To determine the impact of cumulative systolic blood pressure (cumulative SBP) on increased arterial stiffness in a northern Chinese community. A total of 427 participants from the Kailuan study were enrolled. The median age was 59.0 years (interquartile range 52.0, 66.0). Cumulative SBP was calculated from BP measurements recorded in 2006-2022 by quartile. Logistic regression was used to estimate odds ratios (ORs) and confidence intervals (CIs). The prevalence of increased arterial stiffness at the last follow-up was compared with the predicted risk using the area under the curve, net reclassification index at the event rate, and integrated discrimination index, first with baseline SBP and then with cumulative BP values. Increased arterial stiffness was associated with cumulative SBP in Q4 (OR 2.34, 95% CI 1.25-4.40). The association was more significant in females (OR 3.07, 95% CI 1.16-8.28). The OR was 18.56 (95% CI 2.04-278.80) in patients aged ≤50 years and 2.06 (95% CI 1.03-4.15) in those aged >50 years. Participants with higher cumulative SBP had significantly higher carotid-femoral pulse wave velocity and a greater likelihood of higher arterial stiffness. The prevalence of increased arterial stiffness was 30.8% in Q1, 37.7% in Q2, 49.1% in Q3, and 65.1% in Q4 (p < 0.05). Cumulative SBP resulted in significant improvements in the category-free net reclassification index for all participants (0.25, 95% CI 0.02-0.47) and in females (0.43, 95% CI 0.12-0.75). Long-term high cumulative blood pressure is associated with increased arterial stiffness. Cumulative SBP improved risk reclassification for increased artery stiffness when compared to single SBP.

White coat hypertension (WCH) is still a grey zone regarding its management by clinicians, while its link to target organ damage (TOD) is still understudied. The aim of this study was to explore the impact of non-dipping status and nocturnal hypertension on TOD in untreated WCH subjects. A cross-sectional study of 547 individuals with WCH was conducted at a single institution. Patients underwent a thorough clinical examination, including medical history, office BP measurements, echocardiography, carotid artery ultrasonography, serum creatinine level measurements, and ambulatory blood pressure monitoring. Left ventricular hypertrophy (LVH), intima-media thickness of the common carotid artery (IMT-CCA) and estimated Glomerular Filtration Rate (eGFR) were used as TOD indices. The patients were divided into dippers and non-dippers, as well as nocturnal hypertensives and normotensives. Among WCH patients, 49.9% were non-dippers and 33.6% had nocturnal hypertension. Dippers had a significantly lower risk of left ventricular hypertrophy (OR: 0.68, 95%CI: 0.48 - 0.97) and higher mean expected eGFR values (b = 7.03, 95%CI: 3.12 - 10.94) than non-dippers. For IMT-CCA, office systolic and diastolic BP were the only significant predictors (b = 0.02, 95%CI: 0.00 - 0.03 and b = -0.03, 95%CI: -0.05 - -0.01). Office systolic BP was also significantly associated with eGFR (b = -1.68, 95%CI: -2.84 - -0.52). The results of this study indicate that non-dipping status is a significant risk factor for LVH and renal function in WCH subjects. Therefore, nighttime BP patterns, especially non-dipping, should be examined in patients with WCH.

Hypertension is a major global health burden and a leading driver of cardiovascular disease, yet reliable blood-based biomarkers for early disease are still limited. We combined plasma proteomics with explainable machine learning to identify circulating proteins associated with stage 1 hypertension in the Qatar Biobank. Proteomic profiles from 778 participants (554 controls and 224 stage 1 hypertension cases) were analyzed; 1305 proteins were tested for differential expression with adjustment for age and sex, and top features were prioritized before training predictive models. Among the evaluated classifiers, CatBoost performed best (AUROC = 0.7985), and SHapley Additive exPlanations were used to interpret the model. We identified 36 proteins significantly associated with hypertension and observed a characteristic pattern featuring lower Renin, sRAGE, ghrelin, and IL-1RAcP, and higher TFPI, QORL1, HSP70, and C5a in hypertensive individuals. Pathway and network analyses implicated processes related to oxidative stress and vascular function. Together, these results demonstrate Renin, TFPI, sRAGE, QORL1, ghrelin, HSP70, IL-1RAcP, and C5a as candidate circulating biomarkers for hypertension and illustrate the value of explainable AI for translating proteomic signals into potentially clinically interpretable candidates, pending validation in independent and diverse cohorts.

