Mean Nocturnal Systolic Blood Pressure Research Articles

The effects of Olmesartan/amlodipine administered in the Morning or At Night on nocturnal blood pressure reduction in Chinese patients with mild-moderate essential hypertension (OMAN Trial): study protocol for a prospective, multicenter, randomized, open-label clinical trial {1}

IntroductionHypertension increases the risk of cardiovascular disease. Uncontrolled nocturnal blood pressure is prevalent in patients taking antihypertensive medication, with an incidence rate of 30–60%. Although chronotherapy with antihypertensive agents may provide a new direction for effective control of nocturnal blood pressure, the clinical evidence base remains controversial. This research is presently underway to compare the effects of morning and bedtime administration of antihypertensive medication on nocturnal reduction and circadian rhythm of blood pressure in patients with hypertension.Methods and analysisThis study is being performed as a randomized, multicenter, open-label, parallel-group, clinical trial in which 720 participants are to undergo 24-h ambulatory blood pressure measurement (ABPM) and office blood pressure measurement (OBPM) at baseline before being randomly assigned to a morning (6–10 am) or a bedtime (6–10 pm) administration group. Each participant receives one 20/5-mg tablet of olmesartan/amlodipine (OA) daily for 4 weeks and is then followed up at 4-week intervals for a total of 12 weeks. During follow-up, the OA dosage is adjusted according to the ABPM and OBPM results. Patients with uncontrolled hypertension at the first follow-up visit will receive an increase in OA dosage to 1.5 tablets/day. For patients with blood pressure that is still uncontrolled after a further 4 weeks, the dosage of OA can be increased to 2 tablets/day. The primary objective is the reduction in mean nocturnal systolic blood pressure between baseline and week 12. The secondary objectives are the reduction in ambulatory blood pressure at weeks 4 and 12 and the blood pressure control rate at weeks 4, 8, and 12.DiscussionAntihypertensive chronotherapy remains controversial. A superiority test hypothesis design has been adopted for this trial, in which all participants will be taking the same antihypertensive medication. We anticipate that our findings will determine if nocturnal blood pressure control in Chinese patients with essential hypertension varies according to whether antihypertensive medication is taken in the morning or at bedtime. This study may provide scientific evidence for the application of chronotherapy in clinical practice.Trial registrationChiCTR2200059719. Registered on 10 May 2022(http://www.chictr.org.cn/edit.aspx?pid=169782&htm=4) {2a,2b}

Nocturnal blood pressure surge in seconds is a new determinant of left ventricular mass index.

Nocturnal blood pressure (BP) surge in seconds (sec‐surge), which is characterized as acute transient BP elevation over several tens of seconds, could be a predictor of target organ damage. However, it is not clear that the severity of sec‐surge is different between sec‐surges induced by sleep apnea (SA) (apnea/hypopnea detected by polysomnography (PSG) or oxygen desaturation) and those induced by non‐SA factors (rapid eye movement, micro arousal, etc.), and sec‐surge variables associate with left ventricular hypertrophy (LVH) independently of conventional BP variables. The authors assessed these points with 41 patients (mean age 63.2±12.6 years, 29% female) who underwent full PSG, beat‐by‐beat (BbB) BP, and cuff‐oscillometric BP measurement during the night. All patients were included for the analysis comparing sec‐surge severity between inducing factors (SA and non‐SA factors). There were no significant differences in the number of sec‐surges/night between SA‐related sec‐surges and non‐SA‐related sec‐surges (19.5±26.0 vs. 16.4±29.8 events/night). There were also no significant differences in the peak of sec‐surges, defined as the maximum systolic BPs (SBPs) in each sec‐surge, between SA‐related sec‐surges and non‐SA‐related sec‐surges (148.2±18.5 vs. 149.3±19.2 mm Hg). Furthermore, as a result of multiple regression analysis (n = 18), the peak of sec‐surge was significantly and strongly associated with the left ventricular mass index (standardized β = 0.62, p = .02), compared with the mean nocturnal SBPs measured by oscillometric method (β = −0.04, p = .87). This study suggests that peak of sec‐surge could be a better predictor of LVH compared to parameters derived from regular nocturnal oscillometric SBP.

