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Home blood pressure (HBP) measurements are known to be lower than conventional office blood pressure (OBP) measurements. However, this difference might not be consistent across the entire age range and has not been adequately investigated. We assessed the relationship between OBP and HBP with increasing age using the International Database of HOme blood pressure in relation to Cardiovascular Outcome (IDHOCO). OBP, HBP and their difference were assessed across different decades of age. A total of 5689 untreated subjects aged 18-97 years, who had at least two OBP and HBP measurements, were included. Systolic OBP and HBP increased across older age categories (from 112 to 142 mm Hg and from 109 to 136 mm Hg, respectively), with OBP being higher than HBP by ∼7 mm Hg in subjects aged >30 years and lesser in younger subjects (P=0.001). Both diastolic OBP and HBP increased until the age of ∼50 years (from 71 to 79 mm Hg and from 66 to 76 mm Hg, respectively), with OBP being consistently higher than HBP and a trend toward a decreased OBP-HBP difference with aging (P

Aims: In mice, MEOX2/TCF15 heterodimers are highly expressed in heart endothelial cells and are involved in the transcriptional regulation of lipid transport. We investigated whether coronary heart disease (CHD) in humans is associated with variation in these genes. Methods and results: In 2027 participants enrolled in the Flemish Study on Environment, Genes and Health Outcomes (51.0% women; mean age 43.6 years), we genotyped SNPs in MEOX2 and TCF15, measured baseline cardiovascular risk factors, and recorded CHD incidence. Over 15.2 years (median), CHD occurred in 106 participants. For SNPs, we contrasted minor-allele heterozygotes and homozygotes (variant) vs. major-allele homozygotes (reference) and for haplotypes carriers vs. non-carriers. Sex- and age-standardised CHD rates were higher in MEOX2 rs10777, rs12056299, rs7787043, rs4532497, rs1050290 variants, in MEOX2 GTCCGC haplotype carriers (prevalence, 16.5%), but lower in MEOX2 rs6959056 variants (P ≤ 0.04, adjusted for multiple testing). In multivariable-adjusted analyses, the corresponding hazard ratios were ≥1.50 (P ≤ 0.049), 1.77 (P = 0.0054) and 0.62 (P = 0.025), respectively. None of four TCF15 SNPs was associated with coronary risk (P ≥ 0.29). However, CHD risk associated with MEOX2 rs4532497 was confined to TCF15 rs12624577 variant allele carriers (P for interaction = 0.011). The MEOX2 GTCCGC hap-lotype significantly improved the prediction of CHD over and beyond traditional risk factors and was associated with similar population-attributable risk as smoking (18.7% vs. 16.2%). Conclusions: In randomly recruited Flemish, genetic variation in MEOX2, but not TCF15, is a strong predictor of CHD. Further experimental studies should elucidate the underlying molecular mechanisms.

Background: Carboxylation of matrix Gla protein (MGP), a vitamin K dependent process, activates the protein to a powerful inhibitor of arterial calcification. Circulating dephosphorylated and uncarboxylated MGP (dp-ucMGP) and total uncarboxylated MGP (t-ucMGP) are associated with macrovascular disease. The association with microcirculatory disease remains unknown. Methods: In 1174 randomly recruited Flemish (51.4% women; mean age, 38.2 years), we studied the estimated glomerular filtration rate (eGFR) and microalbuminuria, as prototypes of microcirculatory traits, in relation to dp-ucMGP and t-ucMGP. In multivariable linear and logistic regressions, we expressed effect sizes for a doubling of the biomarkers, while accounted for anthropometric characteristics, lifestyle, risk factors and use of medications. Results: Among all participants, geometric means of dp-ucMGP and t-ucMGP were 3.68 mg/L and 45.2 mg/L, respectively. In relation to dp-ucMGP (figure), eGFR decreased by 1.57 mL/min/1.73 m2 (p=0.015), while the risk of renal dysfunction (eGFR

