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Errors in blood pressure (BP) measurement account for a large proportion of misclassified hypertension diagnoses. Ambulatory blood pressure monitoring (ABPM) is often considered to be the gold standard for measurement of BP, but uncertainty remains regarding the degree of measurement error. The aim of this study was to determine reproducibility of sequential ABPM in a population of normotensive and well controlled hypertensive individuals.Individual participant data from three randomized controlled trials, which had recorded ABPM and carotid-femoral pulse wave velocity (PWV) at least twice were combined ( n = 501). We calculated within-individual variability of daytime and night-time BP and compared the variability between normotensive ( n = 324) and hypertensive ( n = 177) individuals. As a secondary analysis, variability of PWV measurements was also calculated, and multivariable linear regression was used to assess characteristics associated with blood pressure variability (BPV).Within-individual coefficient of variation (CoV) for systolic BP was 5.4% (day) and 7.0% (night). Equivalent values for diastolic BP were 6.1% and 8.4%, respectively. No statistically significant difference in CoV was demonstrated between measurements for normotensive and hypertensive individuals. Within-individual CoV for PWV exceeded that of BP measurements (10.7%). BPV was associated with mean pressures, and BMI for night-time measurements. PWV was not independently associated with BPV.The variability of single ABPM measurements will still yield considerable uncertainty regarding true average pressures, potentially resulting in misclassification of hypertensive status and incorrect treatment regimes. Repeated ABPM may be necessary to refine antihypertensive therapy.

We compared the agreement between different techniques to estimate central SBP (cSBP) in children and the relative impact of different methods of measuring peripheral blood pressure (BP).A total of 135 children, aged 12.9 ± 3.0 years including 67 boys, 85 with chronic kidney disease were studied. We measured cSBP using radiofrequency ultrasound carotid wall-tracking (Esaote ART.LAB system, a previously validated reference method), transformation of the radial artery pressure waveform obtained by tonometry (SphygmoCor) and a cuff-based system (cBP301; Centron Diagnostics) during a single visit. Carotid and radial tonometric-derived values were calibrated from mean and diastolic values of brachial BP obtained by aneroid sphygmomanometer. Brachial cuff only values were calibrated from the same aneroid sphygmomanometer values and from oscillometric values obtained from the brachial cuff.cSBP values estimated from radial tonometry were closely correlated with those obtained from the carotid (r = 0.959, mean difference -0.61 ± 3.5 mmHg). cSBP values estimated by the brachial cuff only method agreed reasonably well with those obtained from the carotid (r = 0.847, mean difference 5 ± 7.4 mmHg) when calibrated by the same method but when calibrated by oscillometric values from the brachial cuff, agreement was less good (r = 0.659, mean difference 8.7 ± 11.4 mmHg).Radial tonometry with a radial-to-central transfer function can be used to estimate cSBP in children with acceptable accuracy when compared with the invasively validated carotid reference method. All methods are subject to errors introduced by calibration from peripheral BP.