Association of Framingham score with the parameters of ambulatory blood pressure monitoring

Cardiovascular complications are a major public health problem. The Framingham Risk Score (FS) is a scoring system that assesses the 10-year risk of cardiovascular event. The objective of our study was to evaluate the association of this score with the different parameters of the ambulatory blood pressure monitoring (ABPM). We carried out a retrospective study including patients having an ABPM between January 2015 and December 2016. The FS of each patient was calculated according to the AHA recommendations, including the following parameters: age, sex, smoking, office blood pressure, body mass index, treatment of hypertension and diabetes. The comparison between the groups was carried out by One-Way ANOVA test, and the correlation between FS and ABPM parameters by the Pearson coefficient. A total of 231 patients were included, sex-ratio M/F = 0.83. The results of ABPM showed uncontrolled hypertension (37.2%), controlled hypertension (30.3%), masked hypertension (18.6%) and absence of hypertension (13.9%). Patients with uncontrolled hypertension had the highest FS (35.5 ± 26, P < 0.001). Patients without hypertension had the lowest FS (9.4 ± 10, P < 0.001). The mean FS were 20 ± 19%, 27 ± 24%, 35 ± 30%, 38 ± 28% respectively in the dippers, non-dippers, hyper-dippers and risers ( P = 0.001). Patients with nocturnal hypertension had a higher FS than other patients (29 ± 25 vs. 23 ± 22, P = 0.06). The correlation study showed that FS was negatively correlated with glomerular filtration rate ( r = −0.35, P < 0.001). FS was positively correlated with mean global systolic blood pressure ( r = 0.16, P = 0.017), mean diurnal systolic blood pressure ( r = 0.14, P = 0.4), and mean nocturnal systolic blood pressure ( r = 0.2, P = 0.002). The Framingham score is higher in patients with riser profile and nocturnal hypertension. The ABPM parameters correlated to the Framingham score are 24-hour systolic BP, diurnal systolic BP, and nocturnal systolic BP. Adequate management of other risk factors could balance the blood pressure profile, reduce cardiovascular risk and thus ensure a better quality of life for these patients.

Associations Between Characteristics of Obstructive Sleep Apnea and Nocturnal Blood Pressure Surge.

Research suggests that oxygen desaturation and sleep stage during obstructive sleep apnea (OSA) are related to the magnitude of high blood pressure (BP) in a laboratory setting. However, in a clinical setting, these associations have not been well studied. We used a noninvasive oscillometric BP measurement device to investigate the association between oxygen-triggered BP levels at the end of each OSA episode and the characteristics of the preceding OSA episode. In 42 newly diagnosed OSA patients (average age, 63.5±12.5 years; average apnea-hypopnea index, 32.6±18.2 per hour), 258 BP measurements were obtained at the end of OSA episodes. Hypoxia-peak systolic BP (SBP), defined as the maximum oxygen-triggered SBP value, was significantly higher in rapid eye movement sleep (144.9±19.9 mm Hg) than in non-rapid eye movement stage 1 sleep (129.5±15.1 mm Hg; P<0.001) and non-rapid eye movement stage 2 sleep (129.4±14.7 mm Hg; P<0.001). In a multivariate-linear mixed model, the lowest oxygen saturation percentage during each OSA episode was associated with increased hypoxia-peak SBP (-0.501 mm Hg; P<0.001), nocturnal SBP surge (-0.395 mm Hg; P<0.001), defined as the difference between the hypoxia-peak SBP and the mean nocturnal SBP, and maximum value of SBP surge (-0.468 mm Hg; P<0.001), defined as the difference between the hypoxia-peak SBP and the minimum nocturnal SBP independent of sleep stage. These values were not associated with the duration of each OSA episode. The contribution of rapid eye movement sleep and severe oxygen desaturation to OSA-related BP elevation measured with a noninvasive oscillometric method was determined in a clinical setting.

