Journal of Hypertension最新文献

Objectives: To test the hypothesis that the association of formula-estimated sodium intake from spot urine with cardiovascular disease is independent of spot urinary sodium concentration.

Methods: We included 435 336 participants in the UK Biobank whose sodium intake was estimated from spot urine using INTERSALT, Kawasaki, and Tanaka formulas. Hazard ratios for cardiovascular disease (CVD) events and deaths were estimated using Cox proportional-hazard model adjusted for multiple covariates. Penalized Cox regression was used to assess nonlinear relations. Hazard ratios were recalculated after replacement of the sodium concentration term with sex-specific mean values (women: 67.5 mmol/l; men: 89.8 mmol/l) to assess how other components of the formulas influenced these associations.

Results: Forty-four thousand two hundred and sixty-eight CVD events and 3251 CVD deaths occurred during a median follow-up of 12 years. The mean estimated sodium intake was 143 (SD = 35), 178 (52), and 147 (33) mmol/day based on INTERSALT, Kawasaki, and Tanaka formulas, respectively. For CVD incidence, linear inverse associations were observed for INTERSALT and Tanaka estimates [hazard ratios (95% CIs) for every 50 mmol increase in estimated sodium intake: 0.9 (0.83-0.97) and 0.93 (0.89- 0.97); P -linear = 0.0047 and 0.0021], and a U-shaped association for the Kawasaki estimates ( P -nonlinear = 0.0026). When the sodium concentration term was fixed, inverse associations were seen for all formulas [0.86 (0.77-0.95), 0.96 (0.93-0.99) and 0.94 (0.89-0.99) for INTERSALT, Kawasaki, and Tanaka; P linear = 0.0054, 0.0166 and 0.0188]. For CVD mortality, no association was observed, but a nonlinear association was identified for the INTERSALT equation ( P -nonlinear = 0.0287) after fixing the sodium concentration.

Conclusion: These formula-estimated sodium intakes were associated with CVD incidence and mortality independently of spot urinary sodium concentration. We recommend these formulas not be used in studies associating sodium intake with CVD outcomes to avoid generating misleading evidence.

Introduction: Hypertensive disorders present significant morbidity and mortality during pregnancy. Although ambulatory blood pressure measurement remains the standard of care for normotensive women, self-monitoring at home is increasingly prevalent. The widespread use of smartphones worldwide has sparked interest in mobile applications that leverage the built-in hardware for blood pressure estimation, yet few trials have assessed their accuracy.

Methods: This prospective, longitudinal and monocentric study evaluated the accuracy of the OptiBP algorithm against standard oscillometric blood pressure measurements in a sample of pregnant women. Patients scheduled for elective caesarean sections were enrolled during the preoperative anesthesia consultations. Paired blood pressure measurements using OptiBP and the reference method were obtained at multiple time-points in late pregnancy and the postpartum period. Agreement between methods was assessed using the AAMI/ESH/ISO 81060-2:2018 standard thresholds of 5 ± 8 mmHg for mean ± standard deviation of the error (criterion 1) and patient-specific standard deviation of the mean error (criterion 2) and represented graphically by Bland-Altman scatterplots.

Results: Forty-eight women were enrolled of which 32 completed the protocol, yielding 338 total valid measurement pairs. Mean and standard deviation of the error were -1.78 ± 7.94 and 1.19 ± 7.59, and the patient-specific standard deviation of the mean error was 4.68 and 4.52, for SBP and DBP, respectively.

Conclusion: Compared with blood pressure measurements taken with an oscillometric device, OptiBP's blood pressure estimates meet the AAMI/ESH/ISO 81060-2:2018 criteria.

Background: Heart failure with preserved ejection fraction (HFpEF) is a high prevalence condition, with high rates of hospitalization and mortality. Arterial hypertension is the main risk factor for HFpEF. Among hypertensive patients, alterations in cardiac and vascular morphology identify hypertension-mediated organ damage (HMOD). Cardiac HMOD in terms of ventricular hypertrophy and diastolic dysfunction is a continuum between the preclinical condition (arterial hypertension) and HFpEF. In hypertensive patients, it is currently unknown what is the prevalence of individuals classifiable as being at high risk of developing HFpEF and whether aortic morphofunctional vascular changes are present.

Aim: This study seeks to retrospectively assess the prevalence of echocardiographic alterations consistent with the diagnosis of HFpEF in a cohort of patients with essential arterial hypertension, and the prevalence of vascular HMOD (V-HMOD) in different risk categories of patients.

Methods: Hypertensive outpatients referred at the Hypertension Center of Turin from 2003 to 2021 were retrospectively evaluated. Patients with a previous diagnosis of heart failure and known cardiovascular events were excluded. A predictive model associated with the risk of HFpEF development was calculated using echocardiographic variables. V-HMOD morphological and functional parameters were assessed by ascending aorta diameter and arterial stiffness (carotid-femoral pulse wave velocity, cfPWV).

