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Background: Nocturnal blood pressure (BP) is associated with cardiovascular disease independently of awake BP. However, nocturnal BP measured using an ambulatory monitoring device has limited reproducibility because it is a single-day measurement. We investigated the association between sleep BP measured on multiple days using a timer-equipped home BP monitor and cardiovascular diseases in a general population., Methods: The study population comprised 5814 community residents. Participants were required to sleep with wrapping cuffs on their upper arm and BP was measured automatically at 0 : 00, 2 : 00, and 4 : 00. Actigraph was used to determine BP measured during sleep. Participants were also measured home morning and evening BP manually using the same device., Results: During the 7.3-year mean follow-up period, we observed 117 cases of cardiovascular diseases. The association between sleep BP (per 10 mmHg hazard ratio = 1.31, P  < 0.001) and cardiovascular events remained significant (hazard ratio = 1.22, P  = 0.036) even after adjusting for office BP and confounding factors, such as sleep-disordered breathing. Individuals with sleep-only hypertension ( n  = 1047; hazard ratio = 2.23, P  = 0.005) had a significant cardiovascular risk. Daytime-only hypertension ( n  = 264; hazard ratio = 3.57, P  = 0.001) and combined sleep and daytime hypertension ( n  = 1216; hazard ratio = 3.69, P  < 0.001) was associated with cardiovascular events to the same extent. Sleep BP dipping was not identified as a significant determinant of cardiovascular events., Conclusion: Sleep BP measured using a home BP monitor was independently associated with the incidence of cardiovascular disease in a general population., (Copyright © 2024 Wolters Kluwer Health, Inc. All rights reserved.)

Background: High sleep blood pressure (BP) has been suggested to be an independent risk factor for cardiovascular outcomes. To assess the applicability of sleep BP measured using a timer-equipped home device, we investigated the association between home device-measured sleep BP and large artery stiffness., Methods: We performed a cross-sectional analysis of a dataset from the Nagahama study (N = 5916), a general population-based cohort study. Home morning BP and sleep BP were measured using a timer-equipped cuff-oscillometric device (HEM-7080IC). Office BP, carotid intima--media thickness (IMT), and brachial--ankle pulse wave velocity (baPWV) were measured at the follow-up investigation of the Nagahama study., Results: Sleep hypertension (SBP ≥120 mmHg and/or DBP ≥70 mmHg) was associated with the arterial parameters (IMT: β = 0.051, baPWV: β = 0.141, both P < 0.001) independently of morning hypertension (IMT: β = 0.093, baPWV: β = 0.216, both P < 0.001) irrespective of antihypertensive medication status. Individuals exhibiting isolated sleep hypertension (N = 801) had thicker IMT (0.69 ± 0.14 vs. 0.64 ± 0.13 mm, P = 0.017) and faster baPWV (1,299 ± 197 vs. 1,183 ± 178 cm/s, P < 0.001) than normotensives. A sleep SBP at least 110 mmHg and a sleep DBP at least 65 mmHg were identified as the lower threshold BP values for the association with arterial parameters., Conclusion: Sleep BP measurement using a home device may be a simple way to assess cardiovascular risks overlooked by office and home morning BP measurements.

The sodium-to-potassium ratio (Na/K) of a urine sample is a simple index of salt loading. To practically use Na/K, we aimed to determine whether the Na/K value affects blood pressure (BP) at any age, irrespective of urinary Na and K levels. We analyzed a dataset of the general population (the Nagahama study), including baseline and second-visit measurements performed 5 years after the baseline. Spot urine samples were used for Na/K assessments. A total of 18,505 observations were analyzed using a linear mixed model, including the measurement term as a random effect. Urinary Na/K values showed a positive association with BP. When the highest quartile of Na/K was further divided by the urinary Na/creatinine (Cre) and K/Cre levels, the high-Na/Cre (3.58) and high-K/Cre (0.75) (Na/K = 4.80) groups, as well as the low Na/Cre (1.23) and low-K/Cre (0.26) (Na/K = 4.87) groups, exhibited similar effects on systolic BP (6.82 mmHg [95% CI: 5.72-7.92] and 6.63 mmHg [95% CI: 5.35-7.91], respectively). A similar association was observed in other Na/K quartiles. The positive association of Na/K and Na/Cre with BP was steeper in the older groups, while the inverse association of K/Cre was predominant in the younger population. The results of the multivariate analysis identified interaction terms between age and Na/K, Na/Cre and K/Cre as significant determinants for SBP. The positive association of urinary Na/K with BP was independent of the urinary Na and K levels. The association between Na/K and BP may not be uniform across ages by decade.

