The value of the association of arterial stiffness with left ventricular concentric remodelling/left ventricular hypertrophy (LVH) assessed by echocardiography, for prediction of masked hypertension defined by office and ambulatory blood pressure monitoring (ABPM) in the general population is largely undefined. We investigated this topic in the participants to the Pressioni Monitorate E Loro Associazioni (PAMELA) study.

The study included 272 participants (153 normotensives and 119 with masked hypertension) who attended the second and third survey of the PAMELA study performed after 10 and 25 years from the initial evaluation. Data collection included medical history, physical examination, blood tests, office, ABPM, echocardiographic and Cardio-Ankle Vascular Index (CAVI) measurements.

Compared to normotensive individuals, participants with masked hypertension were younger, had significantly higher office, home, mean 24-h, day-time, night-time SBP/DBP and heart rate. The likelihood of having masked hypertension, was approximately more than two-fold higher [odds ratio (OR) = 2.29, confidence interval (CI): 1.01-5.31, P  = 0.04] in participants with increased CAVI and left ventricular remodelling/LVH compared to their counterparts without organ damage. This association showed a unique value in identifying masked hypertension compared to both isolated markers of organ damage (OR = 1.69, P  = 0.15 for increased CAVI and OR = 0.82, P  = 0.80 for left ventricular remodelling/LVH), after adjusting for age, sex, office SBP/DBP, antihypertensive treatment and diabetes.

The present study offers a new piece of evidence of the key value of looking for both vascular and cardiac organ damage to unmask MH and improve its clinical management in the general population.

We aimed to evaluate the risks of death and cardiovascular death of different subtypes of masked hypertension, defined by either isolated daytime or nighttime blood pressure (BP) elevation, or both, compared with patients with normal both office and 24-h BP.

We selected 4999 patients with masked hypertension (normal office BP and elevated 24-h BP). They were divided in three different categories: isolated daytime masked hypertension (elevated daytime BP and normal nighttime BP, 800 patients), isolated nighttime masked hypertension (elevated nighttime BP and normal daytime BP, 1069 patients) and daytime and nighttime masked hypertension (elevation of both daytime and nighttime BP, 2989). All-cause and cardiovascular death (median follow-up 9.7 years) were assessed in each of these subtypes in comparison to 10 006 patients with normal both office and 24-h BP. Hazard ratios from Cox models after adjustment for clinical confounders were used for such comparisons.

Compared with patients with normal both office and 24-h BP, isolated daytime masked hypertension was not associated with an increased risk of death in models adjusted for clinical confounders [hazard ratio 1.07; 95% confidence interval (CI): 0.80-1.43]. In contrast, isolated nighttime masked hypertension (hazard ratio: 1.39; 95% CI 1.19-1.63) and daytime and nighttime masked hypertension (hazard ratio: 1.22; 95% CI 1.08-1.37) had an increased risk of death in comparison to patients with BP in the normal range. Similar results were observed for cardiovascular death.

The risk of death in masked hypertension is not homogeneous and requires nocturnal BP elevation, either isolated or with daytime elevation. Isolated daytime masked hypertension is not associated with an increased risk of death.

Home blood pressure (BP) variability (BPV) and BP phenotypes such as white-coat hypertension (WCH), white-coat uncontrolled hypertension (WUCH), masked hypertension (MH) and masked uncontrolled hypertension (MUCH) are predictors of adverse cardiovascular events. This study compared home BPV across BP phenotypes built from abnormal office BP (OBP) and home BP monitoring (HBPM) thresholds defined by three distinct societies [European Society of Hypertension (ESH): OBP ≥ 140/90 mmHg and HBPM ≥ 135/85 mmHg; American College of Cardiology/American Heart Association (ACC/AHA): OBP and HBPM ≥ 130/80 mmHg and Brazilian Society of Cardiology (BSC): OBP ≥ 140/90 mmHg and HBPM ≥ 130/80 mmHg].

This cross-sectional study evaluated 51 194 treated (37% men, age = 61 ± 15 years) and 56 100 untreated (41% men, age = 54 ± 16 years) individuals from 1045 Brazilian centers who underwent OBP and HBPM measurements. Systolic and diastolic home BPV were estimated as the: standard deviation, coefficient of variation, and the variability independent of the mean of HBPM.

Results of adjusted analysis showed that home BPV parameters were significantly greater in individuals with WCH/WUCH according to the BSC criteria, in those with MH/MUCH defined by the ACC/AHA criteria, and tended to be greater in individuals with either MH/MUCH or WCH/WUCH defined by the ESH criteria.Furthermore, restricted cubic spline analysis showed a U-shaped association between BPV and the difference between OBP and HBPM in treated and untreated individuals.

Home BPV was greater in WCH/WUCH and/or MH/MUCH depending on the criteria used to define abnormal OBP and HBPM thresholds. These findings underscore the need to standardize abnormal BP criteria in clinical practice.

Hypertension affects one in three adults globally and is the leading modifiable risk factor for cardiovascular disease. Although blood pressure measurements at rest are fundamental to the detection and management of hypertension, abnormal blood pressure responses to exercise, namely, an exaggerated exercise blood pressure (EEBP), can provide additional independent information about current and future hypertension risk. This paper summarizes a symposium entitled, "The Role of Exercise Blood Pressure in Hypertension: Measurement, Mechanisms and Management" included at the 2023 American College of Sports Medicine annual meeting, which presented a timely discussion about the clinical utility of EEBP. Here we will summarize the evidence presented by the speakers including considerations for blood pressure measurement during exercise, an overview of EEBP thresholds and discussion about the value of EEBP during submaximal exercise for the identification and management of hypertension, a summary of the potential physiological mechanisms underpinning an EEBP, and a review of exercise prescription guidelines based on new and emerging evidence as they relate to the American College of Sports Medicine's exercise recommendations for hypertension. We conclude by highlighting areas for future research with the overarching goal of improving the measurement and management of hypertension.

In the in-clinic blood pressure (BP) recording setting, a sizable number of individuals with normal BP and approximately 30% of patients with chronic renal disease (CKD) exhibit elevated outpatient BP records. These individuals are known as masked hypertension (MHTN), and when they are on antihypertensive medications, but their BP is not controlled, they are called masked uncontrolled hypertension (MUHTN). The masked phenomenon (MP) (MHTN and MUHTN) increases susceptibility to end-organ damage (a two-fold greater risk for cardiovascular events and kidney dysfunction). The potential extension of the observed benefits of MP therapy, including a reduction in end-organ damage, remains questionable.