Background In mice MEOX2/TCF15 heterodimers are highly expressed in heart endothelial cells and are involved in the transcriptional regulation of lipid transport. In a general population, we investigated whether genetic variation in these genes predicted coronary heart disease (CHD). Results In 2027 participants randomly recruited from a Flemish population (51.0 % women; mean age 43.6 years), we genotyped six SNPs in MEOX2 and four in TCF15. Over 15.2 years (median), CHD, myocardial infarction, coronary revascularisation and ischaemic cardiomyopathy occurred in 106, 53, 78 and 22 participants. For SNPs, we contrasted CHD risk in minor-allele heterozygotes and homozygotes (variant) vs. major-allele homozygotes (reference) and for haplotypes carriers (variant) vs. non-carriers. In multivariable-adjusted analyses with correction for multiple testing, CHD risk was associated with MEOX2 SNPs (P ≤ 0.049), but not with TCF15 SNPs (P ≥ 0.29). The MEOX2 GTCCGC haplotype (frequency 16.5 %) was associated with the sex- and age-standardised CHD incidence (5.26 vs. 3.03 events per 1000 person-years; P = 0.036); the multivariable-adjusted hazard ratio [HR] of CHD was 1.78 (95 % confidence interval, 1.25–2.56; P = 0.0054). For myocardial infarction, coronary revascularisation, and ischaemic cardiomyopathy, the corresponding HRs were 1.96 (1.16–3.31), 1.87 (1.20–2.91) and 3.16 (1.41–7.09), respectively. The MEOX2 GTCCGC haplotype significantly improved the prediction of CHD over and beyond traditional risk factors and was associated with similar population-attributable risk as smoking (18.7 % vs. 16.2 %). Conclusions Genetic variation in MEOX2, but not TCF15, is a strong predictor of CHD. Further experimental studies should elucidate the underlying molecular mechanisms. Electronic supplementary material The online version of this article (doi:10.1186/s12863-015-0272-2) contains supplementary material, which is available to authorized users.

Background There is limited information on prevalent and incident atrial fibrillation in Chinese. We aimed to investigate the prevalence, incidence, management and risks of atrial fibrillation in an elderly Chinese population. Methods In a population—based prospective study in elderly (≥60 years) Chinese, we performed cardiovascular health examinations including a 12-lead electrocardiogram at baseline in 3,922 participants and biennially during follow-up in 2,017 participants. We collected information on vital status during the whole follow-up period. Results The baseline prevalence of atrial fibrillation was 2.0 % (n = 34) in 1718 men and 1.6 % (n = 36) in 2204 women. During a median 3.8 years of follow-up, the incidence rate of atrial fibrillation (n = 34) was 4.9 per 1000 person-years (95 % confidence interval [CI], 3.4–6.9). In univariate analysis, both the prevalence and incidence of atrial fibrillation were higher with age advancing (P

Blood pressure variability includes short-term, circadian, and long-term components. Assessment of blood pressure variability requires multiple readings obtained within a single or several visits, by home or 24-hour ambulatory blood pressure monitoring, or by beat-to-beat recordings. Factors that affect visit-to-visit and diurnal blood pressure variability, as reviewed elsewhere1–6 include ethnicity,1 sex,2,3 age,2,3 hypertension,3 body mass index,2,3 use of β-blockers,3,4 a history of cardiovascular disease,2,5 renal dysfunction,5 diabetes mellitus,2 a sedentary lifestyle,5 and socioeconomic position.6 The prognostic significance of blood pressure variability remains controversial. Some studies reported association of end-organ damage,7–9 cardiovascular events,4,10–15 or mortality5 with blood pressure variability, whereas others failed to do so or found variability to be inferior to the level of blood pressure.3,16,17 Several publications proposing that the magnitude of the morning blood pressure surge predicted stroke,18 in particular cerebral hemorrhage,19 or cardiovascular endpoints20 remained unconfirmed in recently published large-scale observational studies.21–23 This review will address the current controversy on the morning blood pressure surge, highlight the methodological problems in capturing blood pressure variability, and illustrate how large international population studies and a clinical trial do not support blood pressure variability as target in the management of hypertension. Current indexes of blood pressure variability raise methodological issues related to their poor reproducibility, their interdependence, and their association with the level of blood pressure. We will use the morning surge in blood pressure as a showcase to highlight how inconsistent definitions and poor reproducibility limit the clinical applicability of indexes of blood pressure variability. In 2003, Kario et al18 introduced 2 definitions of …