Objectives: We aimed to analyze associations of sleep disturbance, including sleep disordered breathing, sleep fragmentation, and sleep efficiency, with abnormal nocturnal blood pressure (BP) profiles that may be risk factors for adverse cardiovascular outcomes., Methods: The study included 5854 community residents with 20,725 multi-day measurements. Sleep fragmentation and efficiency were evaluated using a wrist-worn activity monitor. Sleep disordered breathing was assessed using the 3% oxygen desaturation index corrected for actigraphy-determined sleep duration. A timer-equipped standard cuff-oscillometric device was used for home and sleep BP monitoring., Results: Mean nocturnal systolic BP (SBP) change was -8.6 ± 9.7% (-11.1 ± 12.6 mmHg), and inter-day correlation coefficient of the nocturnal SBP change was 0.443. Results of a linear mixed model analysis using daily measured values identified lower sleep efficiency (coefficient = -0.130, p < 0.001) as a determinant for decreased nocturnal SBP dipping beyond the interday variations of these parameters. Number of nocturnal urinations was another strong determinant (coefficient = 1.191, p < 0.001), although the association of sleep efficiency was independent of nocturnal urination, awake SBP, and sleep disordered breathing (coefficient = -0.102, p < 0.001). Sleep efficiency was also independently associated with sleep SBP level (coefficient = -0.138, p < 0.001). Estimated differences in nocturnal SBP dipping and sleep SBP level as a function of the degree of sleep efficiency (less than 80%) reached 1.63% (1.09-2.17%) and 2.16 mmHg (1.49-2.82%), respectively., Conclusion: More attention should be paid to sleep efficiency as a factor in maintaining circadian BP rhythm., (Copyright © 2019 Elsevier B.V. All rights reserved.)

Background: Orthostatic hypertension was associated with worse cardiovascular outcomes, although the factors responsible for an orthostatic rise in blood pressure (BP) are uncertain. We investigated a possible relationship between a stooping posture and orthostatic BP change., Methods: Study participants consisted of 1,992 older individuals. Orthostatic BP change was calculated by systolic BP measured at sitting position, and again 1 and 3 minutes after standing up. Spinal alignment and curvature was assessed by guiding the SpinalMouse device on the surface of the skin along the spine., Results: Mean lumbar lordosis at standing position was 13.4° ± 12.4°. The degree of lumbar lordosis was significantly smaller in orthostatic hypertensive individuals (systolic BP change, ≥+20 mm Hg: 3.3° ± 15.6°, ≥+10 mm Hg: 10.4° ± 14.3°) than in individuals who were orthostatic normotensive (14.2° ± 11.9°). Multiple linear regression analysis identified lumbar lordosis (β = -0.171, P < 0.001) and thoracic kyphosis (β = 0.062, P = 0.007), but not sacral inclination (β = 0.033, P = 0.303), as independent determinants for orthostatic BP change. As waist circumference was another independent determinant, the frequency of orthostatic hypertensive individuals was linearly increased with the combination of abdominal obesity and small degree of lumbar lordosis (control: 9.9%, abdominal obesity: 17.4%, small degree of lordosis: 19.4%, both: 24.1%, P < 0.001). Participants who sustained orthostatic hypertension for 3 minutes after standing up had the smallest degree of lumbar lordosis (5.2° ± 16.4°)., Conclusion: Stooped posture was an overlooked determinant for orthostatic increases in BP.

Background: The aim of this study is to clarify associations between orthostatic blood pressure (BP) change, as well as possible physiological factors, and day-to-day home BP variability, a promising risk factor for cardiovascular outcomes., Methods: Study participants were 6,465 community residents (age 58.3 years). Home BP was measured every morning and evening for 7 days. Orthostatic BP was calculated as the maximum difference between BP measured while sitting and remeasured after 1 and 3 minutes standing., Results: Frequency of individuals who showed orthostatic BP decline was as follows: systolic BP (SBP) change ≥-20 mm Hg: 2.6%, ≥-10 mm Hg: 14.1%. These subgroups showed larger home SBP variability (average real variability: 11.3 ± 5.3, 8.7 ± 3.9 mm Hg) when compared with orthostatic normotensives (7.6 ± 3.7 mm Hg) (all P < 0.001). Multiple linear regression analysis adjusted for major covariates, including seated BP, identified orthostatic BP drop as an independent determinant for morning BP variability (≥-20 mm Hg: β = 0.037, P = 0.003; ≥-10 mm Hg: β = 0.026, P = 0.036) but not for evening BP variability. Carotid hypertrophy was significantly associated with home BP variability (morning: β = 0.052, P = 0.001; evening: β = 0.065, P < 0.001) and showed a U-shaped association with orthostatic BP change. Plasma B-type natriuretic peptide level, a previously suggested factor for BP variability, did not show significant association with morning and evening BP variability., Conclusion: Orthostatic BP decline was significantly associated with morning BP variability. Large artery atherosclerosis was a common risk factor.

