Multiple articles focused on the central arterial systolic (SPTI) and diastolic (DPTI) pressure-time indexes and the subendocardial viability ratio (SEVR). However, whether these indexes contribute to risk stratification in the general population is unknown. SPTI, DPTI and SEVR were noninvasively measured by the SphygmoCor technology. Incidence rates and standardized (per 1-SD increment) multivariable-adjusted hazard ratios (HRs) for cardiovascular (primary) and cardiac endpoints and stroke were evaluated in the International Database of Central Arterial Properties for Risk Stratification (n = 5099). Model refinement was assessed by the area under the curve (AUC) and the integrated discrimination (IDI) and net reclassification (NRI) improvement. Over 4 years (median), 215 cardiovascular, 133 cardiac endpoints and 79 strokes occurred. For SPTI, fully adjusted HRs were 1.37 (95% CI: 1.18-1.59), 1.35 (1.11-1.64) and 1.33 (1.05-1.69) for the cardiovascular and cardiac endpoints and stroke. The corresponding HRs for DPTI were 1.49 (1.31-1.69), 1.23 (1.02-1.48) and 1.74 (1.46-2.07). For SEVR, none of the HRs reached significance. Analyses with these indexes categorized by quartiles were confirmatory. Analyses stratified by various risk factors did not reveal subgroup differences. For the cardiovascular endpoint, adding SPTI or DPTI to the base model improved the AUC, while adding SPTI or DPTI combined with mean arterial pressure, increased IDI by ~1.7% and NRI by ~17% (P < 0.001 for all). Whereas cardiovascular and cardiac endpoints and stroke were related with the non-invasively measured SPTI and DPTI, SEVR was not.

BACKGROUND:The ambulatory arterial stiffness index (AASI) is increasingly used in clinical research and practice. This individual-participant meta-analysis aims to consolidate the prognostic accuracy of AASI in the general population and to derive an end point-based AASI risk threshold. METHODS:In 12 558 individuals enrolled in 14 population studies (48.8% women; mean age, 59.3 years), AASI was derived by regressing 24-hour diastolic on systolic blood pressure (mm Hg/mm Hg). Using Cox regression, the risk-carrying AASI threshold was established by examining stepwise increasing AASI levels and by determining the AASI level, yielding a 10-year risk similar to an office systolic pressure of 140 mm Hg. RESULTS:Over 10.7 years (median), 3027 all-cause deaths and 2183 cardiovascular end points occurred. In all participants, multivariable-adjusted hazard ratios expressing the all-cause deaths and cardiovascular end point risk per 1-SD AASI increment were 1.08 (95% CI, 1.04-1.13) and 1.13 (95% CI, 1.07-1.18). In a randomly defined subset of 8189 individuals, the risk-carrying AASI thresholds converged to 0.50 with hazard ratios (≥0.50 versus <0.50) of 1.14 (95% CI, 1.04-1.26) for all-cause deaths and 1.13 (95% CI, 1.01-1.26) for cardiovascular end point. In the replication sample (n=4369), these hazard ratios were 1.13 (95% CI, 1.01-1.26) and 1.19 (95% CI, 1.04-1.35). AASI continuous or per threshold significantly improved model performance. Analyses of secondary end points and subgroups stratified by sex, age, hypertension status and treatment, history of cardiovascular disease, and nocturnal dipping were confirmatory. CONCLUSIONS:Over and beyond traditional risk factors, AASI improves risk stratification. Exceeding the risk-carrying 0.50 AASI threshold necessitates increased vigilance in managing risk factors before irreversible cardiovascular complications occur.