Background. The level at which low-level lead exposure produces subclinical adverse health effects in adults remains to be established. Methods. The Study for Promotion of Health in Recycling Lead (SPHERL) will enroll 500 newly hired workers, whose blood lead during 2 years of follow-up is expected to increase from levels less than 2 μg/dl, as currently observed in the US population, to 20-30 μg/dl. The main outcome variables to be studied are (i) blood pressure (BP) analyzed as a continuous or categorical variable, both cross-sectionally and longitudinally, and using conventional and ambulatory BP measurement; (ii) indexes of glomerular and tubular renal function, (iii) heart rate variability analyzed in the frequency domain as measure of autonomous sympathetic modulation, (iv) peripheral nerve conductivity velocity, (v) neurocognitive performance, and (vi) quality of life. Expected outcomes. Assuming a 10-fold increase in blood lead, SPHERL will have sufficient statistical power to detect over 2 years a steepening of the age-related rise in systolic BP from 1 to 5 mmHg and a doubling of the age-related decline in the estimated glomerular filtration rate from 3.5 to 7.0 ml/min/1.73 m(2). The longitudinal design of our study complies with the temporality principle of the Bradford-Hill criteria for assessing possible causality between outcomes and exposure. SPHERL will attempt to resolve the apparent contradiction between general population studies showing associations between adverse health effects and low lead exposure with blood lead levels below 5 μg/dl and studies conducted in occupational cohorts indicating that adverse effects of lead exposure occur at much higher blood lead levels. peerreview_statement: The publishing and review policy for this title is described in its Aims & Scope. aims_and_scope_url: http://www.tandfonline.com/action/journalInformation?show=aimsScope&journalCode=iblo20 ispartof: Blood Pressure vol:24 issue:3 pages:147-57 ispartof: location:England status: published

Hypertension guidelines propose home or ambulatory blood pressure monitoring as indispensable after office measurement. However, whether preference should be given to home or ambulatory monitoring remains undetermined. In 831 untreated outpatients (mean age, 50.6 years; 49.8% women), we measured office (3 visits), home (7 days), and 24-h ambulatory blood pressures. We applied hypertension guidelines for cross-classification of patients into normotension or white-coat, masked, or sustained hypertension. Based on office and home blood pressures, the prevalence of white-coat, masked, and sustained hypertension was 61 (10.3%), 166 (20.0%), and 162 (19.5%), respectively. Using daytime (from 8 am to 6 pm ) instead of home blood pressure confirmed the cross-classification in 575 patients (69.2%), downgraded risk from masked hypertension to normotension ( n =24) or from sustained to white-coat hypertension ( n =9) in 33 (4.0%), but upgraded risk from normotension to masked hypertension ( n =179) or from white-coat to sustained hypertension ( n =44) in 223 (26.8%). Analyses based on 24-h ambulatory blood pressure were confirmatory. In adjusted analyses, both the urinary albumin-to-creatinine ratio (+20.6%; confidence interval, 4.4–39.3) and aortic pulse wave velocity (+0.30 m/s; confidence interval, 0.09–0.51) were higher in patients who moved up to a higher risk category. Both indexes of target organ damage and central augmentation index were positively associated ( P ≤0.048) with the odds of being reclassified. In conclusion, for reliably diagnosing hypertension and starting treatment, office measurement should be followed by ambulatory blood pressure monitoring. Using home instead of ambulatory monitoring misses the high-risk diagnoses of masked or sustained hypertension in over 25% of patients.