This review aims to study the diagnostic methodology, epidemiology, pathophysiology, and significance of MP management in end-organs, especially the kidneys, cardiovascular system, and outcomes. To achieve the purposes of this non-systematic comprehensive review, PubMed, Google, and Google Scholar were searched using keywords, texts, and phrases such as masked phenomenon, CKD and HTN, HTN types, HTN definition, CKD progression, masked HTN, MHTN, masked uncontrolled HTN, CKD onset, and cardiovascular system and MHTN. We restricted the search process to the last ten years to search for the latest updates.

MHTN is a variant of HTN that can be missed if medical professionals are unaware of it. Early detection by ambulatory or home BP recording in susceptible individuals reduces end-organ damage and progresses to sustained HTN. Adherence to the available recommendations when dealing with masked phenomena is justifiable; however, further studies and recommendation updates are required.

The prognosis of masked hypertension is controversial. The aims of this meta-analysis were to determine the global prevalence of masked hypertension and to better understand its association with the risk of cardiorenal comorbidities and all-cause mortality.

We searched the PubMed, Embase (OVID), The Cochrane Library, WanFang Data, and CNKI databases for relevant studies published from inception until January 15, 2024. Cohort studies that reported an association of masked hypertension with the risk of cardiorenal comorbidities and all-cause mortality were eligible for meta-analysis.

Twenty-six studies (with 129,061 participants) were included. The median follow-up duration was 7.38 years. The pooled prevalence of masked hypertension was 18% (95% confidence interval [CI] 15%-21%). Compared with normotensive individuals, those with masked hypertension had an increased risk of all-cause mortality (relative risk [RR] 1.64, 95% CI 1.32-2.04) and incident cardiovascular disease (RR 1.57, 95% CI 1.45-1.69). The results were similar regardless of treatment status and in multiple subgroup analyses. Masked hypertension was also associated with increased risks of cardiovascular mortality (RR 1.69, 95% CI 1.02-2.78) and composite renal outcomes (RR 3.57, 95% CI 2.32-5.50).

Masked hypertension is prevalent in adults and associated with increased risks of all-cause mortality, cardiovascular disease, cardiovascular mortality, and composite renal events.

Hypertension, which stands as a leading global health challenge, demands a dynamic approach for its effective management. The traditional methods of managing hypertension, centered on periodic clinic visits for blood pressure measurement and pharmacological interventions, are increasingly being complemented and enhanced by digital technologies. The integration of wearable devices, mobile applications, personalized treatments, and telehealth solutions into healthcare system is reshaping traditional hypertension care. Digitalization of hypertension management extends to population health, in addition to individual patient benefits, aimed at preventing and controlling hypertension on a broader scale. However, this digital revolution in hypertension management brings forth challenges related to data security, data accuracy, equitable access, and standardization of devices by international regulatory agencies. Addressing these issues is equally important to ensure that the benefits of digital technologies are accessible to everyone, irrespective of socio-economic factors. This paper concludes with a forward-looking perspectives, emphasizing the potential of digitalization to modify the landscape of hypertension management.

Hypertension impacts most older adults as one of many multiple chronic conditions. A thorough evaluation is required to assess overall health, cardiovascular status, and comorbid conditions that impact treatment targets. In the absence of severe frailty or dementia, intensive treatment prevents more cardiovascular events than standard treatment and may slow cognitive decline. "Start low and go slow" is not the best strategy for many older adults as fewer cardiovascular events occur when hypertension is controlled within the first 3 to 6 months of treatment.

This review aims to inform the reader of the complexity of blood pressure responses when comparing blood pressure measured in the medical environment to that outside the medical environment. In addition, we summarize what is known about current predictors of white coat hypertension, reevaluate the relationship of white coat hypertension to cardiovascular outcomes, and provide some clinical guidance on management.

Differences in outcomes exist when white coat effect occurs in unmedicated people versus the white coat effects in those on antihypertensive therapy. White coat hypertension is relatively common, carries a small but definite increase in cardiovascular risk, and is prone to conversion to sustained hypertension. Future research will hopefully tease out the roles of ancillary findings that characterize a white coat hypertensive (like modest elevations in creatinine, glucose and triglycerides) in the elevated cardiovascular risk, and test the effectiveness of mitigation strategies in these patients.

This study aimed to elucidate the prognostic role of Masked Morning Hypertension (MMH) in non-dialysis-dependent chronic kidney disease (NDD-CKD).

2,130 NDD-CKD patients of the inpatient department were categorized into four blood pressure (BP) groups: clinical normotension (CH-), clinical hypertension (CH+) with morning hypertension (MH+), and without MH+ (MH-) respectively. The correlation between these four BP types and the primary (all-cause mortality) and secondary endpoints (cardio-cerebrovascular disease [CVD] and end-stage kidney disease [ESKD]) was analyzed.

The prevalence of MH and MMH were 47.4% and 14.98%, respectively. Morning hypertension independently increased the risk of all-cause mortality (P = 0.004) and CVD (P < 0.001) but not ESKD (P = 0.092). Masked morning hypertension was associated with heightened all-cause mortality (HR = 4.22, 95% CI = 1.31-13.59; P = 0.02) and CVD events (HR = 5.14, 95% CI = 1.37-19.23; P = 0.02), with no significant association with ESKD (HR = 1.18, 95% CI = 0.65-2.15; P = 0.60). When considering non-CVD deaths as a competing risk factor, a high cumulative incidence of CVD events was observed in the MMH group (HR = 5.16, 95% CI = 1.39-19.08).

MMH is an independent risk factor for all-cause mortality and combined cardiovascular and cerebrovascular events in NDD-CKD patients, underscoring its prognostic significance. This highlights the need for comprehensive management of MH in this population.

Hypertensive disorders in pregnancy and other adverse pregnancy outcomes (APOs) increase the risk of developing chronic hypertension and cardiovascular disease. Perceptions of stress and neighborhood context also influence blood pressure (BP) fluctuations. We examined if APOs, higher perceived stress, and neighborhood deprivation were associated with hypertension phenotypes a decade after pregnancy in untreated individuals.