BACKGROUND AND AIMS:Hypertension is the predominant modifiable cardiovascular risk factor. This cohort study assessed the association of risk with the percentage of time that the ambulatory blood pressure (ABP) is within the target range (PTTR) proposed by the 2024 European Society of Cardiology (ESC) guidelines for blood pressure (BP) management. METHODS:In a person-level meta-analysis of 14 230 individuals enrolled in 14 population cohorts, systolic and diastolic ABPs were combined to assess 24-h, daytime, and nighttime PTTR with thresholds for non-elevated ABP set at <115/65, <120/70, and <110/60 mmHg, respectively. RESULTS:Median 24-h PTTR was 18% (interquartile range 5-33) corresponding to 4.3 h (1.2-7.9). Over 10.9 years (median), deaths (N = 3117) and cardiovascular endpoints (N = 2265) decreased across increasing 24-h PTTR quartiles from 21.3 to 16.1 and from 20.3 to 11.3 events per 1000 person-years. The standardized multivariable-adjusted hazard ratios for 24-h PTTR were 0.57 (95% confidence interval 0.46-0.71) for mortality and 0.30 (0.23-0.39) for cardiovascular endpoints. Analyses of daytime and nighttime ABP, cardiovascular mortality, coronary endpoints and stroke, and subgroups produced confirmatory results. The 2024 ESC non-elevated 24-h PTTR, compared with the 2018 ESC/European Society of Hypertension non-hypertensive 24-h PTTR, shortened the interval required to reduce relative risk for adverse outcomes from 60% to 18% (14.4-4.3 h). Office BP, compared with 24-h PTTR, misclassified most participants with regard to BP control. CONCLUSIONS:Longer time that ABP is within the 2024 ESC target range is associated with reduced adverse outcomes; PTTR derived from ABP refines risk prediction and compared with office BP avoids misclassification of individuals with regard to BP control.

ABSTRACTPrognostic significance of the timing in the cardiac cycle of the first (TP1) and second (TP2) systolic peak of the central aortic pulse wave is ill‐defined. Incidence rates and standardized multivariable‐adjusted hazard ratios (HRs) of adverse health outcomes associated with TP1 and TP2, estimated by the SphygmoCor software, were assessed in the International Database of Central Arterial Properties for Risk Stratification (IDCARS) (n = 5529). Model refinement was assessed by the integrated discrimination (ID) and net reclassification (NR) improvement. Over 4.1 years (median), 201 participants died and 248 and 159 patients experienced cardiovascular or cardiac endpoints. Mean TP1 and TP2, standardized for cohort, sex, age, and heart rate, were 103 and 228 ms. Shorter TP1 and TP2 were associated with higher mortality and shorter TP1 with a higher risk of cardiovascular and cardiac endpoints (trend p ≤ 0.004). The HRs relating total mortality and cardiovascular endpoints to TP2 were 0.82 (95% confidence interval [CI]: 0.72–0.94) and 0.87 (0.77–0.98), respectively. The HR relating cardiac endpoints to TP1 was 0.81 (0.68–0.97). For total mortality and cardiovascular endpoints in relation to TP2, NRI was significant (p ≤ 0.010), but not for cardiac endpoints in relation to TP1. Integrated discrimination improvement (IDI) was not significant for any endpoint. The HRs relating total mortality to TP2 were smaller (p ≤ 0.026) in women than men (0.67 vs. 0.95) and in older (≥ 60 years) versus younger (< 60 years) participants (0.80 vs. 0.88). Our study adds to the evidence supporting risk stratification based on aortic pulse analysis by showing that TP2 and TP1 carry prognostic information.

BACKGROUND: Wave separation analysis enables individualized evaluation of the aortic pulse wave components. Previous studies focused on the pressure height with overall positive but differing results. In the present analysis, we assessed the associations of the pressure of forward and backward (P for and P ref ) pulse waves with prospective cardiovascular end points, with extended analysis for time to pressure peak (T for and T ref ). METHODS: Participants in 3 IDCARS (International Database of Central Arterial Properties for Risk Stratification) cohorts (Argentina, Belgium, and Finland) aged ≥20 years with valid pulse wave analysis and follow-up data were included. Pulse wave analysis was done using the SphygmoCor device, and pulse wave separation was done using the triangular method. The primary end points consisted of cardiovascular mortality and nonfatal cardiovascular and cerebrovascular events. Multivariable-adjusted Cox regression was used to calculate hazard ratios. RESULTS: A total of 2206 participants (mean age, 57.0 years; 55.0% women) were analyzed. Mean±SDs for P for , P ref , T for , and T for /T ref were 31.0±9.1 mm Hg, 20.8±8.4 mm Hg, 130.8±35.5, and 0.51±0.11, respectively. Over a median follow-up of 4.4 years, 146 (6.6%) participants experienced a primary end point. Every 1 SD increment in P for , T for , and T for /T ref was associated with 27% (95% CI, 1.07–1.49), 25% (95% CI, 1.07–1.45), and 32% (95% CI, 1.12–1.56) higher risk, respectively. Adding T for and T for /T ref to existing risk models improved model prediction (∆Uno’s C, 0.020; P <0.01). CONCLUSIONS: Pulse wave components were predictive of composite cardiovascular end points, with T for /T ref showing significant improvement in risk prediction. Pending further confirmation, the ratio of time to forward and backward pressure peak may be useful to evaluate increased afterload and signify increased cardiovascular risk.