Objective: To evaluate the predictive value for cardiovascular disease incidence (CVD) of brachial-ankle pulse wave velocity (baPWV) based on a general Chinese population. Design and Method: The study group included 4251 participants with an average age of 52.1 ± 12.1 years and a mean baPWV of 14.8 ± 3.3 m/s. Cox regression was used to investigate the prognostic value of baPWV and forced the appropriate interaction term into the regression models to test the absolute risk associated with baPWV at different levels of mean arterial pressure. Results: Over a median follow-up of 4.4 years, the incidence of cardiovascular mortality, stroke and composite cardiovascular endpoints amounted to 21, 48 and 74. We adjusted for sex, age, body mass index, mean arterial pressure, waist-to-hip ratio, total cholesterol, current smoking, alcohol intake, blood glucose and use of antihypertensive drugs. With these adjustments, for each 1-SD increment in baPWV (3.23 m/s), the hazard ratios for an all-cause mortality, cardiovascular mortality, stroke or composite cardiovascular outcomes were 1.41(1.13–1.75), 1.68 (95% CI:1.20–2.35), 1.51 (95% CI:1.27–1.80), 1.57 (95% CI: 1.28–1.93), respectively. At any given level of mean arterial pressure (MAP), a higher baPWV was associated with a higher death rate. The area under curve (AUC) of baPWV was larger than pulse pressure in predicting composite cardiovascular events (Z = 2.45,P = 0.014). Conclusions: In conclusion, baPWV predicted a composite of cardiovascular outcomes above and beyond pulse pressure in a general Chinese population.

Background: Recent studies showing an inverse association between estimated glomerular filtration rate (eGFR), a microvascular trait, and inactive desphospho-uncarboxylated matrix Gla protein (dp-ucMGP) support the hypothesis that after vitamin K dependent activation MGP is renoprotective, but were limited by their cross-sectional design. Methods: In 1009 randomly recruited Flemish (50.6% women), we assessed the association between eGFR and plasma dp-ucMGP, using multivariable-adjusted analyses. Results: From baseline to follow-up 8.9 years later (median), dp-ucMGP increased by 3.7%, whereas eGFR decreased by 4.05 ml/min/1.73 m2 (P < 0.001). In 938 participants with baseline eGFR ≥ 60 ml/min/1.73 m2, incidence of eGFR < 60 ml/min/1.73 m2 at follow-up was 8.0% vs. 4.1% in the top vs. the bottom halve of baseline dp-ucMGP. For each doubling of baseline dp-ucMGP, eGFR at follow-up decreased by 1.36 ml/min/1.73 m2 [95% confidence interval (CI) 0.55–2.17 ml/min/1.73 m2; P = 0.001]. The hazard ratio expressing the risk of progression to eGFR < 60 ml/min/1.73 m2 was 1.67 (95% CI 1.16–2.41; P = 0.006). The hazard ratio relating the presence of microalbuminuria at follow-up to baseline dp-ucMGP was 1.96 (95% CI 1.22–3.12; P = 0.005). Conclusions: In conclusion, circulating inactive dp-ucMGP, a biomarker of poor vitamin K status, predicts renal dysfunction. Possible underlying mechanisms include protection by activated MGP against calcification and inhibition of bone morphogenetic protein signaling pathway.

Background: Molecular pathways leading to stiffening of the central arteries are poorly understood. We searched for differentially expressed proteins by urinary peptidomic analysis in patients with arterial stiffness and healthy controls in a case–control study. Methods: To identify urinary peptides associated with aortic stiffening, we applied capillary electrophoresis coupled to mass spectrometry. We compared 18 cardiovarscular disease-free patients with carotid-femoral pulse wave velocity (PWV > 10 m/s standardised to a heart rate of 75/minute as measured by the SphygmoCor method) with 18 controls matched for sex, age and mean arterial pressure. Results: 69 urinary peptides had a different signal amplitude between cases and controls (P ≤ 0.049). Among 33 peptides with known sequence, 26 were members of the extracellular matrix family, including collagen type I α-1 and α-2, collagen type III α-1, collagen type IV α-5, collagens IX, XXI and XXVII. Collagen type I was down-regulated, whereas collagen type III was up-regulated. Epidermal growth factor receptor (EGFR), a key regulator of myoblast differentiation, and interactions of laminin with other proteins were down-regulated. Atherosclerosis signalling pathways and intrinsic prothrombin activation were the top pathways associated with increased PWV. Potential drug targets included collagen type IV α 3 and transforming growth factor β 3. Angiotensin-converting enzyme inhibitors, which are widely used for vascular protection, were among the possible therapeutic agents. Conclusions: We suggest that stiffening of large elastic arteries involves changes of the extracellular matrix, as reflected by collagen turnover and regulation of myoblast differentiation. Pathway analysis identified potential drug targets, possibly amenable by angiotensin-converting enzyme inhibition.