Background Black African/African-Caribbean individuals with hypertension (BH) are at greater risk of heart failure than those of white European ethnicity (WH). The mechanisms underlying this dissimilarity remain poorly understood. Purpose To investigate the influence of ethnicity on left ventricular (LV) remodelling using multi-parametric cardiovascular magnetic resonance (CMR). Methods BH (n=44), WH (n=38) and healthy-volunteers (HV; n=25, 5 of black ethnicity) underwent comprehensive CMR. The exam included: i) Arterial Stiffness/Afterload pulse-wave-velocity (PWV), aortic elastance (Ea) and systemic vascular resistance (SVR) by phase-contrast velocity-encoding imaging; ii) Ventricular remodelling/Function LV and right ventricular (RV) volumes, mass, ejection fraction (EF), LV peak-filling rate by short-axis cine images; myocardial strains were measured by feature tracking; iii) Left atrial (LA) remodelling/Function volumes and functions by long-axis cine images; iv) Tissue characterisation: extracellular volume by pre/post-contrast T1-mapping and late gadolinium enhancement (LGE) for interstitial and replacement myocardial fibrosis, respectively. Multivariate linear regression models were developed to investigate how LV remodelling associates with ethnicity, arterial afterload, including elastance (Ea) and stiffness [PW], and SVR. Models were adjusted for age, gender, body-mass-index, LV volumes or function and LA volumes. Results Subject characteristics are summarised in the Table. PWV and Ea and SVR were greater in hypertensives, particularly in BH, than HV; this was paralleled by higher LV mass, interventricular septum thickness (IVS), LA volumes but lower LV-EF. These findings were confirmed after adjusting for age. On the Model-1, IVS was associated with Ea (β=0.335, P=0.008) and black ethnicity (β=0.226, P=0.019) but not with SVR or PWV. For each increment of Ea there was a similar increase of IVS in BH and WH (P=0.602 for interaction), however BH had greater IVS than WH at each Ea value (Figure, fully-adjusted Model-1). On Model-2, LV end-diastolic volume was associated with Ea (β=−0.268, P=0.001), SVR (β=−0.319, P=0.019) but not with PWV or ethnicity. However, the inverse relation between LV size and Ea was significantly attenuated in BH (P=0.039 for interaction), (Figure, fully-adjusted Model-2). On model-3, LV-EF was associated with Ea (β=0.223, P=0.009) but not with ethnicity, PWV or SVR. LV-EF reduction for each Ea increment was similar for BH and WH (P=0.597 for interaction). Conclusion BH and WH show a distinctive LV remodelling phenotype. BH had a greater susceptibility to hypertrophy and an attenuated reduction of chamber size in response to arterial afterload. Further research to disentangle the genetic and environmental factors underlying these ethnic group-specific differences is utterly required. Funding Acknowledgement Type of funding sources: None. Figure 1Table 1

Funding Acknowledgements Type of funding sources: Foundation. Main funding source(s): Dr Georgiopoulos was supported by the Onassis Foundation under the special grant & support program for scholars" association members Introduction – Black Afro-Caribbean hypertensives (BAHs) are exposed to a higher risk of heart failure (HF) than white hypertensives (WHs). Arterial afterload is higher in BAHs due to increased arterial stiffness and vascular volume; BAHs develop more often left ventricular (LV) hypertrophy, dilatation and systolic dysfunction than WHs. However, it is unclear whether other racial differences concur to the more pronounced LV remodelling in BAHs. Methods – This cross-sectional study included hypertensive patients undergoing cardiovascular magnetic resonance for their clinical work-up (1.5T Aera Siemens-Healthcare). Clinical history and haemodynamic parameters were collected in all participants; a subset of patients had complete bio-humoral assay of the renin-angiotensin-aldosterone system (RAAs). Arm cuff pressure was measured during CMR. The CMR protocol included: i) Arterial afterload / LV arterial-coupling - pulse-wave-velocity (PWV), aortic (Ea) and LV elastance (Ees) by aorta anatomic and phase-contrast velocity-encoding imaging; ii) ventricular remodelling and function - LV and right ventricular (RV) volumes, mass, EF, LV peak-filling rate by short-axis cine images; global circumferential and longitudinal strains by cine feature tracking; iii) left atrial (LA) remodelling volumes and reservoir, conduit and booster functions by long-axis cine images; iv) tissue characterisation: T2 and pre/post-contrast T1 relaxation times, extracellular volume (ECV) by single mid-ventricular short-axis T1/T2-mapping. Results – 34 BAHs and 35 WHs (52 ± 12 vs 45 ± 14 years, P Conclusion – BAHs have heightened LV remodelling than WHs because of racial predisposition to develop hypertrophy which also encompasses derangements in RAAs. Altogether, these findings may account for the greater risk for HF in BAHs than WHs.

We examined the influence of arterial stiffening and ventricular ejection dynamics on the age-related increase in central pulse pressure. A total of 2033 women aged 18 to 91 years from the Twins UK cohort were studied. Aortic flow and central blood pressure were measured by Doppler sonography and carotid tonometry, respectively. Measured values of central pulse pressure were compared with values predicted from aortic pulse wave velocity and ventricular ejection characteristics. Central pulse pressure at the first shoulder ( P1 ) increased with age from 29.2±8.0 in those 70 years (means±SD; P P2 , usually equal to peak central pulse pressure) increased to a greater extent with age: from 29.1±7.8 mm Hg for those 70 years ( P P2/P1 closely mirrored the ratio of ejection volume to ejection velocity at corresponding time points, and the proportionately greater increase in P2 compared with P1 was explained by increased ventricular ejection up to the time of P2 . This increased from 52.5±13.1 to 59.3±17.8 mL ( P