Background: Numerous studies based on assessment of lithium clearance demonstrated higher sodium reabsorption in renal proximal tubules in individuals with hypertension, overweight, obesity, metabolic syndrome, or diabetes. Aims: We aimed to assess the influence of angiotensin-converting enzyme inhibitors (ACE-I) or angiotensin-II-receptor antagonists (ARB) treatment on sodium handling. Methods: In a sample of 351Caucasian subjects without diuretic treatment with prevailing sodium consumption, we studied associations between renal sodium reabsorption in proximal (FPRNa) and distal (FDRNa) tubules assessed by endogenous lithium clearance and daily sodium intake measured by 24-hour excretion of sodium (UNaV), in the context of obesity and long-term treatment with ACE-I or ARB. Results: In the entire study population, we found a strong negative association between FPRNa and ACE-I/ARB treatment (b = -19.5; SE = 4.9; P <0.001). Subjects with FPRNa above the median value showed a significant adverse association between FPRNa and age (b = -0.06; SE = 0.02; P = 0.003), with no association with ACE-I/ARB treatment (P = 0.68). In contrast, in subjects with FPRNa below the median value, we found a strongly significant adverse relationship between FPRNa and ACE-I/ARB treatment (b = -30.4; SE = 8.60; P <0.001), with no association with age (P = 0.32). Conclusions: ACE-I/ARB long-term treatment modulates FPRNa in the group with lower reabsorption, but not in that with higher than median value for the entire study population.

Objective: Pulse pressure amplification (PPA) is the ratio of brachial-to-aortic pulse pressure and decreases with age and cardiovascular risk factors. In an individual-participant meta-analysis, we aimed to define, calibrate and validate an outcome-driven threshold for PPA in the general population. Design and method: Incidence rates and standardized multivariable-adjusted hazard ratios (HRs) of cardiovascular and coronary endpoints associated with PPA, as assessed by the SphygmoCor software, were evaluated in the International Database of Central Arterial Properties for Risk Stratification (n=5608). Model refinement was assessed by the integrated discrimination (IDI) and net reclassification (NRI) improvement. Results: Over 4.1 years (median), 255 and 109 participants experienced a cardiovascular or coronary endpoint. In a randomly defined discovery subset of 3945 individuals, the rounded risk-carrying PPA thresholds converged at 1.3. The HRs for cardiovascular and coronary endpoints contrasting PPA <1.3 vs >=1.3 were 1.54 (95% confidence interval: 1.00-2.36) and 2.45 (1.20-5.01), respectively. Models were well calibrated, findings were replicated in the remaining 1663 individuals analyzed as test dataset, and NRI was significant for both endpoints. The HRs associating cardiovascular and coronary endpoints per PPA threshold in individuals <60 vs >=60 years were 3.86 vs 1.19 and 6.21 vs 1.77, respectively. Of the younger high-risk individuals, 1107 (67.7%) were women. Conclusions: Over and beyond common risk factors, low PPA defined as a brachial-to-central PP ratio of <1.3 is a forerunner of cardiovascular and coronary complications, in particular in women younger than 60 years. Our study supports pulse wave analysis for risk stratification.