Association of Chronic Nicotine Inhalation with Hypertension in Mice

For decades it has been known that chronic tobacco smoke exposure is a risk factor for hypertension, predisposing to cardiovascular pathologies including stroke and heart failure. However, no prior study has evaluated the role of inhaled nicotine per se. Previous investigations found that subcutaneously‐administered nicotine acutely increases expression of angiotensin‐converting enzyme (ACE) and the angiotensin receptor (AT1R). These findings suggest RAS dysfunction may mediate nicotine‐induced hypertension through either increased expression of pro‐hypertensive proteins (ACE/AT1R) or suppressed expression of compensatory agents (ACE2/MasR).Accordingly, we hypothesized that chronic nicotine inhalation promotes hypertension by inducing RAS dysfunction within autonomic brain nuclei. To test this hypothesis we exposed male (n = 64) and female (n = 44) mice to air (control) or twelve hours of nicotine vapor nightly for eight weeks. Mean nocturnal systolic blood pressure (telemetry) increased between the baseline and final week of nicotine exposure (males: +19.71 ±0.65 mmHg, F = 528.2, n = 5, p &lt; 0.0001; females: +14.04 ±0.85 mmHg, F = 322.7, n = 4, p &lt; 0.0001). In females, a trend towards elevated urinary norepinephrine was observed (t = 1.751, p = 0.0993). In a pilot study, when we exposed rats for 3 weeks to 14 hours of nicotine nightly, the hypothalamic ACE2 mRNA levels were reduced (t = 2.490, p &lt; 0.05). In mice we found a trend towards increased expression of MasR mRNA in this brain region (t = 2.373, p = 0.0766).Together, these findings suggest that nicotine inhalation contributes to high blood pressure, possibly through enhanced sympathetic activity. Mechanistically, our pilot data indicate that impaired ACE2 expression occurs in tandem with a compensatory increase in MasR in the hypothalamus of subjects inhaling nicotine. Future studies will elucidate activity of additional RAS contributors in cell culture and clarify the nature of autonomic dysfunction in vivo (e.g., increased sympathetic output vs decreased vagal tone). Collectively, this project will provide crucial information regarding the risk of hypertension in users of nicotine inhalation devices (i.e. e‐cigarettes), improving the ability of clinicians to treat this condition.Support or Funding InformationThis work was supported by NIH NHLBI grants 1R01 HL135635 and 2R01 HL093178.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Comparative effects of valsartan plus either cilnidipine or hydrochlorothiazide on home morning blood pressure surge evaluated by information and communication technology–based nocturnal home blood pressure monitoring

The authors tested the hypothesis that a valsartan/cilnidipine combination would suppress the home morning blood pressure (BP) surge (HMBPS) more effectively than a valsartan/hydrochlorothiazide combination in patients with morning hypertension, defined as systolic BP (SBP) ≥135mmHg or diastolic BP ≥85mmHg assessed by a self-measuring information and communication technology-based home BP monitoring device more than three times before either combination's administration. This was an 8-week prospective, multicenter, randomized, open-label clinical trial. The HMBPS, which is a new index, was defined as the mean morning SBP minus the mean nocturnal SBP, both measured on the same day. The authors randomly allocated 129 patients to the valsartan/cilnidipine (63 patients; mean 68.4years) or valsartan/hydrochlorothiazide (66 patients; mean 67.3years) combination groups, and the baseline HMBPS values were 17.4mmHg vs 16.9mmHg, respectively (P=.820). At the end of the treatment period, the changes in nocturnal SBP and morning SBP from baseline were significant in both the valsartan/cilnidipine and valsartan/hydrochlorothiazide groups (P<.001): -5.0 vs -10.0mmHg (P=.035) and -10.7 vs -13.6mmHg (P=.142), respectively. HMBPS was significantly decreased from baseline in both groups (P<.001), but there was no significant difference between the two groups: 14.4mmHg vs 14.0mmHg, respectively (P=.892). Valsartan/cilnidipine could not significantly suppress HMBPS compared with valsartan/hydrochlorothiazide. Large-scale randomized controlled studies are needed to assess how reducing HMBPS will affect future cardiovascular outcomes. The information and communication technology-based home BP monitoring device may become an alternative to ambulatory BP monitoring, which has been a gold standard to measure nocturnal BP and the morning BP surge.

Associations of Nocturnal Blood Pressure With Cognition by Self-Identified Race in Middle-Aged and Older Adults: The GENOA (Genetic Epidemiology Network of Arteriopathy) Study.