Objective: Abnormalities in circadian blood pressure (BP) variation, particularly increase in nocturnal BP, have been reported to be risk factors for cardiovascular disease, although the factors associated with BP abnormalities are not fully understood. This study aimed to clarify possible associations of sleep characteristics, including sleep fragmentation, sleep disordered breathing, and nocturia, with sleep BP by simultaneous multiday measurements., Methods: A cross-sectional study evaluated 5959 community participants having home-measured data on nocturnal BP change (sleep BP - awaking BP), sleep characteristics, and sleep disordered breathing. Sleep characteristics including the fragmentation index were assessed using wrist-wearable actigraphy, whereas sleep disordered breathing was assessed by 3% oxygen desaturation index obtained using a finger-type monitor. The number of nocturnal urinations was recorded in a sleep diary., Results: Mean nocturnal SBP change was -8.5 ± 7.9%. A 3% oxygen desaturation index was associated with the BP change independently of the basic covariates (β = 0.051, P = 0.001), although the association became insignificant (P = 0.196) after adjusting the fragmentation index (β = 0.105, P < 0.001). The association of the fragmentation index was also insignificant (P = 0.153) after adjusting measurement season (middle season: β = 0.163, P < 0.001; summer season: β = 0.249, P < 0.001). In contrast, the frequency of urination showed strong and independent association (β = 0.140, P < 0.001), with smaller nocturnal BP drop in participants with frequent urination., Conclusion: Subjective sleep estimates and frequent nocturnal urination may represent a potential risk for circadian BP abnormalities.

Background: Urinary sodium-to-potassium ratio (Na/K) represents a simple measure of sodium load and has been reported to be associated with blood pressure (BP) levels in a cross-sectional setting even with spot measurements. The aim of the present large-scale cohort study is to determine prognostic significance of spot urine Na/K for longitudinal changes in BP levels and renal function., Methods: The present study population consisted of 7,063 individuals from the general population. Clinical parameters were measured at baseline and at a follow-up interval of 5 years., Results: Mean systolic BP was slightly increased during the follow-up period (overall, 124 ± 17 to 125 ± 18 mm Hg; nontreated participants, 119 ± 15 to 122 ± 17 mm Hg). Although, the urinary Na/K demonstrated a linear association with BP in a cross-sectional analysis (P < 0.001), analysis of repeated measured BP values identified baseline Na/K * time interaction, i.e., an intraindividual effect, as an inverse determinant (F = 76.9, P < 0.001) independently of hypertension status and fasting conditions possibly due to regression to the mean of temporary high baseline Na/K values at baseline. Spot urine Na/K values were found to be positively associated with renal function in a cross-sectional analysis (P < 0.001). Although baseline Na/K * time interaction showed inverse associated with renal functional decline (F = 85.8, P < 0.001), this inverse association might not represent physiological relationship in likewise fashion with the analysis for BP., Conclusions: Spot urine Na/K may have limited utility as a prognostic marker of longitudinal BP change, as well as renal functional decline., (© American Journal of Hypertension, Ltd 2017. All rights reserved. For Permissions, please email: journals.permissions@oup.com)

Objectives: We undertook descriptive epidemiology of spot urine sodium-to-potassium ratio (Na/K) in a population sample to clarify the close relationship between Na/K and blood pressure level independently of potential confounding factors., Methods: Study participants consisted of 9144 apparently healthy citizens (aged 54 ± 13 years). All clinical parameters were obtained at baseline., Results: Na/K was significantly higher in hypertensive individuals irrespective of antihypertensive medication status (normotension, 3.12 ± 1.82; untreated hypertension 3.50 ± 1.96; treated hypertension, 3.72 ± 2.53). As urinary Na (β = 0.092, P < 0.001) and K (β = -0.050, P < 0.001) levels were inversely associated with BP, Na/K (β = 0.118, P < 0.001) was more closely associated with BP than Na or K alone, as well as daily salt intake estimated from urinary Na (β = 0.088, P < 0.001). Several factors were significantly associated with Na/K, namely age, sex, obesity, blood pressure, renal function, salt restriction status, serum phosphate and urinary creatinine level, and fasting period and season at urine sample collection. However, the association between Na/K and BP was independent of these factors (adjusted β = 0.112, P < 0.001). No direct association was observed between Na/K and large arterial remodeling assessed by pulse wave analysis (P = 0.496) or retinal arteriolar morphological change (P = 0.431). Further, a genome-wide association study failed to identify any particular genotype influencing urinary Na and K levels., Conclusions: Although we clarified several factors that might affect spot urine Na/K, these relationships were not substantial enough to confound the association between urinary Na/K and BP. A simple measure of Na/K might be more representative of salt loading obtained from spot urine samples than Na excretion alone.