Objective: While the relation of salt intake with blood pressure (BP) is linear, it is U shaped for mortality and cardiovascular disease (CVD). This individual-participant meta-analysis explored whether the relation of hypertension, death or CVD with 24 h urinary sodium excretion (UVNA) or sodium-to-potassium (UNAK) ratio was modified by birth weight (BW). Design and method: Families were randomly enrolled in the Flemish Study on Genes, Environment and Health Outcomes (1985-2004) and the European Project on Genes in Hypertension (1999-2001). Categories of BW, UVNA and UNAK (< = 2500, >2500-4000, >4000 g; <2.3, 2.3-4.6 and >4.6 g; and <1, 1-2, >2, respectively) were coded using deviation-from-mean coding and analyzed by Kaplan-Meier survival functions and linear and Cox regression. Results: The study population was subdivided into the Outcome (n = 1945), Hypertension (n = 1460) and BP cohorts (n = 1039) to analyze the incidence of mortality and cardiovascular endpoints, hypertension and BP changes as function of UVNA changes. The prevalence of low/medium/high BW in the Outcome Cohort was 5.8/84.5/9.7%. Over 16.7 years (median), rates were 4.9%, 8.0% and 27.1% for mortality, CVD and hypertension, respectively, but were not associated with BW. Multivariable-adjusted hazard ratios were not significant for any endpoint in any of the BW, UVNA and UNAK strata. Adult body weight tracked with BW (P<0.0001). The partial r in the low BW group associating changes from baseline to follow-up in UVNA and systolic BP was 0.68 (P = 0.023), but not significant in other BW groups. Conclusions: This study did not substantiate its prior hypothesis, but showed tracking of adult with birth weight and suggest that low BW increases salt sensitivity.

BACKGROUND: Aortic pulse wave velocity (PWV) predicts cardiovascular events (CVEs) and total mortality (TM), but previous studies proposing actionable PWV thresholds have limited generalizability. This individual-participant meta-analysis is aimed at defining, testing calibration, and validating an outcome-driven threshold for PWV, using 2 populations studies, respectively, for derivation IDCARS (International Database of Central Arterial Properties for Risk Stratification) and replication MONICA (Monitoring of Trends and Determinants in Cardiovascular Disease Health Survey – Copenhagen). METHODS: A risk-carrying PWV threshold for CVE and TM was defined by multivariable Cox regression, using stepwise increasing PWV thresholds and by determining the threshold yielding a 5-year risk equivalent with systolic blood pressure of 140 mm Hg. The predictive performance of the PWV threshold was assessed by computing the integrated discrimination improvement and the net reclassification improvement. RESULTS: In well-calibrated models in IDCARS, the risk-carrying PWV thresholds converged at 9 m/s (10 m/s considering the anatomic pulse wave travel distance). With full adjustments applied, the threshold predicted CVE (hazard ratio [CI]: 1.68 [1.15–2.45]) and TM (1.61 [1.01–2.55]) in IDCARS and in MONICA (1.40 [1.09–1.79] and 1.55 [1.23–1.95]). In IDCARS and MONICA, the predictive accuracy of the threshold for both end points was ≈0.75. Integrated discrimination improvement was significant for TM in IDCARS and for both TM and CVE in MONICA, whereas net reclassification improvement was not for any outcome. CONCLUSIONS: PWV integrates multiple risk factors into a single variable and might replace a large panel of traditional risk factors. Exceeding the outcome-driven PWV threshold should motivate clinicians to stringent management of risk factors, in particular hypertension, which over a person’s lifetime causes stiffening of the elastic arteries as waypoint to CVE and death.

Objective: Current guidelines recommend a carotid-femoral pulse wave velocity (cf-PWV) > 10m/s of as a sign of large arterial stiffening, which was mainly based on cross-sectional analyses on the distribution of cf-PWV in healthy populations. Using data from the International Database of Central Arterial Properties for Risk Stratification (IDCARS), we aimed to determine an outcome-driven threshold for cf-PWV. Methods: Adults (> = 18 years) recruited from eight IDCARS centres and followed up for 6 months or longer were qualified for inclusion in the current meta-analysis. Cf PWV was measured using the Sphygmocor device. The primary endpoint consisted of fatal and nonfatal cardiovascular events. Secondary endpoints were total and cardiovascular mortality, and fatal and nonfatal coronary events. We calculated multivariable-adjusted hazard ratios (HRs) versus the average risk of the whole population for cf-PWV ranging from the 10th to the 90th percentile with an increment of 0.1 m/s. We plotted the HRs and their 95% confidence limits versus the increasing cutoff points of cf-PWV with the goal to determine at which level the lower confidence limit crossed unity. Results: Of 3494 participants (mean age: 52.2 years; women: 55.3%; mean cf-PWV: 7.8 m/s) followed up for a median of 5.0 years, 156 (4.5%) experienced the primary endpoint and 104 (3.0%) died. Multivariable adjusted outcome-driven thresholds of cf-PWV (m/s) were 8.6 for the primary cardiovascular endpoint, and 9.1, 8.7 and 8.6 for all-cause and cardiovascular mortality and coronary event, respectively. Subjects with a cf-PWV > = 9 m/s (n = 752, 21.5%), compared with the rest of the population, had an increased risk of the primary cardiovascular endpoint (HR: 1.75; 95% CI: 1.20–2.54, P = 0.004). Conclusions: The outcome-based threshold of > = 9 m/s for cf-PWV is close to the cut-off proposed by the current guidelines, according to which 20% of the IDCARS participants had arterial stiffness and were associated with increased cardiovascular risk.