Hypertension is a major reversible risk factor for cardiovascular complications. According to recent guidelines, hypertension can be subdivided into isolated diastolic, isolated systolic, and systolic and diastolic mixed hypertension using proposed thresholds of various blood pressure components. In the present article, we reviewed the association of cardiovascular outcomes with diastolic blood pressure versus systolic blood pressure and with isolated diastolic hypertension versus systolic and mixed hypertension in observational prospective cohort studies and large-scale individual data-based meta-analysis. Blood pressure was measured either in the clinic or at home or under ambulatory conditions for 24 h in cohort studies. To illustrate the treatment effect of diastolic blood pressure lowering, we also reviewed randomized placebo-controlled outcome trials in diastolic hypertension. Conclusions: The risks conferred by diastolic and systolic blood pressure, irrespective of the methods of blood pressure measurement, are age-dependent. Diastolic blood pressure and isolated diastolic hypertension drive coronary risk in younger subjects, whereas systolic blood pressure is the predominant risk indicator in older people. Reversibility of the risk by diastolic BP lowering treatment in randomized trials confirms that diastolic hypertension is a risk factor that must be treated.

Background We assessed association of retinal arteriolar and venular diameters with central and peripheral blood pressure (BP). Methods We post-processed retinal photographs from 514 participants randomly recruited from a Flemish population (mean age, 50.6 years; 50.8% women), using IVAN software to generate retinal arteriolar (CRAE) and venular (CRVE) equivalents. We measured peripheral BP by mercury sphygmomanometry and central B P by tonometry at the carotid artery. We applied multivariable-adjusted regression analysis. Results For peripheral vs. central BP (mmHg) average levels were 126.6 vs. 122.1 systolic and 79.4 vs. 79.6 diastolic, and 95.1 vs. 97.9 and 47.2 vs. 42.5 for mean and pulse pressure, respectively. CRAE and CRVE averaged 153 μm and 219 μm. Effect sizes (μm) for CRAE for 1 − SD increase in peripheral vs. central BP were −3.77 vs. −3.52 systolic, −3.16 vs. −3.13 diastolic, −3.84 vs. −3.64 for mean BP, and −2.07 vs. −1.83 for pulse pressure ( p ≤ 0.006). Models that included two BP components demonstrated that CRAE decreased ( p ≤ 0.035) with systolic (peripheral vs. central, −2.87 vs. −2.40) and diastolic (−1.58 vs. −1.80) BP. CRAE decreased with mean BP (−3.53 vs. −3.53; p p ≥ 0.19). CRVE was not related to any peripheral or central BP component ( p ≥ 0.062). All CRAE regression slopes on corresponding peripheral and central BP components were similar ( p ≥ 0.28). Conclusion Higher systolic, diastolic and mean BPs were associated with smaller CRAE, regardless of whether BP was measured centrally or peripherally. Central BP does not refine the inverse association of CRAE and CRVE with peripheral BP.

Outcome-driven recommendations about time intervals during which ambulatory blood pressure should be measured to diagnose white-coat or masked hypertension are lacking. We cross-classified 8237 untreated participants (mean age, 50.7 years; 48.4% women) enrolled in 12 population studies, using ≥140/≥90, ≥130/≥80, ≥135/≥85, and ≥120/≥70 mm Hg as hypertension thresholds for conventional, 24-hour, daytime, and nighttime blood pressure. White-coat hypertension was hypertension on conventional measurement with ambulatory normotension, the opposite condition being masked hypertension. Intervals used for classification of participants were daytime, nighttime, and 24 hours, first considered separately, and next combined as 24 hours plus daytime or plus nighttime, or plus both. Depending on time intervals chosen, white-coat and masked hypertension frequencies ranged from 6.3% to 12.5% and from 9.7% to 19.6%, respectively. During 91 046 person-years, 729 participants experienced a cardiovascular event. In multivariable analyses with normotension during all intervals of the day as reference, hazard ratios associated with white-coat hypertension progressively weakened considering daytime only (1.38; P =0.033), nighttime only (1.43; P =0.0074), 24 hours only (1.21; P =0.20), 24 hours plus daytime (1.24; P =0.18), 24 hours plus nighttime (1.15; P =0.39), and 24 hours plus daytime and nighttime (1.16; P =0.41). The hazard ratios comparing masked hypertension with normotension were all significant ( P