Participants were 360 individuals who gave birth between 2008 and 2009 and participated in a research study 8-10 years following pregnancy. Standardized office and home BP readings were obtained, and we applied the AHA/ACC 2017 guidelines to identify sustained, white coat, and masked hypertension phenotypes. We measured personal stress with the perceived stress scale and neighborhood deprivation with the CDC Social Vulnerability Index.

Of the 38.3% (138/360) with any hypertension, 26.1% (36/138) reported a diagnosis of hypertension but were currently untreated. Sustained hypertension was the most common (17.8%), followed by masked and white coat hypertension, both 10.3%. Hypertensive disorders in pregnancy were associated with sustained (odds ratio [OR] 5.54 [95% confidence interval, CI 2.46, 12.46] and white coat phenotypes (OR 4.20 [1.66, 10.60], but not masked hypertension (OR 1.74 [0.62, 4.90]). Giving birth to a small for gestational age infant was also associated with sustained hypertension. In covariate adjusted models, perceived stress, but not neighborhood deprivation, was significantly associated with masked hypertension.

A decade after delivery, APOs were associated with sustained and white coat hypertension, but not masked hypertension. Exploration of the mechanisms underlying, and clinical implications of, these associations is warranted.

Using high awake blood pressure (BP; ≥130/80 mm Hg) on ambulatory BP monitoring (ABPM) as a reference, the purpose of this study was to determine the accuracy of high office BP (≥130/80 mm Hg) at an initial visit and high confirmatory office BP (≥130/80 mm Hg), and separately, high home BP (≥130/80 mm Hg) among participants with high office BP (≥130/80 mm Hg) at an initial office visit.

The accuracy of office BP measurements using the oscillometric method for detecting high BP on ABPM was determined among 379 participants with complete office BP and ABPM data in the IDH (Improving the Detection of Hypertension) study. For detecting high BP on ABPM, the accuracy of high confirmatory office BP using the oscillometric method and, separately, high home BP was also determined among the subgroup of 122 participants with high office BP at an initial visit and complete home BP monitoring data. High office BP had moderate sensitivity (0.61 [95% CI, 0.53-0.68]) and high specificity (0.85 [95% CI, 0.80-0.90]) for high awake BP. High confirmatory office BP and high home BP had moderate sensitivity (0.69 [95% CI, 0.59-0.79] and 0.79 [95% CI, 0.71-0.87], respectively) and low and moderate specificity (0.44 [95% CI, 0.27-0.61] and 0.72 [95% CI, 0.56-0.88], respectively).

Many individuals with high BP on ABPM do not have high office BP. Confirmatory office BP and home blood pressure monitoring also had limited ability to identify individuals with high BP on ABPM.

Cardio-cerebrovascular diseases (CVDs) are the most common cause of death worldwide. Various CVD risk assessment tools have been developed. In South Korea, the Korea Occupational Safety & Health Agency (KOSHA) and the National Health Insurance Service (NHIS) have provided CVD risk assessments with health checkups. Since 2018, the KOSHA guide has stated that NHIS CVD risk assessment tool could be used as an alternative of KOSHA assessment tool for evaluating CVD risk of workers. The objective of this study was to determine the correlation and agreement between the KOSHA and the NHIS CVD risk assessment tools.

Subjects of this study were 17,485 examinees aged 20 to 64 years who had undergone medical examinations from January 2021 to December 2021 at a general hospital. We classified subjects into low-risk, moderate-risk, high-risk, and highest-risk groups according to KOSHA and NHIS's CVD risk assessment tools. We then compared them with cross-analysis, Spearman correlation analysis, and linearly weighted kappa coefficient.

The correlation between KOSHA and NHIS tools was statistically significant (p-value < 0.001), with a correlation coefficient of 0.403 and a kappa coefficient of 0.203. When we compared risk group distribution using KOSHA and NHIS tools, CVD risk of 6,498 (37.1%) participants showed a concordance. Compared to the NHIS tool, the KOSHA tool classified 9,908 (56.7%) participants into a lower risk category and 1,079 (6.2%) participants into a higher risk category.

In this study, KOSHA and NHIS tools showed a moderate correlation with a fair agreement. The NHIS tool showed a tendency to classify participants to higher CVD risk group than the KOSHA tool. To prevent CVD more effectively, a higher estimation tool among verified CVD risk assessment methods should be selected and managements such as early intervention and treatment of risk factors should be performed targeting the high-risk group.

Seasonal variation of blood pressure (BP) is a topic in cardiology that has gained more attention throughout the years. Although it is extensively documented that BP increases in seasons coupled with lower temperatures, there are still many gaps in this knowledge field that need to be explored. Notably, seasonal variation of BP phenotypes, such as masked and white coat hypertension, and the impact of air pollution, latitude, and altitude on seasonal variation of BP are still poorly described in the literature, and the levels of the existing evidence are low. Therefore, further investigations on these topics are needed to provide robust evidence that can be used in clinical practice.

Masked hypertension is associated with cardiovascular disease (CVD). However, previous large studies have not used the same device to measure office and home blood pressure (BP) and adhered to current home BP measurement recommendations of the European Society of Hypertension. We aimed to characterize masked hypertension and explore its relation to manifestations of CVD.

A randomly selected cohort of 5057 participants aged 50-64 years from the Swedish CardioPulmonary BioImage Study (SCAPIS) was evaluated with office and home BP using the semi-automatic Omron M10-IT oscillometric device. Additional analyses included pulse wave velocity (PWV) and coronary artery calcium score (CACS).

Of participants, 4122 did not have current antihypertensive treatment, and were thus included in our analyses. Of these, 2634 (63.9%) had sustained normotension, and 172 (4.2%) had masked hypertension. Participants with masked hypertension vs. sustained normotension were more often men (66.9 vs. 46.2%, P  < 0.001). Those with masked hypertension had higher mean PWV [9.3 (95% confidence interval, 95% CI 9.1-9.5) vs. 8.3 (95% CI 8.2-8.4) m/s, P  < 0.001] and odds ratio for CACS at least 100 [1.65 (95% CI 1.02-2.68), P  = 0.040]. These associations were similar in a posthoc analysis of masked hypertension and sustained normotension, matched for age, sex and systolic office BP.

Masked hypertension was associated with markers of CVD. This suggests that home BP is a better predictor of risk, even when the recordings are performed with the same measurement device, in a population-based setting with randomized recruitment.