Background: The role of pulse pressure (PP) ‘widening’ at older and younger age as a cardiovascular risk factor is still controversial. Mean PP, as determined from repeated blood pressure (BP) readings, can be expressed as a sum of two components: ‘elastic PP’ (elPP) and ‘stiffening PP’ (stPP) associated, respectively, with stiffness at the diastole and its relative change during the systole. We investigated the association of 24-h ambulatory PP, elPP, and stPP (‘PP variables’) with mortality and composite cardiovascular events in different age classes. Method: Longitudinal population-based cohort study of adults with baseline observations that included 24-h ambulatory BP. Age classes were age 40 or less, 40–50, 50–60, 60–70, and over 70 years. Co-primary endpoints were total mortality and composite cardiovascular events. The relative risk expressed by hazard ratio per 1SD increase for each of the PP variables was calculated from multivariable-adjusted Cox regression models. Results: The 11 848 participants from 13 cohorts (age 53 ± 16 years, 50% men) were followed for up for 13.7 ± 6.7 years. A total of 2946 participants died (18.1 per 1000 person-years) and 2093 experienced a fatal or nonfatal cardiovascular event (12.9 per 1000 person-years). Mean PP, elPP, and stPP were, respectively, 49.7, 43.5, and 6.2 mmHg, and elPP and stPP were uncorrelated (r = −0.07). At age 50–60 years, all PP variables displayed association with risk for almost all outcomes. From age over 60 years to age over 70 years, hazard ratios of of PP and elPP were similar and decreased gradually but differently for pulse rate lower than or higher than 70 bpm, whereas stPP lacked predictive power in most cases. For age 40 years or less, elPP showed protective power for coronary events, whereas stPP and PP predicted stroke events. Adjusted and unadjusted hazard ratio variations were similar over the entire age range. Conclusion: This study provides a new basis for associating PP components with outcome and arterial properties in different age groups and at different pulse rates for both old and young age. The similarity between adjusted and unadjusted hazard ratios supports the clinical usefulness of PP components but further studies are needed to assess the prognostic significance of the PP components, especially at the young age.

Abstract OBJECTIVE To address to what extent central hemodynamic measurements, improve risk stratification, and determine outcome-based diagnostic thresholds, we constructed the International Database of Central Arterial Properties for Risk Stratification (IDCARS), allowing a participant-level meta-analysis. The purpose of this article was to describe the characteristics of IDCARS participants and to highlight research perspectives. METHODS Longitudinal or cross-sectional cohort studies with central blood pressure measured with the SphygmoCor devices and software were included. RESULTS The database included 10,930 subjects (54.8% women; median age 46.0 years) from 13 studies in Europe, Africa, Asia, and South America. The prevalence of office hypertension was 4,446 (40.1%), of which 2,713 (61.0%) were treated, and of diabetes mellitus was 629 (5.8%). The peripheral and central systolic/diastolic blood pressure averaged 129.5/78.7 mm Hg and 118.2/79.7 mm Hg, respectively. Mean aortic pulse wave velocity was 7.3 m per seconds. Among 6,871 participants enrolled in 9 longitudinal studies, the median follow-up was 4.2 years (5th–95th percentile interval, 1.3–12.2 years). During 38,957 person-years of follow-up, 339 participants experienced a composite cardiovascular event and 212 died, 67 of cardiovascular disease. CONCLUSIONS IDCARS will provide a unique opportunity to investigate hypotheses on central hemodynamic measurements that could not reliably be studied in individual studies. The results of these analyses might inform guidelines and be of help to clinicians involved in the management of patients with suspected or established hypertension.