BackgroundWhether the association of blood pressure (BP) during sleep (nocturnal BP) with cognition differs by race is unknown.Methods and ResultsParticipants in the GENOA (Genetic Epidemiology Network of Arteriopathy) Study underwent ambulatory BP measurements, brain magnetic resonance imaging, and cognitive function testing (the Rey Auditory Verbal Learning Test, the Digit Symbol Substitution Task, and the Trail Making Test Part B) between 2000 and 2007. We examined multivariable linear regression models of the nocturnal BP‐cognition association. Among 755 participants (mean age, 63 years; 64% women; 42% self‐identified black race; 76% taking antihypertensive medication), mean nocturnal systolic BP (SBP)/diastolic BP was 126/69 mm Hg, daytime SBP/diastolic BP level was 139/82 mm Hg, and mean reduction in SBP from day to night (dipping) was 9%. Among the entire sample, a race interaction was observed in Digit Symbol Substitution Task and Trail Making Test Part B (both P<0.15). Race‐stratified analyses showed that a 1‐SD increase in nocturnal SBP levels was associated with poorer Digit Symbol Substitution Task and log‐transformed Trail Making Test Part B scores (unstandardized regression coefficient [95% confidence interval]: −1.98 [−3.28 to −0.69] and 0.06 [0.004–0.12]; both P<0.05) in black but not white individuals. Additional adjustments for white matter hyperintensity volumes or brain atrophy, measured via brain magnetic resonance imaging, did not change the results. Results were similar when nocturnal SBP dipping was assessed as the exposure, yet daytime SBP levels yielded no association with cognition.ConclusionsNocturnal SBP measurements may be useful in assessing the potential risk for lower cognitive function in middle‐aged and older adults, particularly in black individuals.

Nocturnal Blood Pressure Dipping is Abolished in Old-Elderly Hospitalized Patients.

During sleep there is reduction of blood pressure (BP) caused by a decrease of the sympathetic nervous tone. This nocturnal "dipping" phenomenon, assessable with ambulatory blood pressure monitoring (ABPM), is blunted with increasing age. To assess the effect of hospitalization on night-time BP fall in old-elderly patients. We analysed 78 ABPM of old-elderly hospitalized patients (mean age 91±0.5years) and those of 18 outpatients as control group. The nocturnal BP fall was assessed calculating: the dipping value (DV) i.e. the difference between mean diurnal systolic BP (mDSBP) and mean nocturnal systolic BP (mNSBP) and the "dipping pattern" i.e. mNSBP/mDSBPx100. Hospitalized patients showed a lower rate of normal dipping patterns (9 vs. 39%), an higher rate of reverse dippers (59 vs. 28%; p<0.05) and a lower DV (-0.9±1 vs. 9±4mmHg; p<0.05) than patients of control group. At multivariate regression analysis including age, gender and hospitalization, DV was significantly correlated only with the hospitalization (β -0.3, t -2.9; p<0.05). In old-elderly hospitalized patients nocturnal BP fall is abolished. This enhancement of the age related reduction of nocturnal BP dipping may be due to the stress associated with hospital environment.

Novel Triggered Nocturnal Blood Pressure Monitoring for Sleep Apnea Syndrome: Distribution and Reproducibility of Hypoxia-Triggered Nocturnal Blood Pressure Measurements.

Obstructive sleep apnea (OSA) causes blood pressure (BP) surges during sleep, which may lead to increased sleep-onset cardiovascular events. The authors recently developed a triggered nocturnal BP monitoring system that initiates BP measurements when oxygen desaturation falls below a variable threshold. The distribution and reproducibility of hypoxia-triggered nocturnal BP parameters compared with those of fixed-interval nocturnal BP parameters for two consecutive nights in 147 OSA patients (mean age 59.4 years, 86.4% men) were evaluated. The mean and distribution (standard deviation [SD]) of the hypoxia-peak systolic BP (SBP) were significantly greater than that of the mean nocturnal SBP (mean±SD: 148.8±20.5 vs 123.4±14.2 mm Hg, P<.001). The repeatability coefficient (expressed as %MV) of hypoxia-peak SBP between night 1 and night 2 was comparable to that of mean nocturnal SBP (43% vs 32%). In conclusion, hypoxia-peak nocturnal BP was much higher than mean nocturnal BP, and it was as reproducible as mean nocturnal BP.

Nocturnal Blood Pressure Variability in Patients with Obstructive Sleep Apnea Syndrome.