Aims Haemodynamic determinants of blood pressure (BP) include cardiac output (CO), systemic vascular resistance (SVR), and arterial stiffness. We investigated the heritability of these phenotypes, their association with BP-related single-nucleotide polymorphisms (SNPs), and the causal association between BP and arterial stiffness. Methods and results We assessed BP, central BP components, and haemodynamic properties (during a single visit) including CO, SVR, and pulse wave velocity (PWV, measure of arterial stiffness) in 3531 (1934 monozygotic, 1586 dizygotic) female TwinsUK participants. Heritability was estimated using structural equation modelling. Association with 984 BP-associated SNP was examined using least absolute shrinkage and selection operator (LASSO) and generalized estimating equation regression. One and two-sample Mendelian randomization (MR) was used to estimate the causal direction between BP and arterial stiffness including data on 436 419 UK Biobank participants. We found high heritability for systolic and pulsatile components of BP (>50%) and PWV (65%) with overlapping genes accounting for >50% of their observed correlation. Environmental factors explained most of the variability of CO and SVR (>80%). Regression identified SNPs (n = 5) known to be associated with BP to also be associated with PWV. One-sample MR showed evidence of bi-directional causal association between BP and PWV in TwinsUK participants. Two-sample MR, confirmed a bi-directional causal effect of PWV on BP (inverse variance weighted (IVW) beta = 0.11, P < 0.02) and BP on arterial stiffness (IVW beta = 0.004, P < 0.0001). Conclusion The genetic basis of BP is mediated not only by genes regulating BP but also by genes that influence arterial stiffness. Mendelian randomization indicates a bi-directional causal association between BP and arterial stiffness.

Supplemental Digital Content is available in the text., We examined the influence of arterial stiffening and ventricular ejection dynamics on the age-related increase in central pulse pressure. A total of 2033 women aged 18 to 91 years from the Twins UK cohort were studied. Aortic flow and central blood pressure were measured by Doppler sonography and carotid tonometry, respectively. Measured values of central pulse pressure were compared with values predicted from aortic pulse wave velocity and ventricular ejection characteristics. Central pulse pressure at the first shoulder (P1) increased with age from 29.2±8.0 in those 70 years (means±SD; P70 years (P

Differences between central aortic root (c) and peripheral (p) systolic blood pressure (SBP) may be particularly marked in children, but noninvasive methods for assessing cSBP in children have not been validated. We compared estimates of cSBP obtained from radiofrequency ultrasound wall tracking of the carotid artery (ART.LAB system) with that measured directly by a catheter in the aortic root at the time of arterial cannulation. Carotid waveforms were calibrated from invasive measurements of mean and diastolic pressures. In 9 children aged 10.5±5.0 years (mean±SD), cSBP obtained from carotid wall tracking was highly correlated with invasive measures of cSBP ( r =0.99) with mean (±SD) difference 3.9±2.5 mm Hg. Second, we compared values of cSBP obtained from the carotid with those obtained using noninvasive applanation tonometry at the radial artery and a radial-to-aortic transfer function (SphygmoCor). Both carotid and radial tonometric measurements were calibrated from the same peripheral mean and diastolic measurements of blood pressure obtained by sphygmomanometry. In 84 children aged 13.2±3.2 years, there was excellent agreement between the 2 methods ( r =0.95; P

AimsVascular ageing is characterized by arterial stiffening, dilation, and arterial wall thickening. We investigated the extent to which these changes are related and their heritability during 5 year follow-up in the Twins UK cohort.Methods and resultsCarotid-femoral pulse wave velocity (PWVcf), carotid diameter, carotid distensibility, and carotid intima-media thickness (IMT) were measured in 762 female twins (mean age 57.9 ± 8.6 years) at two time-points over an average follow-up of 4.9 ± 1.5 years. Magnetic resonance imaging (MRI) was performed in a sub-sample of 38 women to measure aortic pulse wave velocity (PWVaorta), diameter, and wall thickness. Heritability of changes in arterial wall properties was estimated using structural equation modelling. Annual increases in PWVcf, carotid diameter, distensibility, and IMT were 0.139 m/s, 0.028 mm, −0.4 kPa−1, and 0.011 mm per year, respectively. In regression analysis, predictors of progression in PWVcf included age, mean arterial pressure (MAP), and heart rate (HR) at baseline, and progression in MAP, HR, and body mass index (BMI). Predictors of progression in IMT included progression in MAP, BMI, and triglyceride levels. Progression of PWV and distensibility correlated with progression in carotid diameter but not with IMT. Heritability of progression of PWVcf, diameter, and IMT was 55%, 21%, and 8%, respectively. In a sub-sample of women that underwent MRI, aortic wall thickness increased by 0.19 mm/year, but aortic wall thickening was not correlated with an increase in lumen diameter or PWVaorta.ConclusionArterial stiffening, as measured by PWVcf, and dilation are heritable but independent of arterial wall thickening. Genetic and cardiovascular risk factors contribute differently to progression of PWV and IMT.

