possible mechanisms by which inflammation could lead to arterial stiffening. (1) Inflammation is associated with endothelial dysfunction and this can regulate arterial stiffness via changes in smooth muscle tone. (2) Inflammation leads to increased synthesis of matrix metalloproteinases, which can degrade elastin, resulting in stiffening. (3) Several mediators of inflammation may directly stimulate vascular calcification, whereas endogenous inhibitors of vascular calcification are downregulated during inflammation, both of which can lead to stiffening. (4) During inflammation arterial glycosaminoglycan (GAG) synthesis is upregulated. In animal models, an overproduction of certain GAGs in the aorta results in stiffening of the arterial wall by thinning of elastic lamellae. (5) Finally, direct vascular inflammation could lead to arterial stiffening by changing the composition of extracellular matrix. This review aims to discuss potential mechanisms by which inflammation could lead to aortic stiffening.

The last 15 years have seen an explosion of interest in large artery haemodynamics, and arterial stiffness in particular. A number of devices are now available to assess arterial stiffness, and although many are in routine use, they do not necessarily provide identical information. The aim of this statement is to provide guidelines for the process of validating new devices. The focus of the article is aortic pulse wave velocity. We hope that equipment manufacturers, and researchers will both find these guidelines helpful, and that they will allow greater standardization of aortic pulse wave velocity measurements.

Central blood pressure is increasingly considered to be more predictive of cardiovascular events than peripheral pressure. Central systolic pressure (cSBP) can be estimated from the late systolic shoulder (pSBP2) of the radial pulse waveform. The Omron HEM-9000AI utilizes this technique to non-invasively measure cSBP through semi-automated applanation tonometry. The aim of this study was to compare the Omron HEM-9000AI with an existing device, the SphygmoCor, and to test its reproducibility. 33 subjects were tested using both the Omron and the SphygmoCor devices, which identify pSBP2 in the radial waveform, and estimate cSBP and peripheral augmentation index (pAIx) using their inbuilt software. 10 subjects were retested after a period of 24 h to determine reproducibility. There was a strong correlation (r = 0.94; P < 0.001), and no difference between mean values of pSBP2 (0.8 ± 4.8 mmHg; P = 0.4) measured by the two devices. However estimates of cSBP were significantly higher in the Omron than the SphygmoCor (12.2 ± 4.6 mmHg; P < 0.001), despite significant correlation (r = 0.95; P < 0.001). pAIx measurements were correlated (r = 0.85; P < 0.001) with no significant difference between absolute values (mean difference = 1 ± 9.2%; P = 0.6). Results from both devices were reproducible, with significant correlation and insignificant mean differences for values of cSBP and pAIx. pSBP2 values were highly correlated, but a direct analysis with invasive measurements is necessary to determine which estimate of cSBP is most accurate. Excluding this discrepancy, the Omron system is potentially useful for measuring pSBP2 and pAIx in large scale trials.