Results: Eight hundred and four patients (34.8% women) were analyzed, age 53.1 ± 14 years; left ventricular mass index (LVMi) and E / e' ratio were impaired in 15.9 and 29.1% of cases, respectively. Dividing them into tertiles according to score: score 1 or less (30.2%); score 2-3 (47.4%); score at least 3 (22.7%). Patients identified at high risk of HFpEF (score ≥3) had higher age, BMI and blood pressure than the other two groups ( P  < 0.05); they showed a significantly higher prevalence of female patients (42.3%), treatment with at least two antihypertensive drugs (40.1%), diabetes (7.1%), and dyslipidemia (28%; P  < 0.05), with a larger ascending aorta diameter (35.5 ± 5.5 mm, P  < 0.05) and higher cfPWV (8.8 ± 2.4 m/s, P  < 0.05).

Conclusion: At least one in five hypertensive patients, referred to an outpatient echocardiographic examination, has C-HMOD compatible with a high-risk category of HFpEF and have a significant increase in V-HMOD. This reinforces the notion that arterial hypertension and HFpEF are not two distinctly separate conditions but a continuum of pathophysiologic alterations.

Background: People with diabetes often have increased blood pressure (BP) variability because of autonomic dysfunction and arterial stiffness, making it a critical factor in predicting clinical outcomes. We investigated the reproducibility of long-term visit-to-visit BP variability (VVV) and the minimum number of BP readings to reliably determine VVV in people with diabetes.

Methods: This multicenter retrospective study used data from electronic health records of the Korea University Medical Center database. Altogether, 10 475 people with diabetes who had more than nine BP readings during a maximum period of 2 years were identified. This study focused on the coefficient of variation of these readings and their correlation with major adverse cardiovascular events (MACE) over a 3-year follow-up period.

Results: The mean age of the participants was 65.2 years. Of these, 53.2% were men, and 87.4% had hypertension. The mean coefficient of variation of multiple SBP readings that best predicted the 3-year MACE were 8.4, 9.5, 9.0, 9.0, and 9.7 for three, five, seven, nine, and all readings, respectively. Patients with high VVV (coefficient of variation of five SBP readings >9) exhibited a higher incidence of 3-year MACE (10.1%) than those with low VVV (5.4%, P  < 0.001). In the multivariable analysis, high VVV of both SBP and DBP were independently associated with 3-year MACE.

Conclusion: Long-term VVV in the BP is a reproducible and reliable predictor of cardiovascular outcomes in people with diabetes. A minimum of five BP measurements are recommended for effective intraindividual VVV estimation and cardiovascular risk assessment.

Background: Arterial stiffness is a key cardiovascular risk factor influenced by conditions like hypertension, obesity and kidney function. Although large arteries have been extensively studied, small conduit arteries remain less investigated. This study aims to explore the impact of kidney function on small conduit artery stiffness in two distinct groups: normotensive individuals with severe obesity and normal-weight hypertensive individuals.

Methods: Thirty-three severely obese (OB) individuals, 33 hypertensive (HT) individuals, and 33 normotensive, normal-weight control participants, matched for age and sex, were recruited. Eleven participants (33%) in both the OB and HT groups had estimated glomerular filtration rate (eGFR) less than 60 ml/min/1.73 m 2 . Aortic stiffness (carotid-femoral pulse wave velocity) was recorded. Ultrasound images of common carotid, radial, and interdigital arteries were acquired for the assessment of geometry, distensibility coefficient, circumferential wall stress, and Young's elastic modulus (Einc).

Results: The OB group exhibited higher radial stiffness (both Einc and distensibility coefficient) compared to the HT and control groups, independent of radial diameter adjustments. An inverse correlation between eGFR and radial Einc was noted only in the OB group ( P  = 0.002). Conversely, a direct correlation between eGFR and carotid distensibility coefficient was found only in the HT group ( P  = 0.001). In multivariable analysis, eGFR and BMI were the only predictors of radial Einc in the overall population.

Conclusion: Severe obesity and reduced eGFR synergistically increase radial artery stiffness, a phenomenon not observed in essential hypertension. This study suggests that moderate chronic kidney disease exacerbates vascular alterations in obese individuals, highlighting the need for further research on the role of small conduit arteries in cardiovascular risk.

Background: The arterial stiffening is attributed to the intrinsic structural stiffening and/or load-dependent stiffening by increased blood pressure (BP). The respective lifetime alterations and major determinants of the two components with normal aging are not clear.