Background: Whether cardiovascular risk is more tightly associated with central (cSBP) than brachial (bSBP) systolic pressure remains debated, because of their close correlation and uncertain thresholds to differentiate cSBP into normotension versus hypertension. Methods: In a person-level meta-analysis of the International Database of Central Arterial Properties for Risk Stratification (n=5576; 54.1% women; mean age 54.2 years), outcome-driven thresholds for cSBP were determined and whether the cross-classification of cSBP and bSBP improved risk stratification was explored. cSBP was tonometrically estimated from the radial pulse wave using SphygmoCor software. Results: Over 4.1 years (median), 255 composite cardiovascular end points occurred. In multivariable bootstrapped analyses, cSBP thresholds (in mm Hg) of 110.5 (95% CI, 109.1–111.8), 120.2 (119.4–121.0), 130.0 (129.6–130.3), and 149.5 (148.4–150.5) generated 5-year cardiovascular risks equivalent to the American College of Cardiology/American Heart Association bSBP thresholds of 120, 130, 140, and 160. Applying 120/130 mm Hg as cSBP/bSBP thresholds delineated concordant central and brachial normotension (43.1%) and hypertension (48.2%) versus isolated brachial hypertension (5.0%) and isolated central hypertension (3.7%). With concordant normotension as reference, the multivariable hazard ratios for the cardiovascular end point were 1.30 (95% CI, 0.58–2.94) for isolated brachial hypertension, 2.28 (1.21–4.30) for isolated central hypertension, and 2.02 (1.41–2.91) for concordant hypertension. The increased cardiovascular risk associated with isolated central and concordant hypertension was paralleled by cerebrovascular end points with hazard ratios of 3.71 (1.37–10.06) and 2.60 (1.35–5.00), respectively. Conclusions: Irrespective of the brachial blood pressure status, central hypertension increased cardiovascular and cerebrovascular risk indicating the importance of controlling central hypertension.

Objective. To evaluate changes in blood pressure (BP) values in patients with established coronary artery disease (CAD) over 20 years (1997–2017). Materials and Methods. Consecutive patients aged <71 years and hospitalized for acute coronary syndrome or myocardial revascularization procedures were recruited and interviewed 6–18 months after their discharge from the hospital. BP was measured in 1997–1998, 1999–2000, 2006–2007, 2011–2013, and 2016–2017. The same five hospitals took part in the surveys at each time point. Results. We examined 412 patients in 1997–1998, 427 in 1999–2000, 422 in 2006–2007, 462 in 2011–2013, and 272 in 2016–2017. The proportion of patients with BP at the recommended goal was 49.2% in 1997–98, 44.5% in 1999–2000, 44.7% in 2006–07, 51.1% in 2011–13, and 58.8% in 2016–17 ( p < 0.001 ). Mean systolic and diastolic BP decreased significantly independent of age, sex, and education (systolic BP: 137.9 ± 21.4 mmHg in 1997–98, 139.5 ± 21.6 mmHg in 1999–2000, 136.1 ± 20.3 mmHg in 2006–07, 134.8 ± 22.0 mmHg in 2011–13, and 134.2 ± 18.6 mmHg in 2016–17, p < 0.001 ; diastolic BP: 83.4 ± 11.0 mmHg in 1997–98, 84.8 ± 12.0 mmHg in 1999–2000, 85.2 ± 11.0 mmHg in 2006–07, 80.9 ± 12.5 mmHg in 2011–13, and 81.1 ± 10.4 mmHg in 2016–17; p < 0.001 ). Conclusion. The analysis of five multicenter surveys provides evidence of a decrease in BP in patients with established CAD over two decades. This trend is independent of age, sex, and the education level of the patients.