Background— Data on risk associated with 24-hour ambulatory diastolic (DBP 24 ) versus systolic (SBP 24 ) blood pressure are scarce. Methods and Results— We recorded 24-hour blood pressure and health outcomes in 8341 untreated people (mean age, 50.8 years; 46.6% women) randomly recruited from 12 populations. We computed hazard ratios (HRs) using multivariable-adjusted Cox regression. Over 11.2 years (median), 927 (11.1%) participants died, 356 (4.3%) from cardiovascular causes, and 744 (8.9%) experienced a fatal or nonfatal cardiovascular event. Isolated diastolic hypertension (DBP 24 ≥80 mm Hg) did not increase the risk of total mortality, cardiovascular mortality, or stroke (HRs≤1.54; P ≥0.18), but was associated with a higher risk of fatal combined with nonfatal cardiovascular, cardiac, or coronary events (HRs≥1.75; P ≤0.0054). Isolated systolic hypertension (SBP 24 ≥130 mm Hg) and mixed diastolic plus systolic hypertension were associated with increased risks of all aforementioned end points ( P ≤0.0012). Below age 50, DBP 24 was the main driver of risk, reaching significance for total (HR for 1-SD increase, 2.05; P =0.0039) and cardiovascular mortality (HR, 4.07; P =0.0032) and for all cardiovascular end points combined (HR, 1.74; P =0.039) with a nonsignificant contribution of SBP 24 (HR≤0.92; P ≥0.068); above age 50, SBP 24 predicted all end points (HR≥1.19; P ≤0.0002) with a nonsignificant contribution of DBP 24 (0.96≤HR≤1.14; P ≥0.10). The interactions of age with SBP 24 and DBP 24 were significant for all cardiovascular and coronary events ( P ≤0.043). Conclusions— The risks conferred by DBP 24 and SBP 24 are age dependent. DBP 24 and isolated diastolic hypertension drive coronary complications below age 50, whereas above age 50 SBP 24 and isolated systolic and mixed hypertension are the predominant risk factors.

BACKGROUND: Guidelines propose classification of conventional blood pressure (CBP) into normotension (

Objective: We assessed association of retinal micro-vessel diameter with central and peripheral BP. Methods: We post-processed retinal photographs taken in 514 subjects randomly selected from a Flemish population (mean age, 50.6 years; 50.8% women), using IVAN software to generate retinal arteriolar (CRAE) and venular (CRVE) equivalents. We measured peripheral and central BP by mercury sphygmomanometry and tonometry at the carotid artery (SphygmoCor software), respectively. We applied stepwise regression, considering as covariables in addition to BP sex, age, body mass index, smoking, drinking, antihypertensive drug treatment, and serum cholesterol. Results: CRAE and CRVE averaged 153μm and 219μm. Effect sizes (ìm) for CRAE for 1–SD increase in peripheral vs. central BP were –3.77 vs. –3.52 systolic, –3.16 vs. –3.13 diastolic, –3.84 vs. –3.64 for mean BP, and –2.07 vs. –1.83 for pulse pressure (P≤0.006). Models that included two BP components demonstrated that CRAE decreased (P≤0.035) with systolic (peripheral vs. central, –2.87 vs. –2.40) and diastolic (–1.58 vs. –1.80) BP. CRAE decreased with mean BP (–3.53 vs. –3.53; P

Objectives: Cerebral artery critical closing pressure (CCP) is an estimated parameter with no single accepted method of calculation. Variation between methods could be significant. This study investigates two models to estimate CCP using arterial blood pressure (BP) and middle cerebral artery flow velocity (FV) waveforms, quantifying the difference between radial and aortic BP as the BP input signal. Methods: Suspected and untreated hypertensive subjects (n=445, 203 female, 50±10 years, range 21 to 73 years old), referred to Ruijin Hospital in Shanghai, China, for 24-hours BP monitoring, were recruited. Radial BP and FV waveforms were acquired by applanation tonometry and transcranial Doppler respectively. Aortic BP waveforms were synthesised from the radial waveform using a validated transfer function (SphygmoCor®). CCP was estimated using the relationship between BP and FV waveforms by both linear regression (LR), and the first harmonic (H1) in Fourier decomposition. The difference between the two models was quantified if the BP waveform input signal was radial or aortic and compared by Student’s paired t-test. Results: Use of aortic instead of radial BP resulted in a 29% increase in estimated CCP using the LR model, and 25% increase using the H1 model (Figure, p