Background: Arterial stiffness as measured by PWV along the aorta is an important determinant of cardiovascular risk. PWV is known to be dependent on contemporaneous blood pressure (BP) but its dependence on long-term BP has not been established. Methods: Subjects from Twins UK who had tonometric measures of carotid-femoral PWV with previous longitudinal measures of blood pressure (n = 2094) and, in a sub-sample, PWV (n=956) were studied. Brachial artery pulse pressure (PP) and mean arterial pressure (MAP) were averaged over the period of longitudinal follow-up to obtain measures of historical PP and MAP (PPH and MAPH). The relationship of PWV to contemporaneous PP and MAP (PPC and MAPC) was compared with that to PPH and MAPH. Results: The average duration of blood pressure measurement was 14.0 ± 4.3 years.PWV correlated strongly with PPC (r = 0.542, p < 0.001), PPH (r = 0.474,p < 0.001), MAPC (r = 0.462, p < 0.001) and MAPH (r = 0.360, p < 0.001). In multiple regression analysis incorporating historical and contemporaneous values of PP and MAP as well as age and heart rate, PWV was significantly associated with PPC, MAPC and PPH but not with MAPH. In the sub-study in which historical values of PWV were available, PWV increased by 0.75 ± 1.42 m/s, over an average of 5.5 ± 1.7years. The change in PWV was associated with MAPC and with PPH (β = 0.144, p < 0.001). Conclusions: These results are consistent with strong dependence of PWV on contemporaneous BP but also historical values of pulse pressure which may drive arterial stiffening.

We thank Papaioannou and colleagues for their interest in our study.1 They raise several related concerns regarding the influence of errors in the determination of peripheral blood pressure (BP; which our study did not address) on estimates of central blood pressure.2 We agree that this is a most important point. All of the current noninvasive methods for measuring central blood pressure require calibration from peripheral BP measurements. However, errors in peripheral BP are transferred to central blood pressure, so that the difference between central and peripheral systolic blood pressure is affected little by peripheral calibration3 and the ratio of central to peripheral pulse pressure is not affected by calibration. Thus, if relative differences (eg, effects of treatment on central versus peripheral BP) are of interest, the issue of calibration is less critical. For absolute measurements …

We compared large artery mechanical properties in children with nondialysis stages of chronic kidney disease with those in children with normal renal function, examining the potential effect of blood pressure (BP) components and level of renal dysfunction. Common carotid artery mechanical properties, carotid-femoral pulse wave velocity, and carotid and peripheral BP were measured in children (n=226) with nondialysis chronic kidney disease (n=188; 11.9±3.7 years; 26%, 25%, 30%, 16%, and 3% in stages 1, 2, 3, 4 and 5, respectively) and healthy controls (n=38; 11.5±3.3 years). In children with nondialysis chronic kidney disease when compared with healthy controls, at similar levels of peripheral and carotid BP, carotid artery diastolic diameter and wall thickness were similar. In those with suboptimal BP (≥75th percentile), indices of arterial elasticity indicated greater stiffness than in healthy normotensive controls (distensibility: 92±31 versus 114±33 kPa −1 ×10 −3 , P =0.03; compliance: 2.1±0.7 versus 2.6±0.7 m 2 kPa −1 ×10 −6 , P =0.02; Young elastic modulus: 0.151±0.068 versus 0.109±0.049 kPa×10 3 , P =0.02; and wall stress: 83.6±23.5 versus 68.7±14.9 kPa, P =0.02). In all children, mechanical properties were independently related to carotid and peripheral BP components but not to estimated glomerular filtration rate. In children with nondialysis chronic kidney disease, changes in elastic properties of the carotid artery are primarily related to BP and not to glomerular renal function.