Abstract Background Pulse pressure (PP) reflects the age-related stiffening of the central arteries, but no study addressed the management of the PP-related risk over the human lifespan. Methods In 4,663 young (18–49 years) and 7,185 older adults (≥50 years), brachial PP was recorded over 24 hours. Total mortality and all major cardiovascular events (MACEs) combined were coprimary endpoints. Cardiovascular death, coronary events, and stroke were secondary endpoints. Results In young adults (median follow-up, 14.1 years; mean PP, 45.1 mm Hg), greater PP was not associated with absolute risk; the endpoint rates were ≤2.01 per 1,000 person-years. The adjusted hazard ratios expressed per 10-mm Hg PP increments were less than unity (P ≤ 0.027) for MACE (0.67; 95% confidence interval [CI], 0.47–0.96) and cardiovascular death (0.33; 95% CI, 0.11–0.75). In older adults (median follow-up, 13.1 years; mean PP, 52.7 mm Hg), the endpoint rates, expressing absolute risk, ranged from 22.5 to 45.4 per 1,000 person-years and the adjusted hazard ratios, reflecting relative risk, from 1.09 to 1.54 (P < 0.0001). The PP-related relative risks of death, MACE, and stroke decreased >3-fold from age 55 to 75 years, whereas absolute risk rose by a factor 3. Conclusions From 50 years onwards, the PP-related relative risk decreases, whereas absolute risk increases. From a lifecourse perspective, young adulthood provides a window of opportunity to manage risk factors and prevent target organ damage as forerunner of premature death and MACE. In older adults, treatment should address absolute risk, thereby extending life in years and quality.

The prognostic implications of isolated diastolic hypertension (IDH), as defined by 2017 American College of Cardiology (ACC)/American Heart Association (AHA) guidelines, have not been tested using ambulatory blood pressure (BP) monitor thresholds (ie, 24-hour mean systolic BP <125 mm Hg and diastolic BP >= 75 mm Hg). We analyzed data from 11 135 participants in the IDACO (International Database on Ambulatory Blood Pressure in Relation to Cardiovascular Outcomes). Using 24-hour mean ambulatory BP monitor values, we performed Cox regression testing independent associations of IDH with death or cardiovascular events. Analyses were conducted in the cohort overall, as well as after age stratification (<50 years versus >= 50 years). The median age at baseline was 54.7 years and 49% were female. Over a median follow-up of 13.8 years, 2836 participants died, and 2049 experienced a cardiovascular event. Overall, irrespective of age, IDH on 24-hour ambulatory BP monitor defined by 2017 American College of Cardiology/American Heart Association criteria was not significantly associated with death (hazard ratio, 0.95 [95% CI, 0.79-1.13]) or cardiovascular events (hazard ratio, 1.14 [95% CI, 0.94-1.40]), compared with normotension. However, among the subgroup <50 years old, IDH was associated with excess risk for cardiovascular events (2.87 [95% CI, 1.72-4.80]), with evidence for effect modification based on age (P interaction <0.001). In conclusion, using ambulatory BP monitor data, this study suggests that IDH defined by 2017 American College of Cardiology/American Heart Association criteria is not a risk factor for cardiovascular disease in adults aged 50 years or older but is a risk factor among younger adults. Thus, age is an important consideration in the clinical management of adults with IDH.

Abstract Background Hypertension and diabetes cause chronic kidney disease (CKD) and diastolic left ventricular dysfunction (DVD) as forerunners of disability and death. Home blood pressure telemonitoring (HTM) and urinary peptidomic profiling (UPP) are technologies enabling prevention. Methods UPRIGHT-HTM (Urinary Proteomics Combined with Home Blood Pressure Telemonitoring for Health Care Reform [NCT04299529]) is an investigator-initiated 5-year clinical trial with patient-centred design, which will randomise 1148 patients to be recruited in Europe, sub-Saharan Africa and South America. During the whole study, HTM data will be collected and freely accessible for patients and caregivers. The UPP, measured at enrolment only, will be communicated early during follow-up to 50% of patients and their caregivers (intervention), but only at trial closure in 50% (control). The hypothesis is that early knowledge of the UPP risk profile will lead to more rigorous risk factor management and result in benefit. Eligible patients, aged 55–75 years old, are asymptomatic, but have ≥5 CKD- or DVD-related risk factors, preferably including hypertension, type-2 diabetes, or both. The primary endpoint is a composite of new-onset intermediate and hard cardiovascular and renal outcomes. Demonstrating that combining UPP with HTM is feasible in a multicultural context and defining the molecular signatures of early CKD and DVD are secondary endpoints. Expected outcomes The expected outcome is that application of UPP on top of HTM will be superior to HTM alone in the prevention of CKD and DVD and associated complications and that UPP allows shifting emphasis from treating to preventing disease, thereby empowering patients.

