In a comparative meta-analysis, we investigated the prognostic value of masked hypertension and masked uncontrolled hypertension defined by ambulatory or home blood pressure (BP) monitoring. We searched English literature published till 2 September 2018 to identify prospective observational studies. Masked hypertension was defined as a normal clinic BP (<140/90 mmHg) in the presence of an elevated 24 h, daytime or night-time ambulatory or home BP. Clinical outcomes included all-cause and cardiovascular mortality, and fatal and nonfatal cardiovascular, stroke, cardiac, coronary and renal disease events. In total, 21 studies (n = 130 318) were included. Overall, compared with normotensive participants, masked hypertensive patients had a 5.7/2.9 mmHg higher clinic BP and 18.7/9.8 mmHg higher out-of-office BP. The pooled risk ratio for masked hypertension versus normotension was 1.67 (95% confidence interval, 1.32–2.13) and 2.19 (1.72–2.78) for all-cause (eight studies) and cardiovascular mortality (three studies), respectively, and 1.71 (1.53–1.91), 1.95 (1.36–2.80), 1.76 (1.33–2.33), 1.62 (0.27–9.60), 3.85 (2.03–7.31) for fatal and nonfatal cardiovascular (15 studies), stroke (two studies), cardiac (two studies), coronary (two studies) and renal disease events (two studies), respectively. Risk ratios for all-cause mortality (1.78 versus 1.40, P = 0.16) and fatal and nonfatal cardiovascular events (1.81 versus 1.61, P = 0.29) were similar between studies on ambulatory and home BP monitoring in the overall analyses. The analyses in subgroups according to treatment status (untreated, treated or mixed) and sampling approach (population or referred patients) were confirmatory. Masked hypertension and masked uncontrolled hypertension were associated with unfavorable clinical outcomes, regardless of the out-of-office BP monitoring techniques.

Background: Smokers may smoke cigarettes during ambulatory or home blood pressure (BP) monitoring but not clinic measurement. We investigated the prevalence of masked hypertension in relation to cigarette smoking in Chinese outpatients enrolled in a multicenter registry. Methods: Our study included 1646 men [494 (30.0%) current smokers]. We defined masked hypertension as a normal clinic SBP/DBP (<140/90 mmHg) and elevated daytime (≥135/85 mmHg) or night-time (≥120/70 mmHg) ambulatory or morning or evening home SBP/DBP (≥135/85 mmHg). Results: In all men, multiple logistic regression showed that current cigarette smoking was significantly associated with daytime [prevalence 18.7%, odds ratio (OR) 1.69, 95% confidence interval 1.27–2.25, P = 0.0003] but not night-time (prevalence 27.1%, P = 0.32) ambulatory masked hypertension and associated with evening (prevalence 14.6%, OR 1.81, confidence interval 1.33–2.47, P = 0.0002) but not morning (prevalence 17.6%, P = 0.29) home masked hypertension. The associations were more pronounced for heavy smoking (≥20 cigarettes/day) relative to never smoking for both masked daytime ambulatory (OR 1.97, P = 0.001) and evening home hypertension (OR 2.40, P < 0.0001) or in patients over 55 years of age (P for interaction in relation to daytime ambulatory masked hypertension = 0.005). In men with clinic normotension (n = 742), the associations were also significant (P < 0.01), particularly in those with a normal to high-normal clinic BP (n = 619, P < 0.04). Conclusion: Cigarette smoking was associated with increased odds of masked daytime ambulatory and evening home hypertension, especially in heavy smoking or older men.

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.

Isolated nocturnal hypertension (INH) is a special type of out‐of‐office hypertension. Its determinants and pathophysiology remain unclear. In a nested case‐control study, we intend to investigate the host, environmental, and genetic factors in relation to INH. Among 2030 outpatients screened from December 2008 till June 2015, 128 patients with INH were identified, and then 128 normotensives were matched according to sex and age. INH was an elevated nocturnal blood pressure (BP ≥120/70 mmHg) in the presence of a normal daytime BP (< 135/85 mmHg). Host factors included age, sex, body mass index, smoking and drinking, sleep time and duration, heart rate, serum lipids, and serum creatinine. Environmental cues encompassed season, ambient temperature, atmospheric pressure, humidity, and wind speed, and genetic cues 29 single‐nucleotide polymorphisms (SNPs) in 12 clock genes. Daytime and nighttime BPs averaged 124.9/80.7 and 114.5/73.7 mmHg, respectively, in the INH patients and 121.0/76.5 and 101.8/63.3 mmHg in the normotensive controls. Stepwise logistic regression analyses revealed that INH was associated with nighttime heart rate (P = .0018), sleep duration (P = .0499), and relative humidity (P = .0747). The odds ratios (95% CI) for each 10 beats/min faster nighttime heart rate and 10% lower relative humidity were 1.82 (1.25‐2.65) and 0.82 (0.67‐1.00), respectively. Irrespective of the genetic models, no significant association was observed between INH and the SNPs (P ≥ .054). In conclusion, INH was associated with host and environmental factors rather than genetic markers.

Blacks are more prone to salt‐sensitive hypertension than Whites. This cross‐sectional analysis of a multi‐ethnic cohort aimed to search for proteins potentially involved in the susceptibility to salt sensitivity, hypertension, and hypertension‐related complications. The study included individuals enrolled in African Prospective Study on the Early Detection and Identification of Cardiovascular Disease and Hypertension (African‐PREDICT), Flemish Study of the Environment, Genes and Health Outcomes (FLEMENGHO), Prospective Cohort Study in Patients with Type 2 Diabetes Mellitus for Validation of Biomarkers (PROVALID)‐Austria, and Urinary Proteomics Combined with Home Blood Pressure Telemonitoring for Health Care Reform Trial (UPRIGHT‐HTM). Sequenced urinary peptides detectable in 70% of participants allowed the identification of parental proteins and were compared between Blacks and Whites. Of 513 urinary peptides, 300 had significantly different levels among healthy Black (n = 476) and White (n = 483) South Africans sharing the same environment. Analyses contrasting 582 Blacks versus 1731 Whites, and Sub‐Saharan Blacks versus European Whites replicated the findings. COL4A1, COL4A2, FGA, PROC, MGP, MYOCD, FYXD2, and UMOD were identified as the most likely candidates underlying the racially different susceptibility to salt sensitivity, hypertension, and related complications. Enriched pathways included hemostasis, platelet activity, collagens, biology of the extracellular matrix, and protein digestion and absorption. Our study suggests that MGP and MYOCD being involved in cardiovascular function, FGA and PROC in coagulation, FYXD2 and UMOD in salt homeostasis, and COL4A1 and COL4A2 as major components of the glomerular basement membrane are among the many proteins potentially incriminated in the higher susceptibility of Blacks compared to Whites to salt sensitivity, hypertension, and its complication. Nevertheless, these eight proteins and their associated pathways deserve further exploration in molecular and human studies as potential targets for intervention to reduce the excess risk of hypertension and cardiovascular complications in Blacks versus Whites.

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.