Patients with hypertension have worse acute COVID-19 outcomes, but the long-term effects of SARS-CoV-2 infection is unclear. We conducted a retrospective cohort study of adults with hypertension and no prior cardiovascular events in the Montefiore Health System, comparing those with and without COVID-19 over up to 4.5 years post-infection. Outcomes included first-time myocardial infarction (MI), heart failure (HF), stroke, all-cause mortality, and major adverse cardiovascular events (MACE). Multivariate regression and inverse-probability weighting adjusted for demographics, comorbidities, socioeconomic status, and COVID-19 vaccination. Adjusted hazard ratios (HRs) with 95% confidence intervals were calculated. Sub-analyses examined hypertension stage and acute COVID-19 blood biomarkers in relation to outcomes. Among 75,180 hypertensive patients, hospitalized COVID-19 was associated with increased risk of first-time MI (adjusted HR = 1.40 [1.21-1.63]), HF (1.59 [1.45-1.75]), stroke (1.35 [1.17-1.57]), all-cause mortality (2.51 [2.17-2.90]), and MACE (1.65 [1.54-1.77]) compared to COVID-negative individuals. Non-hospitalized COVID-19 patients had elevated risks of HF (1.17 [1.06-1.30]) and MACE (1.14 [1.05-1.23]). Hospitalized COVID-19 was associated with an increase in MACE risk by 75% in those with normal blood pressure, and by 126% and 148% in those with elevated blood pressure and stage 1 hypertension, respectively. Abnormal C-reactive protein, creatinine, lactate dehydrogenase, D-dimer, hemoglobin, and neutrophil-to-lymphocyte ratio predicted higher MACE risk. COVID-19, irrespective of disease severity, puts hypertensive patients at greater risks of worse cardiovascular outcomes, especially those with more advanced hypertension. These findings underscore the importance of long-term cardiovascular monitoring in this vulnerable population.

Pulse pressure amplification (PPA) is a measure of arterial function and wave reflection dynamics. The potential contribution of low-grade systemic inflammation to PPA-particularly in the context of overweight and obesity (OW/OB)-remains unclear, especially in young adults. We assessed differences in PPA and inflammatory markers (leptin, interleukin-6, interleukin-8, tumour necrosis factor-α, adiponectin, interleukin-10, and C-reactive protein) in young adults stratified by body composition. We further determined the relationship of PPA and inflammatory markers within these groups. This cross-sectional study included 1202 adults aged between 20-30 years. Participants were stratified into groups with underweight (N = 82) healthy weight (N = 598), overweight (N = 326) and obesity (N = 196). PPA was defined as the ratio of brachial pulse pressure to central pulse pressure. Inflammatory biomarkers were measured in serum. PPA was lower in the OW and OB groups (p < 0.001), while the inflammatory profile (tumour necrosis factor-α, adiponectin, leptin and C-reactive protein) was also more adverse in the OW and OB groups (all p < 0.001). In multivariate adjusted regression analysis, PPA was adversely associated with tumour necrosis factor-α, adiponectin, leptin and C-reactive protein in the OW or OB groups only (all p < 0.025). In young adults, a higher BMI is associated with a lower PPA and higher levels of inflammatory markers. Adverse associations between PPA as a measure of arterial function and several inflammatory markers are also seen in the setting of increased adiposity, highlighting inflammation as a potential mechanistic link between adiposity and changes in arterial function.

This study aimed to compare the inter-arm blood pressure difference (IAD) based on the first reading versus the average of the second and the third readings using computer-programmed blood pressure measurement (CCBPM) in 3067 rural community residents. The detection rate of abnormal systolic IAD (sIAD) was 9.1% based on the first reading, compared to 5.6% based on the average reading-a difference of approximately 40%. These findings suggest that CCBPM should be used with the average of the second and the third readings for sIAD evaluation.

While elevated arterial stiffness is recognized as a predictor of atrial fibrillation (AF), the relationship between long-term pulse pressure (PP) and the incidence of AF remains to be fully elucidated. We assessed the influence of time-averaged cumulative PP in midlife on incident AF. The analysis included 9150 adults from the Atherosclerosis Risk in Communities (ARIC) cohort who were free of AF at visit 4. The time-averaged cumulative blood pressure (BP) was calculated as the sum of the averaged BPs from the adjacent consecutive visits (visits 1-4), with the values being indexed to the total exposure time. At visit 4, the mean age of the study population was 62.9 years, with 4045 (44.2%) of the population being male. In 1455 individuals (15.9%) with a median follow-up of 16 years, incident AF was seen. The greatest predictor of incident AF, as indicated by the decline in the -2 Log likelihood statistic, was time-averaged cumulative PP, which was linked to an elevated risk for AF (HR = 1.20 (1.13-1.27)) in adjusted Cox models (per 1-SD increment). The correlation between incident AF and time-averaged cumulative systolic blood pressure (SBP) was 1.14 (1.07-1.22). In contrast, the diastolic relation tended to be opposite (HR = 0.94 (0.88-1.00)). Moreover, among persons aged < 65 years, without hypertension or antihypertensive treatment, these associations were even more remarkable (P < 0.05 for all interactions). Time-averaged cumulative PP in midlife was an important risk factor for incident AF with the strongest predictive effect, especially in persons who were younger, normotensive, or without antihypertensive treatment.