White-coat hypertension (WCH) has been defined as an increased blood pressure (BP) in the doctor's office and a normal BP outside the office by 24 hr ambulatory BP monitoring (ABPM) or home BP measurement. It is generated by fear and anxiety of whether an abnormal value could be found and indicate the existence of hypertension. When first described, it was defined as a neuro-defense reaction related to the presence of the doctor in their office or clinic and associated with an increase in heart rate. Initially it was considered a benign condition, not associated with the hypertension mediated organ damage (HMOD) and not requiring treatment. However, recent studies have shown that WCH is not a benign condition and is associated with HMOD and cardiovascular (CV) events (CVE). According to recent ACC/AHA guidelines, the outside of office normal BP should be < 130/80 mmHg and according to the ESC/ESH guidelines, the outside of office normal BP should be < 135/85 mmHg. The prevalence of WCH varies by different studies from 15% to 40% and up to 50% in older subjects. Currently, the management of WCH if not associated with CV risk factors should be conservative with healthy lifestyle changes and exercise. Drug therapy should be considered if these measures do not work or in the presence of CV risk factors, HMOD, or preexisting cardiovascular disease.

The 3F study (Fit&Fun with Football) demonstrated a significant reduction in blood pressure, antihypertensive medication, body weight, stress and depression through health football. Health football could be a popular tool to unleash the full preventive potential of physical activity. This work analyses the effect of health football on hypertensive subgroups: dipper, nondipper, white-coat hypertension (WCH), sustained hypertension, (un)treated hypertensive patients (UH, TH).

A prospective interventional study with 1-year follow-up. Football group (FG): n  = 103, 'health'-football training (1×/week, 90 min) led by licensed football coaches. Physical inactive, hypertensive patients older than 45 years were compared with a control group (CG) ( n  = 105). Subgroups were divided by ambulatory blood pressure monitoring (ABPM), casual blood pressure (CBP), medication schedule and compared by blood pressure (BP), laboratory results and weight.

In all three subgroups (WCH vs. sustained hypertension, TH vs. UH, D vs. ND), health football reduced BP and weight significantly compared with the CG, and compared with the admission. An even greater effect in CBP was found in people with WCH than in sustained hypertension (FG: WCH: 141-127 mmHg, sustained Hypertension (SH): 142-132 mmHg; CG: WCH: 141-143 mmHg, SH: 140-141 mmHg). In contrast, the significant reduction in CBP and ABPM was comparable in treated and untreated patients, although antihypertensive drugs were reduced significantly more frequently in FG than in CG. BP reduction in nondippers and dippers was also comparable. In the nondipper group, nocturnal BP was significantly reduced in the FB (122.0-111.5 mmHg), but not in the CG or the dippers.

All evaluated football subgroups achieved a significant BP reduction (compared with CG). This applied to dipper, nondipper, (un)treated hypertension, WCH and SH. All mentioned subgroups displayed a clear benefit. The even greater reduction in BP in WCH demonstrates the importance of physical activity before the additional prescription of antihypertensive medications, underscoring the recommendations of the ESC and ISH in WCH.

There is little information about the reproducibility of the white coat effect, which was treated as a continuous variable. To investigate a long-term interval reproducibility of the white-coat effect as a continuous variable. We selected 153 participants without antihypertensive treatment (men, 22.9%; age, 64.4 years) from the general population of Ohasama, Japan, to assess the repeatedly measured white-coat effect (the difference between blood pressures at the office and home) in a 4-year interval. The reproducibility was assessed by testing the intraclass correlation coefficient (two-way random effect model-single measures). The white-coat effect for systolic/diastolic blood pressure slightly decreased by 0.17/1.56 mmHg at the 4-year visit on average. The Bland-Altman plots showed no significant systemic error for the white-coat effects (P ≥ 0.24). The intraclass correlation coefficient (95% confidence interval) of the white-coat effect for systolic blood pressure, office systolic blood pressure, and home systolic blood pressure were 0.41 (0.27-0.53), 0.64 (0.52-0.74), and 0.74 (0.47-0.86), respectively. Change in the white-coat effect was mainly affected by a change in office blood pressure. Long-term reproducibility of the white-coat effect is limited in the general population without antihypertensive treatment. The change in the white-coat effect is mainly caused by office blood pressure variation.

Alcoholic beverages are common components of diets worldwide and understanding their effects on humans' health is crucial. Because hypertension is the leading risk factor for cardiovascular diseases and all-cause mortality, the relationship of alcohol consumption with blood pressure (BP) has been the subject of extensive investigation. For the purpose of this review, we searched the terms "alcohol", "ethanol", and "arterial hypertension" on Pubmed MeSH and selected the most relevant studies. Short-term studies showed a biphasic BP response after ingestion of high doses of alcohol, and sustained alcohol consumption above 30 g/day, significantly, and dose-dependently, increased the risk for hypertension. These untoward effects of alcoholic beverages on BP can be mediated by a multiplicity of neurohormonal mechanisms. In addition to the effects on BP, excess alcohol intake might contribute to cardiac and renal hypertensive organ damage, although some studies suggest possible benefits of moderate alcohol consumption on additional cardiovascular risk factors, such as diabetes and lipoprotein(a). Some intervention studies and cumulative analyses support the evidence of a benefit of the reduction/withdrawal of alcohol consumption on BP and cardiovascular outcomes. This is why guidelines of scientific societies recommend avoidance or limitation of alcohol intake below one unit/day for women and two units/day for men. This narrative article overviews all these topics, providing an update of the current knowledge on the relationship between alcohol and BP.

A growing body of evidence supports the view that masked hypertension (MH) (i.e. normal office and elevated out-of-office BP) is a blood pressure (BP) phenotype associated with increased risk of subclinical organ damage, cardiovascular disease and death as compared to true normotension. Whether left ventricular (LV) systolic function is impaired in individuals with MH is still a poorly defined topic. Therefore, we aimed to provide a new piece of information on LV systolic dysfunction in the untreated MH setting, focusing on speckle tracking echocardiography (STE) studies investigating LV global longitudinal strain (GLS), a more sensitive index of systolic function than conventional LV ejection fraction (LVEF).

A computerized search was performed using Pub-Med, OVID, EMBASE and Cochrane library databases from inception until June 30, 2022. Full articles reporting data on LV GLS in MH, as assessed by ambulatory BP monitoring (ABPM), and normotensive controls were considered suitable for the purposes of review and meta-analysis.