Aortic pulse wave velocity (aPWV), a major prognostic indicator of cardiovascular events, may be augmented in hypertension as a result of the aorta being stretched by a higher distending blood pressure or by a structural change. We used a novel technique to modulate intrathoracic pressure and thus aortic transmural pressure (TMP) to examine the variation of intrathoracic aPWV with TMP in hypertensive (n=20; mean±SD age, 52.1±15.3 years; blood pressure, 159.6±21.2/92.0±15.9 mm Hg) and normotensive (n=20; age, 55.5±11.1 years; blood pressure, 124.5±11.9/72.6±9.1 mm Hg) subjects. aPWV was measured using dual Doppler probes to insonate the right brachiocephalic artery and aorta at the level of the diaphragm. Resting aPWV was greater in hypertensive compared with normotensive subjects (897±50 cm/s versus 784±43 cm/s; P P

Objectives: To investigate large artery viscoelastic properties in children with non-dialysis stages of CKD and compare these with healthy children with normal renal function and (ii) to evaluate the impact of blood pressure components following adjustment for level of renal dysfunction. Methods: Prospective single centre study including 226 children [188 children with non-dialysis CKD (11.9 3.7 years) and 38 controls (11.5 3.3 years)] were recruited from tertiary out-patient clinics. Common carotid artery parameters were non-invasively determined using a high-definition echotracking system. Peripheral and central BP were also measured noninvasively. Results: When compared to controls, in children with CKD with similar levels of peripheral and central BP, anatomical measures of arterial properties such as lumen diameter and carotid wall thickness remained comparable. In those with BP >75th percentile there were significant differences between elastic properties of the carotid artery when compared with controls: distensibility (92 31 versus 114 33 kPa-1 x 103, pZ0.03), compliance (2.1 0.7 versus 2.6 0.7 m2 kPa-1 x 106, pZ0.02), Young’s elastic modulus (0.151 0.068 versus 0.109 0.049 kPa x 10-3, pZ0.02) and wall stress (83.6 23.5 versus 68.7 14.9 kPa, pZ0.02). These differences were independent of glomerular filtration rate (GFR). Multivariate regression analyses displayed brachial mean arterial pressure (MAP), carotid systolic and carotid pulse pressure were all associated with carotid artery functional elasticity following adjustment for age, body mass index and GFR. Conclusions: Changes in elasticity of the carotid artery is one of the earliest identifiable alterations in children with non-dialysis CKD but is primarily explained by level of blood pressure and not that of renal function.

Aortic pulse wave velocity (aPWV), a major prognostic indicator of cardiovascular events, may be augmented in hypertension as a result of the aorta being stretched by a higher distending blood pressure or by a structural change. We used a novel technique to modulate intrathoracic pressure and thus aortic transmural pressure (TMP) to examine the variation of intrathoracic aPWV with TMP in hypertensive (n=20; mean±SD age, 52.1±15.3 years; blood pressure, 159.6±21.2/92.0±15.9 mm Hg) and normotensive (n=20; age, 55.5±11.1 years; blood pressure, 124.5±11.9/72.6±9.1 mm Hg) subjects. aPWV was measured using dual Doppler probes to insonate the right brachiocephalic artery and aorta at the level of the diaphragm. Resting aPWV was greater in hypertensive compared with normotensive subjects (897±50 cm/s versus 784±43 cm/s; P P

Background: Pulse wave velocity (PWV), a measure ofarterial stiffness strongly predictive of cardiovascular riskin adults, is usually measured by sequential ECG-referenced carotid and femoral tonometry. A simplifiedtechnique, more suitable for use in children, employssimultaneous volumetric recording from a sensor appliedover the carotid artery and a cuff applied over thefemoral artery or arm and thigh pressure cuffs appliedover the brachial and femoral arteries. The purpose ofthis study was to compare PWV computed over thecarotid-femoral path (PWVcf) with that over thebrachial-femoral path (PWVbf) using a volumetric system(Vicorder) and to compare values of PWVcf obtained bythe volumetric and a tonometric method (SphygmoCor)in children.Method: Vicorder PWVcf and PWVbf were comparedin 156 children (3–18 years, 110 with chronickidney disease), and PWVcf by Vicorder wascompared to PWVcf by SphygmoCor in a subset of122 patients.Results: PWVcf by Vicorder was moderately correlatedwith PWVcf by SphygmoCor (R¼0.50, P