Objectives: Although central blood pressure (BP) is considered to be more closely associated with large arterial remodeling and cardiovascular outcomes than brachial BP, few studies have investigated these associations with changes in small arteries. As morphological changes in retinal vessels might be associated with cardiovascular outcomes, we conducted a cross-sectional study to investigate the association of central BP with retinal vessel caliber., Methods: The study included 8054 Japanese participants. Central BP was estimated by the radial arterial waveform by calibrating brachial BP. Central retinal arteriolar equivalent (CRAE) was computationally measured using fundus photography., Results: CRAE was most strongly associated with central SBP (r = -0.324, P < 0.001), followed by DBP (r = -0.292, P < 0.001) and central pulse pressure (PP; r = -0.226, P < 0.001). The correlation coefficient between SBP and CRAE was significantly greater in central SBP than in brachial SBP (r = -0.300, P < 0.001). After adjustment for possible covariates, brachial SBP (β = -0.221, P < 0.001) and central SBP (β = -0.239, P < 0.001) were independently associated with CRAE. Further, higher brachial SBP (β = -0.226, P < 0.001) and smaller PP amplification (β = 0.092, P < 0.001) were identified as independent determinants of narrowing of CRAE in the same equation, which indicated the superiority of central BP. Central BP-determined hypertensive individuals had a significantly narrower CRAE independent of brachial BP (central/brachial: hypertension/hypertension 121.4 ± 11.5, hypertension/normotension 120.9 ± 11.2, normotension/hypertension 125.1 ± 11.9, normotension/normotension 128.1 ± 11.5 μm)., Conclusion: Central BP was more closely associated with the narrowing of CRAE than brachial BP. Slight increases in central BP might be involved in the morphological changes in small retinal arteries, even in individuals with optimal brachial BP.

Central blood pressure (BP) has been suggested to be a better predictor of cardiovascular disease risk than brachial BP. Given that central BP and arterial waveform are both influenced by insulin resistance, major initiators of insulin resistance, such as serum-free fatty acid (FFA), are suspected of potentially being involved in central hemodynamics. To confirm that insulin signaling is an important modulator of central hemodynamics, we investigated this hypothesis in a large-scale general population. Brachial BP and radial arterial waveform were measured simultaneously in 9393 middle-aged to elderly individuals. The augmentation index was calculated from the radial waveform as the ratio of the height of the late systolic peak to that of the first peak. Central systolic BP was defined as the absolute pressure of the late systolic peak of the waveform. Differences in central and brachial pulse pressure (PP) were considered to represent PP amplification. PP amplification differed significantly among serum FFA level quartiles (Q1, 7.8±5.3; Q2, 8.6±5.0; Q3, 9.3±5.7; Q4, 10.3±6.1 mm Hg; P<0.001), and the maximum difference in combination with diabetes mellitus status was 4.9 mm Hg. Multivariate analysis adjusted for major covariates indicated that higher serum FFA was an independent determinant for higher PP amplification (β=0.145, P<0.001) and lower augmentation index (β=-0.122, P<0.001) and central systolic BP (β=-0.044, P<0.001), whereas the association between FFA and PP amplification significantly decreased (β=0.022, P<0.001) after further adjustment for augmentation index. Serum FFA is an overlooked factor favorably influencing central hemodynamics. A low-magnitude reflection pressure wave might be involved in this paradoxical relationship., (© 2014 American Heart Association, Inc.)

Background: Central systolic blood pressure (cSBP) has been postulated to correlate closely with cardiovascular risk. Identifying factors associated with cSBP is therefore important. Prolonged QT interval is known to be associated with cardiovascular outcomes and might also be associated with the arterial waveform and cSBP. We investigated the possible associations between electrocardiogram wave interval and cSBP in general population samples., Methods: Brachial blood pressure and radial arterial waveform were measured simultaneously. Augmentation index (AIx) was calculated from the radial waveform as the ratio of the height of the late systolic peak to that of the first peak. cSBP was defined as the absolute pressure of the late systolic peak., Results: In the first panel (n = 8,085), QT interval was strongly association with AIx (r = 0.330; P < 0.001). This association remained significant even in the heart rate-adjusted analysis (r = 0.184; P < 0.001). Although subjects with a longer QT interval were older and had higher blood pressure, heart rate, and pulse wave velocity, multivariable analysis with adjustment for these covariables nevertheless identified longer corrected QT interval as an independent determinant of increased AIx and smaller pulse pressure amplification (PPa; brachial SBP minus cSBP) (β = -0.066; P < 0.001). This association was replicated in the independent second panel (n = 1,412) (β = -0.105; P < 0.001). In contrast, QRS interval was positively associated with PPa (β = 0.056; P < 0.001)., Conclusions: Longer QT interval and short QRS duration were significantly associated with arterial waveform and PPa. Our results provide a clue to the elucidation of unidentified mechanisms of the increased cardiovascular outcome and mortality risks in subjects with longer QT interval.