Obstructive sleep apnea (OSA) is a common respiratory disorder associated with hypertension and cardiovascular complications. Blood pressure variability may be a sign of risk of cardiovascular events. The aim of this study was to investigate the hypothesis that severe OSA syndrome is associated with increased blood pressure variability. Based on respiratory polygraphy, 58 patients were categorized into two groups: severe OSA with apnea/hypopnea index (AHI) greater than 29 episodes per hour (mean 52.2 ± 19.0/h) and mild-to-moderate OSA with AHI between 5 and 30 episodes per hour (mean 20.2 ± 7.8/h). A 24-h noninvasive blood pressure monitoring was performed. The standard deviation of mean blood pressure was used as the indicator of blood pressure variability. In patients with severe, compared with mild-to-moderate OSA, a higher mean nocturnal systolic blood pressure (133.2 ± 17.4mmHg vs. 117.7 ± 31.2mmHg, p < 0.05) and diastolic blood pressure (80.9 ± 13.1mmHg vs. 73.8 ± 9.2, p < 0.01), nocturnal systolic blood pressure variability (12.1 ± 6.0 vs. 7.6 ± 4.3, p < 0.01) and diastolic blood pressure variability (10.5 ± 6.1 vs. 7.3 ± 4.0 p < 0.05), nocturnal mean blood pressure variability (9.1 ± 4.9 mmHg vs. 6.8 ± 3.5 mmHg) were detected. The findings of the study point to increased nocturnal systolic and diastolic arterial blood pressure and blood pressure variability as risk factors of cardiovascular complications in patients with severe OSA.

Effects of Obstructive Sleep Apnea Hypopnea Syndrome on Blood Pressure and C-Reactive Protein in Male Hypertension Patients.

BackgroundThe influences of obstructive sleep apnea hypopnea syndrome (OSAHS) on blood pressure and C-reactive protein (CRP) were observed, and the underlying mechanism was investigated.MethodsRespiratory sleep monitoring was performed on 188 male patients who were newly diagnosed with hypertension. Based on the apnea hypopnea index (AHI) results, patients were divided into a normal control group (AHI ≤ 5, n = 35), a mild OSAHS group (5 < AHI ≤ 15, n = 28), a moderate OSAHS group (15 < AHI ≤ 30, n = 57), and a severe OSAHS group (AHI > 30, n = 68). Ambulatory blood pressure monitoring was conducted on patients in each group, and blood samples were collected to detect indicators, including fasting blood glucose (FBG), triglyceride (TG), low-density lipoprotein-cholesterol (LDL-C), high-density lipoprotein-cholesterol (HDL-C), and high-sensitivity CRP (hs-CRP).ResultsTG and hs-CRP in patients in the moderate and severe OSAHS groups were higher than those in the normal control group (P < 0.01, P < 0.05). Additionally, their mean nocturnal systolic blood pressure (nSBP) and nocturnal diastolic blood pressure (nDBP) were higher than those in the normal control group (P < 0.01, P < 0.05). However, the percentage of blood pressure reduction at night was significantly lower than that in the normal control group (P < 0.01). AHI and hs-CRP positively correlated with nSBP (adjusted R2 = 0.46) and nDBP (adjusted R2 = 0.38) and negatively correlated with the nocturnal blood pressure reduction percentage (adjusted R2 = 0.48).ConclusionModerate and severe OSAHS induced increases in nocturnal blood pressure and CRP content in the body, resulting in further damage to the circadian rhythms of blood pressure.

PP.17.18

Objective: Evaluate circadian blood pressure (BP) variation in hypertensive patients and analyze it's association with kidney function. Design and method: Retrospective analysis of 24-h BP monitoring results in 63 hypertensive patients and their clinical, laboratory data was performed. According to nocturnal fall (NF) of BP patients were categorized into following groups. Group A were dippers (NF 10–20%), group B were non-dippers (NF 0–10%), group C were risers (NF < 0%) and group D were extreme dippers (NF > 20%). The relation between circadian BP and renal function was compared with dipping pattern of the patients. Statistical analysis was performed using SPSS 22.0 program. P < 0,05 was considered statistically significant. Results: Results: The 24-h BP monitoring was performed in 63 patients, 26 (41,26%) of them were males, 37 (58,73%) were females. Their mean age was 53,1 ± 18,14 years. Group A consisted of 18 (28,57%) patients, group B of 35 (55,56%) patients, group C of 8 (12,70%) patients and group D of 2 (3,17%) patients. Group D was excluded from further analysis due to low numbers. Mean nocturnal systolic/diastolic BP was 125 ± 19,24/72,61 ± 9,17 mmHg in group A, 135,71 ± 23,22/79,02 ± 14,79 mmHg in group B and 144,25 ± 30,98/77,38 ± 15,7 mmHg in group C, respectively. The differences between the groups in patients mean age and gender were not statistically significant (p = 0,261 and p = 0,286, respectively). We found a statistically significant negative correlation between mean nocturnal systolic BP and glomerular filtration rate (GFR) (r = -0,32; p = 0,011) and positive correlation between mean nocturnal systolic BP and serum creatinine concentration (r = 0,263; p = 0,038). There were no significant differences between groups regarding other values studied, such as cholesterol levels and poteinuria. Conclusions: Abnormal circadian BP pattern was found in more than 70% of patients. We found a statistically significant correlation between circadian BP variation and kidney function: increased nocturnal systolic BP correlated with decreased GFR and increased serum creatinine concentration.