Hypertension (HTN) is a mitochondrial and metabolic disease. However, cause-effect connections between mitochondrial dysfunction and HTN remains uncharted. we focused on mitochondria-related genes, identifying potential causal-genes-relevant blood pressure (BP) using mitochondria-related genome-wide Mendelian randomization (MR). Through the summary statistics from cis-expression quantitative trait loci (cis-eQTL) datasets (human blood and artery), mitochondrial transcription factor A (TFAM), and genome-wide association studies (GWAS) datasets of BP indices (systolic blood pressure [SBP], diastolic blood pressure [DBP], pulse pressure [PP], and mean arterial pressure [MAP]) and HTN. we conducted a MR analysis to explore the potential causal relationship between mitochondrial-related genes and the BP indices, HTN. Sensitivity analysis and Bayesian colocalization were employed to validate this causal relationship. In aorta, HIBCH expression was negatively associated with SBP; OCIAD1 expression was positively associated with MAP. In tibial artery, HIBCH expression was negatively associated with SBP; OCIAD1 expression was positively associated with SBP, PP, and MAP; SLC25A37 was positively associated with MAP. In blood, LACTB expression was negatively associated with SBP, PP, and MAP; OCIAD1 expression was negatively associated with SBP and PP; and MTX1 expression was negatively associated with MAP. HARS2 expression was positively associated with SBP and PP; RAB24 and PRELID1 expression was positively associated with DBP; and NME6 expression was positively associated with SBP and DBP. In conclusion, the regulation of blood pressure correlates with mitochondria-related genes (HIBCH, SLC25A37 and OCIAD1 in artery; LACTB, OCIAD1, MTX1, HARS2, RAB24, PRELID1 and NME6 in blood). This study provides scientific evidence for specifically regulating BP phenotypes.

Cardiovascular diseases, the leading global cause of mortality, are frequently driven by hypertension, which contributes to left ventricular hypertrophy (LVH) and heart failure. Although ejection fraction (EF) remains the standard metric for assessing left ventricular function, it often fails to detect early dysfunction. Speckle-tracking echocardiography (STE) provides a more sensitive approach to identifying subclinical myocardial strain changes before EF declines. This cross-sectional, case-control study evaluated 90 participants divided into three groups: 30 healthy controls (Group I), 40 hypertensive patients without LVH (Group II), and 20 hypertensive patients with LVH (Group III). All underwent clinical evaluation, conventional echocardiography, and 2D-STE. Results showed that Group III had significantly greater septal and posterior wall diastolic thickness (p = 0.001) and higher LV mass index (p = 0.001) compared to Groups I and II. 2D-STE revealed reduced apical (AP2Ls, AP3Ls) and global longitudinal strain (GLS) in Groups II and III versus controls. Basal and mid-segment strains were also lower in disease groups, with mid-inferolateral segments showing more pronounced impairment in Group III. These findings highlight that Group III exhibited the most severe structural and functional cardiac alterations. The study demonstrates the superiority of 2D-STE over conventional echocardiography in detecting subclinical LV dysfunction in hypertensive patients, particularly those with LVH, through impaired longitudinal strain measurements. Early integration of 2D-STE into clinical practice could facilitate timely interventions to mitigate myocardial remodeling and heart failure progression.

Despite consistent evidence of the cardioprotective benefits of reduced-sodium salt, it remains an underutilised intervention. Understanding how reduced-sodium salt is perceived is required to scale-up its use. This review summarises end user and healthcare professional knowledge, attitudes, and behaviours about reduced-sodium salt. We systematically searched four databases (inception to February 2024) and identified studies reporting knowledge, attitudes and behaviours towards reduced-sodium salt. Twenty-nine studies from 11 countries were included, 18 of which were intervention studies involving reduced-sodium salt and 11 were descriptive studies examining perceptions among the general community and healthcare professionals. Among intervention studies, there was high overall acceptability but mixed findings on taste. Outcomes related to use or willingness to use were mostly positive especially following cost-subsidisation. Among descriptive studies, there was low awareness (ranging from 0-32%) and reported use (10-16%) of reduced-sodium salt among the general community. Barriers to use included low availability and higher costs compared to regular salt. Awareness was higher among healthcare professionals (71%). Overall, most studies found high acceptability and willingness to use following exposure to reduced-sodium salt, despite some detecting taste differences. Greater awareness coupled with strategies to improve availability and affordability are important to scale-up the use of reduced-sodium salt.