A total of 329 untreated individuals with MH and 376 normotensive controls were included in six studies. While pooled average LVEF was not different between groups [64.5 ± 1.5 and 64.5 ± 1.3%, respectively, standard means difference (SMD): -0.002 ± 0.08, confidence interval (CI): 0.15/-0.15, P = 0.98), LV GLS was worse in MH patients than in normotensive counterparts (-18.5 ± 0.70 vs. -20.0 ± 0.34%, SMD: 0.68 ± 0.28, CI: 0.12/1.24, P < 0.01).

Our findings suggest that early changes in LV systolic function not detectable by conventional echocardiography in the MH setting can be unmasked by STE and that its implementation of STE in current practice may improve the detection of subclinical organ damage of adverse prognostic significance.

Single-night disease misclassification of OSA due to night-to-night variability may contribute to inconsistent findings in OSA trials.

Does multinight quantification of OSA severity provide more precise estimates of associations with incident hypertension?

A total of 3,831 participants without hypertension at baseline were included in simulation analyses. Included participants had ≥ 28 days of nightly apnea-hypopnea index (AHI) recordings via an under-mattress sensor and ≥ 3 separate BP measurements over a 3-month baseline period followed by ≥ 3 separate BP measurements 6 to 9 months postbaseline. Incident hypertension was defined as a mean systolic BP ≥ 140 mm Hg or a mean diastolic BP ≥ 90 mm Hg. Simulated trials (1,000) were performed, using bootstrap methods to investigate the effect of variable numbers of nights (x = 1-56 per participant) to quantify AHI and the ability to detect associations between OSA and incident hypertension via logistic regression adjusted for age, sex, and BMI.

Participants were middle-aged (mean ± SD, 52 ± 12 y), mostly men (91%), and overweight (BMI, 28 ± 5 kg/m²). Single-night quantification of OSA failed to detect an association with hypertension risk in 42% of simulated trials (α = 0.05). Conversely, 100% of trials detected an association when AHI was quantified over ≥ 28 nights. Point estimates of hypertension risk were also 50% higher and uncertainty was 5 times lower during multinight vs single-night simulation trials.

Multinight monitoring of OSA allows for better estimates of hypertension risk and potentially other adverse health outcomes associated with OSA. These findings have important implications for clinical care and OSA trial design.

The aim of this study was to provide prediction models for masked uncontrolled hypertension (MUCH) detected by ambulatory blood pressure (BP) monitoring in an Italian population. We studied 738 treated hypertensive patients with normal clinic BPs classified as having controlled hypertension (CH) or MUCH if their daytime BP was < or ≥135/85 mmHg regardless of nighttime BP, respectively, or CH or MUCH if their 24-h BP was < or ≥130/80 mmHg regardless of daytime or nighttime BP, respectively. We detected 215 (29%) and 275 (37%) patients with MUCH using daytime and 24-h BP thresholds, respectively. Multivariate logistic regression analysis showed that males, those with a smoking habit, left ventricular hypertrophy (LVH), and a clinic systolic BP between 130−139 mmHg and/or clinic diastolic BP between 85−89 mmHg were associated with MUCH. The area under the receiver operating characteristic curve showed good accuracy at 0.78 (95% CI 0.75−0.81, p < 0.0001) and 0.77 (95% CI 0.73−0.80, p < 0.0001) for MUCH defined by daytime and 24 h BP, respectively. Internal validation suggested a good predictive performance of the models. Males, those with a smoking habit, LVH, and high-normal clinic BP are indicators of MUCH and models including these factors provide good diagnostic accuracy in identifying this ambulatory BP phenotype.

We have previously shown that masked hypertension (MH) and sustained hypertension (SH) contribute to the progression of diabetic nephropathy. Although the risk of target organ damage and cardiovascular events in MH and SH is significantly higher than that in normotension and white coat hypertension, the role of MH or SH in cardiovascular events has never been reported in studies specific to diabetic patients. Therefore, in this study, we aimed to determine whether blood pressure control status contributes to the development of new cardiovascular events. A longitudinal study of 1082 patients with type 2 diabetes mellitus and no history of cardiovascular events was conducted. Patients were instructed to have their blood pressure measured three times, every morning and evening, for 14 consecutive days. Hypertension status was classified into four groups based on the systolic blood pressure measurements in the clinic and at home. The primary endpoint was the first cardiovascular event. After a median follow-up of 7.0 (interquartile range, 4.0-9.0) years, 119 patients developed cardiovascular events. The hazard ratio (95% confidence interval) for the risk of developing cardiovascular events was significantly higher in the SH group than in the controlled blood pressure group (1.63 [1.02-2.59]). SH is a useful predictor of cardiovascular events. Both at home and in the clinic, blood pressure monitoring should be assessed in routine clinical practice to predict future cardiovascular events in patients with type 2 diabetes.

Individuals with masked hypertension (MHT) have a greater risk of adverse cardiovascular outcomes than normotensive (NT) individuals. Exploring metabolomic differences between NT and MHT individuals may help provide a better understanding of the etiology of MHT. We analyzed data from 910 young participants (83% NT and 17% MHT) (mean age 24 ± 3 years) from the African-PREDICT and 210 older participants (63% NT and 37% MHT) from the SABPA (mean age 42 ± 9.6 years) studies. Clinic and ambulatory blood pressures (BPs) were used to define BP phenotypes. Urinary amino acids and acylcarnitines were measured using liquid chromatography time-of-flight mass spectrometry in SABPA and liquid chromatography tandem mass spectrometry in the African-PREDICT studies. In the SABPA study, amino acids (leucine/isoleucine, valine, methionine, phenylalanine), free carnitine (C0-carnitine), and acylcarnitines C3 (propionyl)-, C4 (butyryl)-carnitine and total acylcarnitine) were higher in MHT than NT adults. In the African-PREDICT study, C0- and C5-carnitines were higher in MHT individuals. With unadjusted analyses in NT adults from the SABPA study, ambulatory SBP correlated positively with only C3-carnitine. In MHT individuals, positive correlations of ambulatory SBP with leucine/isoleucine, valine, methionine, phenylalanine, C0-carnitine and C3-carnitine were evident (all p < 0.05). In the African-PREDICT study, ambulatory SBP correlated positively with C0-carnitine (r = 0.101; p = 0.006) and C5-carnitine (r = 0.195; p < 0.001) in NT adults and C5-carnitine in MHT individuals (r = 0.169; p = 0.034). We demonstrated differences between the metabolomic profiles of NT and MHT adults, which may reflect different stages in the alteration of branched-chain amino acid metabolism early on and later in life.