No previous study addressed the relative contributions of environmental and genetic cues to the diurnal blood pressure rhythmicity. We firstly investigated the explained variance of environmental and clock genes in relation to the night-to-day ratio (NDR) and morning surge (MS), respectively. From 24-h ambulatory recordings of systolic blood pressure (SBP) obtained in untreated Chinese patients (51% women; mean age, 51 years), we computed NDR in 897 and MS in 637. Environmental cues included season, mean daily outdoor temperature, atmospheric pressure, humidity and weekday and the genetic cues variation in the clock genes BMAL1 (rs6486121), CRY2 (rs10838524) and CLOCK (rs1801260). SBP averaged (±SD) 126.7 ± 11.9 mmHg, NDR 0.86 ± 0.07 and MS 24.8 ± 10.7 mmHg. In adjusted analyses, NDR was 2.4% higher in summer and 1.8% lower in winter (P

Background Uric acid has been associated with blood pressure and hypertension. During the final stage of purine metabolism xanthine oxidoreductase (XOR) produces uric acid, while at the same time reactive oxygen species are formed. We hypothesized that uric acid production, as assessed indirectly from XOR variants, is associated with hypertension (figure 1). Objectives The aim of the present study is to investigate the association of variants in the XOR gene with blood pressure and the development of hypertension. Methods Analyses were conducted in the prospective Flemish FLEMENGHO and European EPOGH study. Among 2769 participants (48.3% men; mean age 40.7 years) we genotyped 25 XOR SNPs and measured blood pressure at baseline and follow-up (median 8.8 years). The relation between variants of the XOR gene with changes in pulse pressure and mean arterial pressure over time; and incidence of hypertension, were analysed using multivariable mixed models and cox-regression, respectively. Results Compared with major allele homozygotes, pulse pressure increased approximately 2 mm Hg more in minor allele carriers of rs11904439 (P=value 0.01), whereas mean arterial pressure and diastolic blood pressure increased approximately 1 mm Hg less in minor allele carriers of rs2043013 (P=0.01). In 2050 participants normotensive at baseline, hazard ratios contrasting risk of hypertension in minor allele carriers vs. major allele homozygotes was 1.31 (95% confidence interval [CI] 1.03–1.68) for rs11904439 and 1.69 (95% CI 1.11–2.57) for rs148756340. With the false discovery rate set at 0.25, the aforementioned associations retained significance. The changes in systolic blood pressure from baseline to follow-up and the serum levels of uric acid at baseline (n=1949) were not associated with XOR. Conclusions In conclusion, pending confirmation in appropriately powered cohort studies, our findings suggest that variation in uric acid production, as captured by genetic variation in XOR, might be a predictor of changes in pulse pressure, mean arterial pressure and in the risk of hypertension. Acknowledgement The authors gratefully acknowledge the clerical assistance of Mrs Renilde Wolfs. Disclosure of Interest None declared

Previous studies have demonstrated that urinary angiotensinogen excretion, a biomarker of the intrarenal renin-angiotensin system activity, is associated with clinic blood pressure (BP). In the present study, we investigated the determinants of urinary angiotensinogen excretion and its associations with ambulatory BP.The study participants were suspected hypertensive patients being off antihypertensive medication for at least 2 weeks and referred to our hypertension clinic for 24-h ambulatory BP monitoring. Ambulatory hypertension was defined as a 24-h BP of at least 130 mmHg systolic or 80 mmHg diastolic. We collected a first morning urine sample for the measurement of angiotensinogen by ELISA kits.The 446 participants (mean age 51.7 years) included 218 (48.9%) men, and 275 (61.7%) patients had ambulatory hypertension. In addition to age and sex, 24-h urinary sodium excretion was an independent determinant of urinary angiotensinogen-to-creatinine ratio (P = 0.0008). Urinary angiotensinogen-to-creatinine ratio was 34% (P = 0.04) and 82% (P ≤ 0.0001) higher in tertiles 2 and 3 of 24-h urinary sodium excretion, respectively, than in tertile 1. In multivariate analyses, urinary angiotensinogen-to-creatinine ratio was significantly and positively associated with clinic and ambulatory BP (P ≤ 0.02) and the prevalence of ambulatory hypertension [odds ratio (95% confidence interval) associated with two-time increase, 1.24 (1.09-1.39); P = 0.0007].Urinary angiotensinogen excretion is higher with greater urinary sodium excretion, and is associated with clinic and ambulatory BP.