Methods: A total of 3053 healthy adults (1922 women) aged 18-79 years were enrolled. The carotid intima-media thickness, diameter, and local BPs were automatically determined by the radio frequency ultrasound system. The Peterson and Young elastic moduli were then calculated to represent total arterial stiffness. Structural stiffness was recalculated at a reference BP of 120/80 mmHg with established models. Load-dependent stiffness was the difference between total and structural stiffness.

Results: Both structural and load-dependent stiffness increased with aging, with much larger changes in the structural components. The age-related increasing rates were higher in women for the structural stiffness than men ( P  < 0.05), but similar for the load-dependent stiffness. The clinical characteristics and arterial stiffness were widely correlated, but most correlations were quite weak ( r  < 0.3) other than BPs. Multiple regression analyses adjusted for sex, age and other clinical correlates showed that structural stiffness increased with pulse pressure (PP) and load-dependent stiffness increased with mean arterial pressure (MAP), respectively.

Conclusion: The age-related arterial stiffening is mainly caused by the intrinsic structural stiffening, which demonstrated significant age-sex interaction. BPs were the major clinical determinants of arterial stiffness, with PP and MAP associated with different arterial stiffness components. The differentiation of the structural and load-dependent arterial stiffness should be highlighted for the optimal vascular health management.

The aim of this meta-analysis was to assess the efficacy and safety of sacubitril-valsartan in hypertension patients with end-stage kidney disease (ESKD) undergoing dialysis. We searched the Medline, Cochrane, Embase, Web of Science, and ClinicalTrials.gov databases for studies reporting outcomes after SV treatment. All analyses were performed utilizing the random effects models. Nineteen studies comprising 1597 patients with concomitant hypertension and ESKD undergoing dialysis were included. After sacubitril-valsartan treatment, significant reductions in both SBP and DBP were observed (mean change in SBP: -11.09 mmHg [95% confidence interval, 95% CI: -14.51,-7.66] and DBP: -4.37 mmHg [-6.36,-2.38]). Compared to conventional treatment, patients treated with sacubitril-valsartan had a lower risk of cardiovascular hospitalization (risk ratio: 0.63 [0.44,0.90]). Sacubitril-valsartan treatment showed a trend toward reducing the risk of all-cause mortality, although this was not statistically significant (risk ratio: 0.66 [0.27,1.60]). Evaluation of echocardiographic parameters among studies including hypertension patients with heart failure indicated that SV improved LVEF (mean change: +7.04%[+3.19, +10.90]), however this effect was more pronounced in the HFrEF patients ( Pinteraction =0.0003). Sacubitril-valsartan also reduced LVSd, LVDd, LAD, and E/e' ratio ( P  < 0.05). The risks of severe hyperkalemia and symptomatic hypotension were comparable between sacubitril-valsartan treatment and conventional treatment ( P  > 0.05). The present study revealed that sacubitril-valsartan treatment is well tolerated and could have potential benefits in hypertension patients with ESKD on dialysis by effectively controlling blood pressure, improving LVEF, reversing cardiac remodeling, and reducing the risk of cardiovascular hospitalization.

Background: Central SBP purports to aid hypertension management. This concept is founded on cross-sectional studies; however, findings are mixed and few report longitudinal relationships between changes in blood pressure (BP) and outcomes. This study aimed to determine associations of changes in brachial BP and central BP with changes in left ventricular mass index (LVMi), as an important hypertension-related clinical outcome.

Methods: Standard brachial BP and central BP (Vicorder, Skidmore Medical, UK; a type 1 device, using SBP/DBP calibration) were measured at the same time as cardiac MRI for LVMi among adults from the UK Biobank Cohort Study assessed prospectively at two time points (2014+ and 2019+). Analysis was by linear regression adjusted for demographic and clinical characteristics.

Results: Data were evaluable for 681 participants (aged 50.1 ± 7.1 years, 54% women) followed over 3.2 ± 1.6 years [mean ± standard deviation (SD)]. Cross-sectional analysis showed the association of brachial SBP with LVMi [ β  ± standard error (SE) 3.47 × 10 -2  ± 6.39 × 10 -3  g/m 2.7 /mmHg] and central SBP with LVMi ( β  ± SE = 3.52 × 10 -2  ± 6.40 × 10 -3  g/m 2.7 /mmHg) were comparable ( P  < 0.001 both). In longitudinal analysis, associations between the changes in BP and changes in LVMi were identical for both central and brachial SBP ( β  ± SE = 0.011 ± 0.003 g/m 2.7 /mmHg; P  < 0.001 both). Findings were unchanged if participants were stratified by age, LVMi quartile, BP category or central BP phenotype.

Conclusion: Changes over time in standard brachial BP provide similar information to central BP on changes over time in LVMi. Whether these findings are generalizable must be further investigated in other cohorts and by other types of central BP devices.