Home blood pressure measurement (HBPM) has the advantage of measuring blood pressure (BP) multiple times over a long period. HBPM effectively diagnoses stress-induced transient BP elevations (i.e., white coat hypertension), insufficient BP control throughout the day (i.e., masked hypertension), and even BP variability. In most cases, HBPM may increase self-awareness of BP, increasing the compliance of treatment. Cumulative evidence has reported better improved predictive values of HBPM in cardiovascular morbidity and mortality than office BP monitoring. In this position paper, the Korean Society of Hypertension Home Blood Pressure Forum provides comprehensive information and clinical importance on HBPM.

The pathophysiologic mechanisms of masked hypertension are still debated. The aim of this study was to investigate whether the blood pressure response to standing is a determinant of masked hypertension in young individuals.

We studied 1078 individuals (mean age 33.2 ± 8.5 years) with stage-1 untreated hypertension at baseline. Orthostatic response was defined as the difference between six SBP measurements in the orthostatic and supine postures. People with a response more than 6.5 mmHg (upper decile) were defined as hyperreactors. After 3 months of follow-up, 24-h ambulatory BP was measured and the participants were classified as normotensives (N = 120), white-coat hypertensive individuals (N = 168), masked hypertensive individuals (N = 166) and sustained hypertensive individuals (N = 624). In 591 participants, 24-h urinary epinephrine was also measured.

Orthostatic response was an independent predictor of masked hypertension after 3 months (P = 0.001). In the whole group, the odds ratio for the Hyperreactors was 2.5 [95% confidence interval (95% CI) 1.5-4.0, P < 0.001]. In the participants stratified by orthostatic response and urinary epinephrine, the odds ratio for masked hypertension was 4.2 (95% CI, 1.8-9.9, P = 0.001) in the hyperreactors with epinephrine above the median and was 2.6 (95% CI, 0.9-7.3, P = 0.069) in those with epinephrine below the median. The association between orthostatic response and masked hypertension was confirmed in the cross-sectional analysis after 3 months (P < 0.001).

The present findings indicate that hyperreactivity to standing is a significant determinant of masked hypertension. The odds ratio for masked hypertension was even quadrupled in people with an orthostatic response more than 6.5 mmHg and high urinary epinephrine suggesting a role of sympathoadrenergic activity in the pathogenesis of masked hypertension.

Little evidence is available on whether antihypertensive treatment lowers cardiovascular risk in white-coat hypertension (WCH). Protection might be indirectly inferred, however, from the blood pressure (BP) effects of treatment as in trials BP reduction is linearly related to outcome reduction. We analyzed the effect of antihypertensive treatment on office and ambulatory BP in WCH using data from the Plaque HYpertension Lipid-Lowering Italian Study (PHYLLIS).

: Office and ambulatory blood pressure were measured in 470 hypertensive patients randomized to fosinopril or hydrochlorothiazide alone or combined with a statin before treatment and at 6 month or yearly intervals during 2.6 years of follow-up. Patients were divided into two groups according to whether before randomization to treatment office and 24-h mean BP were elevated (sustained hypertension) or office BP was elevated but 24-h BP values were normal (WCH).

: In both sustained hypertension and WCH antihypertensive treatment was associated with an early marked office BP reduction, which persisted virtually unchanged throughout the treatment period. In contrast, 24-h (and day and night) BP showed a marked and persistent treatment-related fall in sustained hypertension but no change in WCH. The results were similar when data were separately analyzed in patients under fosinopril or diuretic, with or without statin treatment.

: In WCH, antihypertensive treatment can effectively and durably reduce office BP. This reduction is accompanied by the inability to lower ambulatory BP from the normal values characterizing this condition at baseline. This appears to be unrelated to the type of treatment employed.

Recent US blood pressure (BP) guidelines recommend using ambulatory BP monitoring (ABPM) or home BP monitoring (HBPM) to screen adults for masked hypertension. However, limited evidence exists of the expected long-term effects of screening for and treating masked hypertension.

We estimated the lifetime health and economic outcomes of screening for and treating masked hypertension using the Cardiovascular Disease (CVD) Policy Model, a validated microsimulation model. We simulated a cohort of 100,000 US adults aged ≥20 years with suspected masked hypertension (i.e., office BP 120-129/<80 mm Hg, not taking antihypertensive medications, without CVD history). We compared usual care only (i.e., no screening), usual care plus ABPM, and usual care plus HBPM. We projected total direct healthcare costs (2021 USD), quality-adjusted life years (QALYs), and incremental cost-effectiveness ratios. Future costs and QALYs were discounted 3% annually. Secondary outcomes included CVD events and serious adverse events.

Relative to usual care, adding masked hypertension screening and treatment with ABPM and HBPM was projected to prevent 14.3 and 20.5 CVD events per 100,000 person-years, increase the proportion experiencing any treatment-related serious adverse events by 2.7 and 5.1 percentage points, and increase mean total costs by $1,076 and $1,046, respectively. Compared with usual care, adding ABPM was estimated to cost $85,164/QALY gained. HBPM resulted in lower QALYs than usual care due to increased treatment-related adverse events and pill-taking disutility.

The results from our simulation study suggest screening with ABPM and treating masked hypertension is cost-effective in US adults with suspected masked hypertension.

The PRedicting Out-of-OFfice Blood Pressure (PROOF-BP) algorithm accurately predicted out-of-office blood pressure (BP) among adults with suspected high BP in the United Kingdom and Canada. We tested the accuracy of PROOF-BP in a diverse US population and evaluated a newly developed US-specific algorithm (PROOF-BP-US).

Adults with ≥2 office BP readings and ≥10 awake BP readings on 24-hour ambulatory BP monitoring from 4 pooled US studies were included. We compared mean awake BP with predicted out-of-office BP using PROOF-BP and PROOF-BP-US. Our primary outcomes were hypertensive out-of-office systolic BP (SBP) ≥130 mm Hg and diastolic BP (DBP) ≥80 mm Hg.