BACKGROUND Masked hypertension (MH) has 10-15% prevalence and carries risk similar to that of sustained hypertension, but its short-term persistence remains uncertain. METHODS Forty-five patients with MH (mean age 52.2 years; 37.8% women) were enrolled in the placebo arm of a randomized clinical trial of Chinese medicine (NCT02156024) and followed up for 4 weeks. MH was office normotension (

Objective:Hypertension guidelines propose home (HBP) or ambulatory (ABP) blood pressure monitoring as indispensable after office measurement (OBP). However, whether preference should be given to HBP or ABP remains undetermined.Design and method:We recruited 831 consecutive patients (mean age, 50.6 y

Background The metabolic signature associated with subclinical diastolic left ventricular (LV) dysfunction in the population remains ill defined. Methods and Results In 711 randomly recruited Flemish (50.8% women; mean age, 50.8 years), we assessed echocardiographic Doppler indexes of diastolic LV function in relation to 44 circulating metabolites determined by nuclear magnetic resonance spectroscopy. In multivariable‐adjusted regression analysis with Bonferroni correction of significance levels applied, peak a’ decreased ( P ≤0.048) and e’/a’ increased ( P ≤0.044) with circulating tyrosine, high‐density lipoprotein apolipoproteins, glucose+glutamine, and an unidentified molecule. Effect sizes expressed per 1‐SD increment in the metabolite ranged from −0.277 to −0.203 cm/s for peak a’ and from +0.047 to +0.054 for e’/a’. In addition, peak a’ decreased ( P ≤0.031) with glucose+2‐aminobutyrate (−0.261 cm/s) and glucose+2‐phosphoglycerate (−0.209 cm/s). In partial least square discriminant analysis (PLS‐DA), metabolites associated with normal diastolic LV function (n=538) included glucose+glutamine, glucose+2‐aminobutyrate, and glucose+2‐phosphoglycerate, whereas those siding with abnormal function encompassed 4‐aminobutyrate, 4‐hydroxybutyrate, creatinine, and phosphocholine. In receiver operating characteristics plots, adding 3 latent factors identified by PLS‐DA to prohormone brain natriuretic peptide increased ( P

Background: We assessed association of retinal arteriolar and venular diameters with central and peripheral blood pressure (BP).

The association of target organ damage with 24-hour systolic and diastolic blood pressure levels and ambulatory hypertension subtypes has not yet been examined in untreated Chinese patients. We measured left ventricular mass index by echocardiography (n=619), the urinary albumin:creatinine ratio (n=1047), and aortic pulse wave velocity by tonometry (n=1013) in 1047 untreated subjects (mean age, 50.6 years; 48.9% women). Normotension was a 24-hour systolic/diastolic blood pressure P ≤0.003) left ventricular mass index (+4.31 g/m 2 ), urinary albumin:creatinine ratio (+1.63 mg/mmol), and pulse wave velocity (+0.76 m/s); and isolated diastolic hypertension was associated with similar left ventricular mass index and pulse wave velocity ( P ≥0.39), but higher urinary albumin:creatinine ratio (+1.24 mg/mmol; P =0.002). In younger participants (2 ( P =0.009/0.79) for left ventricular mass index, +1.15/+1.14 mg/mmol ( P =0.02/0.04) for the urinary albumin:creatinine ratio, and +0.54/–0.05 m/s ( P 2 ( P =0.045/0.88), +1.23/+1.05 mg/mmol ( P =0.002/0.54), and +0.76/–0.49 m/s ( P