Objective: We aimed to determine the outcome-driven thresholds for central systolic blood pressure (cSBP) based on the new ACC/AHA hypertension classification and to explore the characteristics and prognosis associated with central systolic hypertension (cSHT). Design and method: In 5580 participants enrolled from 9 populations (mean age 54.2 years; 54.1% women), cSBP was estimated tonometrically from the radial waveform (SphygmoCor, Atcor, Australia). We determined the thresholds for cSBP, resulting in 5-year cardiovascular risks similar to those associated with the 2017 ACC/AHA classification of brachial systolic blood pressure (bSBP). Statistical methods included analysis of covariance, the log-rank test and proportional hazards regression. Results: Over 4.1 years (median), 203 persons died (6.4 per 1000 person years) and 252 experienced a composite cardiovascular endpoint (8.2 per 1000 person-years). After rounding to the nearest 5 mm Hg, approximate thresholds for elevated cSBP and stages 1 and 2 and severe cSHT were 110, 120, 130 and 150 mm Hg, respectively. In 3659 untreated subjects, those with isolated cSHT (cSBP > = 120 mmHg, n = 137, 3.7%), compared to the participants with central (cSBP < 120 mmHg) and brachial (bSBP <130 mmHg) normotension (n = 1953, 53.4%), were older, more likely being female, had smaller height, slower heart rate and higher augmentation index. The opposite was true for isolated brachial hypertension (bSHT; bSBP > = 130 mmHg, n = 192, 5.3%). Among 1921 treated patients, the use of b-blockers was more frequent (50% vs. 36.2%, P = 0.027), whereas in isolated cSHT (n = 72, 3.8%) compared with controlled cSBP, RAAS inhibitors less often used (50% vs. 65.3%, P = 0.013). Among all participants, with brachial and central normotension as reference, the multivariable-adjusted hazard ratios (95% confidence interval) of the composite cardiovascular events were 1.29 (0.57–2.90; P = 0.54) for isolated bSHT, 2.30 (1.22–4.33; P = 0.01) for isolated cSHT, and 2.00 (1.39–2.88; P = 0.002) for concordant cSHT and bSHT. Conclusions: Outcome-driven thresholds of central systolic BP were approximately 10 mm Hg lower than their brachial counterparts. cSHT, either isolated (4%) or combined bSHT (90%), was characterised by greater systolic augmentation and was associated with higher cardiovascular risk.

BACKGROUND Body mass reduction in overweight and obese people so as to reduce blood pressure, low‑density lipoprotein cholesterol level, and the risk of type 2 diabetes as well as to lower the risk of recurrent cardiovascular events is strongly recommended in current guidelines. OBJECTIVES To evaluate changes in body mass index (BMI) and waist circumference in patients with established coronary artery disease over a 20‑year period (1997-2017). PATIENTS AND METHODS Consecutive patients younger than 71 years of age and hospitalized for acute coronary syndrome or myocardial revascularization procedures were recruited and interviewed 6 to 18 months after their discharge from hospital. Weight, height, and waist circumference were measured in 1997 to 1998, 1999 to 2000, 2006 to 2007, 2011 to 2013, and 2016 to 2017. The same 5 hospitals took part in the surveys each time. RESULTS We examined 412 patients in 1997 to 1998 (survey 1), 427 in 1999 to 2000 (survey 2), 422 in 2006 to 2007 (survey 3), 462 in 2011 to 2013 (survey 4), and 272 in 2016 to 2017 (survey 5). The proportion of obese patients was 24.5% in survey 1, 27.2% in survey 2, 34.1% in survey 3, 35.9% in survey 4, and 40.4% in survey 5 (P <0.001). The proportion of patients with central obesity also increased significantly (32.5% in survey 1, 40.5% in survey 2, 51.4% in survey 3, 48.6% in survey 4, and 61.3% in survey 5; P <0.001). BMI increased significantly in men, but not in women, whereas the mean waist circumference increased in both sexes. BMI and waist circumference increased irrespective of age and education. CONCLUSIONS The analysis of 5 multicenter surveys showed a gradual increase in BMI and waist circumference in patients with established coronary artery disease over the course of 2 decades.

survey, the study sample consisted of consecutive patients hospitalized for coronary artery bypass grafting or percutaneous coronary inter-vention, or myocardial infarction, or unstable angina. As the age limit in the first (1997–1998) and the second (1999–2000) surveys was set be-low 71 years at the time of hospitalization, we excluded all older participants of the other 3 surveys from the present analysis. The to after the index hospitalization. Data on medications were using a standard ques-tionnaire declarations.