We included 3,058 adults, mean (SD) age was 52.0 (11.9) years, 38% were male, and 54% were Black. The area under the receiver-operator characteristic (AUROC) curve (95% confidence interval) for hypertensive out-of-office SBP was 0.81 (0.79-0.82) and DBP was 0.76 (0.74-0.78) for PROOF-BP. For PROOF-BP-US, the AUROC curve for hypertensive out-of-office SBP was 0.82 (0.81-0.83) and for DBP was 0.81 (0.79-0.83). The optimal predicted out-of-office BP ranges for out-of-office BP measurement referral were 120-134/75-84 mm Hg for PROOF-BP and 125-134/75-84 mm Hg for PROOF-BP-US. The 2017 American College of Cardiology/American Heart Association BP guideline (referral range 130-159/80-99 mm Hg) would refer 93.1% of adults not taking antihypertensive medications with office BP ≥130/80 mm Hg in the National Health and Nutrition Examination Survey for out-of-office BP measurement, compared with 53.1% using PROOF-BP and 46.8% using PROOF-BP-US.

PROOF-BP and PROOF-BP-US accurately predicted out-of-office hypertension in a diverse sample of US adults.

Perioperative hypotension has been repeatedly associated with organ injury and worse outcome, yet many interventions to reduce morbidity by attempting to avoid or reverse hypotension have floundered. In part, this reflects uncertainty as to what threshold of hypotension is relevant in the perioperative setting. Shifting population-based definitions for hypertension, plus uncertainty regarding individualised norms before surgery, both present major challenges in constructing useful clinical guidelines that may help improve clinical outcomes. Aside from these major pragmatic challenges, a wealth of biological mechanisms that underpin the development of higher blood pressure, particularly with increasing age, suggest that hypotension (however defined) or lower blood pressure per se does not account solely for developing organ injury after major surgery. The mosaic theory of hypertension, first proposed more than 60 yr ago, incorporates multiple, complementary mechanistic pathways through which clinical (macrovascular) attempts to minimise perioperative organ injury may unintentionally subvert protective or adaptive pathways that are fundamental in shaping the integrative host response to injury and inflammation. Consideration of the mosaic framework is critical for a more complete understanding of the perioperative response to acute sterile and infectious inflammation. The largely arbitrary treatment of perioperative blood pressure remains rudimentary in the context of multiple complex adaptive hypertensive endotypes, defined by distinct functional or pathobiological mechanisms, including the regulation of reactive oxygen species, autonomic dysfunction, and inflammation. Developing coherent strategies for the management of perioperative hypotension requires smarter, mechanistically solid interventions delivered by RCTs where observer bias is minimised.

Blood-pressure-lowering therapy with antihypertensive drugs can reduce the risk of cardiovascular morbidity and mortality in patients with hypertension. However, patients treated with antihypertensive drugs generally have a worse prognosis than untreated individuals. Consistent with the results obtained from epidemiological studies, a clinical study showed that endothelial function was impaired more in treated patients with hypertension than in untreated individuals with the same blood pressure level, suggesting that blood-pressure-lowering therapy with currently available antihypertensive drugs cannot restore endothelial function to the level of that in untreated individuals. Several mechanisms of endothelial dysfunction in treated patients are postulated: irreversible damage to the endothelium caused by higher cumulative elevated blood pressure exposure over time; the persistence of the primary causes of hypertension even after the initiation of antihypertensive drug treatment, including an activated renin-angiotensin-aldosterone system, oxidative stress, and inflammation; and higher global cardiovascular risk related not only to conventional cardiovascular risk factors but also to undetectable nonconventional risk factors. Lifestyle modifications/nonpharmacological interventions should be strongly recommended for both untreated and treated individuals with hypertension. Lifestyle modifications/nonpharmacological interventions may directly correct the primary causes of hypertension, which can improve endothelial function and consequently reduce cardiovascular risk regardless of the use or nonuse of antihypertensive drugs.

Masked uncontrolled hypertension (MUCH) is at higher cardiovascular risk than controlled hypertension (CH). In previous studies, patients with MUCH were considered as a unique group though those receiving ≤2 drugs could be defined as having nonresistant MUCH (NRMUCH) and those receiving ≥3 drugs as having resistant MUCH (RMUCH). The aim of this study was to assess the prognostic value of NRMUCH and RMUCH detected by ambulatory blood pressure (BP) monitoring. Cardiovascular risk was evaluated in 738 treated hypertensive patients with normal clinic BP. Patients were classified as having CH or MUCH if daytime BP < or ≥ 135/85 mmHg, respectively, regardless of nighttime BP, or CH or MUCH if 24-h BP < or ≥ 130/80 mmHg, respectively, regardless of daytime or nighttime BP. By daytime or 24-h BP, the authors detected 523 (71%), 178 (24%), and 37 (5%) or 463 (63%), 231 (31%), and 44 (6%) patients with CH, NRMUCH, and RMUCH, respectively. During the follow-up (median 10 years), 148 events occurred. After adjustment for covariates, compared to CH, the hazard ratio (HR), 95% confidence interval (CI), for cardiovascular events was 1.81, 1.27-2.57, and 2.99, 1.73-5.16, in NRMUCH and RMUCH defined by daytime BP, respectively, and 1.58, 1.12-2.23, and 2.21, 1.27-3.82, in NRMUCH and RMUCH defined by 24-h BP, respectively. If RMUCH was compared with NRMUCH, the risk tended to be higher in RMUCH but did not attain statistical significance (P = .08 and P = .23 by daytime and 24-h BP thresholds, respectively). In conclusion, both NRMUCH and RMUCH are at increased cardiovascular risk than CH.

The risk profile of white-coat hypertension/effect (WCH/E) remains unclear. This study aimed to investigate the relationship between WCH/E, markers of cardiovascular risk and cerebrovascular events.

This is a sub-group analysis of The Arterial Stiffness In lacunar Stroke and Transient ischemic attack (ASIST) study, which recruited 96 patients aged at least 40 years old with a diagnosis of transient ischemic attack or lacunar stroke in the preceding 14 days. Thirty-two patients with target blood pressure (clinic blood pressure <140/90 mmHg and daytime ambulatory blood pressure <135/85 mmHg) and 30 patients with WCH/E (clinic blood pressure ≥140/90 mmHg and daytime ambulatory blood pressure <135/85 mmHg) were included in the analysis.