The effect of catheter based renal denervation on nocturnal blood pressure and nocturnal pulse pressure in patients with true resistant hypertension: National heart institute Malaysia experience

Introduction: Nocturnal hypertension and increased pulse pressure (PP) are relevant predictors of poor cardiovascular outcomes. According to the American Heart Association Council on High Blood pressure research, nocturnal blood pressure (NBP) 125/75 is deemed abnormal. At present, there is limited data on the effect of renal denervation therapy (RDN) on the NBP and nocturnal pulse pressure (NPP) in patients with True Resistant Hypertension (TRH). Purpose: To assess the change in the NBP and NPP from baseline to 1,3,6 and 12 months follow up in TRH patients who have undergone RDN at a tertiary cardiac centre between Sept 2011 and August 2012. Methods: 15 patients underwent RDN using the Symplicity™ renal denervation system. Ambulatory blood pressure monitoring (ABPM) was performed using the Bpro® device and NBP is recorded between 12 midnight to 6am. Inclusion and exclusion criteria are similar to the SYMPLICITY HTN1 and 2 trials. Results: There was a reduction of mean nocturnal systolic blood pressure (NSBP) from a baseline of 149.9±16.2mmHg to 137.2±13mmHg at 1 month (p value=0.0485), 134.3±18.2mmHg at 3 months (p value=0.0302), 131.2±10.6mmHg at 6 months (p value=0.0055) and 121.2±11.8mmHg at 12 months (p value=0.0019). There was a reduction of mean nocturnal diastolic blood pressure (NDBP) from a baseline of 80.6±13.6mmHg to 65.4±11.5 (p value=0.0382) at 12 months. There was a reduction of mean NPP from a baseline of 69.3±11.8mmHg to 54.1±13.1mmHg at 6 months (p value=0.0077) and 55.8±6.9mmHg at 12 months (p value=0.0276) ![Figure][1] Figure 1. Time course of nocturnal BP change. Conclusions: Renal denervation therapy causes early significant reduction of nocturnal blood pressure and nocturnal pulse pressure. This reduction is persistent and progressive over 1 year. [1]: pending:yes

Nighttime Blood Pressure and New-Onset Left Ventricular Hypertrophy

The relationship between circadian blood pressure (BP) variations and the extent of subclinical cardiac organ damage is still debated. In a general population, we investigated the association of night-to-day BP fall, as well as nocturnal BP level (mean and lowest values), with left ventricular (LV) hypertrophy and the value of both BP parameters in predicting new-onset LV hypertrophy. Office BP, 24-hour ambulatory BP values, and laboratory investigations were assessed on entry in 1682 subjects (50.2% men; mean age, 50.2±13.7 years) of the Pressioni Arteriose Monitorate E Loro Associazioni. Echocardiographic LV mass was measured at the initial evaluation and 10 years later. Multiple regression analyses, including daytime systolic BP (SBP), age, sex, and body mass index, showed that the lowest SBP level and the extent of nocturnal SBP decline were independently related to baseline LV mass. After adjustment for several confounders, both mean nocturnal SBP (relative risk for each 10-mm Hg increase in SBP, 1.15; 95% confidence interval, 1.01–1.23; P &lt;0.0001) and the lowest SBP level (relative risk for each 10-mm Hg increase in SBP, 1.10; 95% confidence interval, 1.02–1.19; P =0.01) were independent predictors of new-onset LV hypertrophy. This was not the case for the magnitude of nighttime SBP fall (hazard ratio for each 10% decrease in SBP, 0.91; 95% confidence interval, 0.80–1.04; P =0.18). In a general population, nighttime BP level rather than the nocturnal BP decline may be regarded as a reliable parameter for predicting the development of LV hypertrophy in subjects with normal LV mass. This finding may have important implications for optimizing cardiovascular prevention in the general population.