Patients with WCH/E were older and had a higher BMI. Central SBP (145 ± 13 vs. 118 ± 8 mmHg, P < 0.001) and DBP (82 ± 8 vs. 76 ± 7 mmHg, P = 0.004) were higher in those with WCH/E. They also had higher arterial stiffness measured by carotid-femoral pulse wave velocity (11.9 ± 3.0 vs. 9.6 ± 2.3 m/s, P = 0.002) and cardio-ankle vascular index (10.3 ± 1.3 vs. 9.4 ± 1.7, P = 0.027). Regression analysis showed an independent relationship between WCH/E and both measures of arterial stiffness. Lacunar strokes were more prevalent in those with WCH/E (47 vs. 22%, P = 0.039) and individuals in this group were more likely to have had a lacunar stroke than a transient ischemic attack (odds ratio 9.6, 95% CI 1.5-62.6, P = 0.02).

In this cohort of patients with lacunar stroke and transient ischemic attack, WCH/E was associated with elevated markers of cardiovascular risk and a higher prevalence of lacunar stroke. These results suggest that WCH/E is associated with adverse cardiovascular risk.

Masked hypertension - a blood pressure (BP) phenotype characterized by a clinic BP in the normal range but elevated BP outside the office - is associated with early hypertension-mediated organ damage. This study examined early target organ manifestations of masked hypertension diagnosed by home (HBPM) and ambulatory (ABPM) BP monitoring.

Left ventricular (LV) structure and diastolic function measured by echocardiography, microalbuminuria, and coronary artery calcification were evaluated in 420 patients with high clinic BP (SBP 120-150 mmHg or DBP 80-95 mmHg). Evidence of hypertension-mediated organ damage was compared in patients with sustained normotension, masked hypertension, and sustained hypertension based on measurements by HBPM, daytime ABPM, and 24-h ABPM.

The 420 participants averaged 48 (12) [mean (SD)] years of age; the average clinic BP was 130 (13)/81 (8) mmHg. In individuals with masked hypertension diagnosed by HBPM, indexed LV mass, relative wall thickness, and e' and E/e' (indices of LV relaxation), were generally intermediate between values observed in normotensives and sustained hypertensive patients, and were significantly greater in masked hypertension than normotensives. Similar trends were observed when masked hypertension was diagnosed by ABPM but a diagnosis of masked hypertension was not as reliably associated with LV remodeling or impaired LV relaxation in comparison to normotensives. There were trends towards greater likelihoods of detectable urinary microalbumin and coronary calcification in masked hypertension than in normotensives.

These results support previous studies demonstrating early hypertension-mediated organ damage in patients with masked hypertension, and suggest that HBPM may be superior to ABPM in identifying patients with masked hypertension who have early LV remodeling and diastolic LV dysfunction.

Hypertension is the most common cardiovascular (CV) risk factor, strongly and independently associated with an increased risk of major CV outcomes, including myocardial infarction, stroke, congestive heart failure, renal disease and death due to CV causes. Effective control of hypertension is of key importance for reducing the risk of hypertension-related CV complications, as well as for reducing the global burden of CV mortality. However, several studies reported relatively poor rates of control of high blood pressure (BP) in a setting of real-life practice. To improve hypertension management and control, national and international scientific societies proposed several educational and therapeutic interventions, among which the systematic implementation of out-of-office BP measurements represents a key element. Indeed, proper assessment of individual BP profile, including home, clinic and 24-h ambulatory BP levels, may improve awareness of the disease, ensure high level of adherence to prescribed medications in treated hypertensive patients, and thus contribute to ameliorate BP control in treated hypertensive outpatients. In line with these purposes, recent European guidelines have released practical recommendations and clear indications on how, when and how properly measuring BP levels in different clinical settings, with different techniques and different methods. This review aimed at discussing current applications and potential limitations of European guidelines on how to measure BP in office and out-of-office conditions, and their potential implications in the daily clinical management of hypertension.

High blood pressure (BP) is a leading risk factor for cardiovascular disease (CVD). The identification of high BP is conventionally based on in-clinic (resting) BP measures, performed within primary health care settings. However, many cases of high BP go unrecognised or remain inadequately controlled. Thus, there is a need for complementary settings and methods for BP assessment to identify and control high BP more effectively. Exaggerated exercise BP is associated with increased CVD risk and may be a medium to improve identification and control of high BP because it is suggestive of high BP gone undetected on the basis of standard in-clinic BP measures at rest. This paper provides the evidence to support a pathway to aid identification and control of high BP in clinical exercise settings via the measurement of exercise BP. It is recommended that exercise professionals conducting exercise testing should measure BP at a fixed submaximal exercise workload at moderate intensity (e.g., ~70% age-predicted heart rate maximum, stage 1-2 of a standard Bruce treadmill protocol). If exercise systolic BP is raised (≥170 mmHg), uncontrolled high BP should be assumed and should trigger correspondence with a primary care physician to encourage follow-up care to ascertain true BP control (i.e., home, or ambulatory BP) alongside a hypertension-guided exercise and lifestyle intervention to lower CVD risk related to high BP.

According to some guidelines, white-coat hypertension (WCH) carries little or no increase of cardiovascular risk in the absence of organ damage (OD), but no data are available on this issue.

Using the population data from PAMELA (Pressioni Arteriose Monitorate E Loro Associazioni), we evaluated cardiovascular and total mortality over a median follow-up of 29 years in WCH (elevated office and normal 24-hour or home blood pressure [BP]) and normotensive controls (normal in- and out-of-office blood pressure) with no echocardiographic left ventricular hypertrophy and no reduction of estimated glomerular filtration rate. Patients with sustained hypertension (SH, in- and out-of-office blood pressure elevation) and normotensive, WCH, and SH with cardiac and renal OD served as controls.

In the 1423 subjects analyzed, there were 165 cardiovascular and 526 all-cause deaths. After adjustment for confounders, no-OD WCH exhibited a risk of fatal cardiovascular events lower than that of no-OD SH but greater than that of no-ODN (hazard ratio, 2.0 [95% CI, 1.1-3.6], P=0.02), this being the case also for all-cause mortality. Compared with no-OD normotensive, no-OD WCH also exhibited a greater 10-year adjusted risk to develop new SH or OD. Similar findings were obtained in normotensive, WCH, and SH with OD.

The present study provides the first evidence that WCH with no OD is accompanied by a noticeable increase in long-term risk of mortality, new hypertension, and new OD, thereby differing from normotensive.