Circadian blood pressure variation after acute stroke

We aimed to characterise the patterns of circadian blood pressure (BP) variation after acute stroke and determine whether any relationship exists between these patterns and stroke outcome. BP was recorded manually every 4 h for 48 h following acute stroke. Patients were classified according to the percentage fall in mean systolic BP (SBP) at night compared to during the day as: dippers (fall ⩾ 10–<20%); extreme dippers (⩾20%); non–dippers (⩾0–<10%); and reverse dippers (<0%, that is, a rise in mean nocturnal SBP compared to mean daytime SBP). One hundred and seventy-three stroke patients were included in the study (83 men, 90 women; mean age 74.3 years). Four patients (2.3%) were extreme dippers, 25 (14.5%) dippers, 80 (46.2%) non-dippers and 64 (36.9%) reverse dippers. There was a non-significant trend in the proportion of patients who were dead or dependent at 3 months in the extreme dipper ( p = 0.59) and reverse dipper ( p = 0.35) groups. Non-dipping and reverse-dipping were relatively common patterns of circadian BP variation seen in acute stroke patients. These patterns were not clearly associated with outcome.

Diurnal variation of blood pressure; reproducibility and association with left ventricular hypertrophy in hemodialysis patients

The objective of this paper is to describe the pattern of diurnal blood pressure (BP) change in hemodialysis patients, determine the association of the non-dipping pattern of diurnal BP with left ventricular mass index (LVMI), and to determine if the nocturnal profile of BP is reproducible when repeated over time. In a cross-sectional study, ambulatory blood pressure monitoring (ABPM) was performed over a midweek 44-h period and echocardiography was performed on the interdialytic day. Patients with a night/day systolic and diastolic BP ratio on both days >0.9 were defined as non-dippers. Ambulatory blood pressure monitoring was repeated at 6 and 12 months follow-up. Of the 59 patients, 88% were African-American, and 48% were non-dippers. Mean LVMI was significantly higher in the non-dipper (68.3+/-25 g/height) compared to the dipper patients (55.6+/-16, P<0.05). Mean nocturnal systolic BP (r=0.35) and the night/day systolic BP ratio (r=0.39) had a higher correlation with M-mode LVMI than pre-dialysis (r=0.32). After adjustment for 44-h mean SBP, night/day systolic BP ratio remained independently associated with LVMI (beta coefficient 147.62, P=0.004). Of 12 patients who had a non-dipper profile at baseline, 11 (92%) demonstrated the same profile after 6 months and 1 year of follow-up. Many hemodialysis patients demonstrate a non-dipper profile; the degree of decline in nocturnal BP is independently associated with LVMI even after adjustment for mean BP. Patients who are identified as non-dippers consistently reproduce the same profile over time.

Nocturnal blood pressure elevation is related to adrenomedullary hyperactivity, but not to hyperinsulinemia, in nonobese normoalbuminuric type 1 diabetes.

We tested the hypothesis that insulin is an independent risk factor for elevated blood pressure. As our model we selected type 1 diabetes with peripheral circulatory hyperinsulinemia induced by sc insulin treatment. In 15 nonobese normoalbuminuric patients with type 1 diabetes (23.7 +/- 0.8 yr old) and in 15 healthy controls matched for age, sex, and body weight, ambulatory blood pressure was recorded over 24 h. The areas under the curve of free insulin (605 +/- 135 vs. 275 +/- 35 pmol/L.h; P = 0.03) and basal plasma epinephrine concentrations were higher (170 +/- 10 vs. 130 +/- 10 pmol/L; P = 0.02), and the basal aldosterone level was lower (220 +/- 40 vs. 410 +/- 50 pmol/L; P = 0.009) in the patients. The nocturnal decline in systolic blood pressure was less pronounced (13 +/- 1 vs. 19 +/- 2 mm Hg; P = 0.007) in the patients. Multivariate adjustment (r2 = 0.75; P = 0.0002) showed an effect of basal plasma epinephrine and norepinephrine levels and body mass index on the mean nocturnal systolic blood pressure, but showed no effect of age, sex, hemoglobin A1c, aldosterone, or, in particular, insulin. We found a blunted nocturnal fall in blood pressure in nonobese, normoalbuminuric type 1 diabetic patients. These patients showed increased adrenomedullary activity, and this predominantly contributed to the blood pressure alterations. We also found hyperinsulinemia in these patients, but, after controlling for covariates, blood pressure was independent of the insulin level.