Sleep Systolic Blood Pressure Research Articles

Abstract P181: Young Adult Risk Factor Burden and Sleep Hypertension in Middle-Age: the Coronary Artery Risk Development in Young Adults Study

Introduction: Developing cardiovascular disease (CVD) risk factors at younger ages increases the risk for clinic hypertension. Few data report if earlier exposure to CVD risk factors impacts blood pressure (BP) during sleep. Hypothesis: Test whether exposure to CVD risk factors in young adulthood predicts sleep systolic BP (SBP) and sleep hypertension status in middle age, independent of risk factor levels in middle age. Methods: In 1985-86, the Coronary Artery Risk Development in Young Adults study enrolled 5115 adults 18-30 years old. CVD risk factors (i.e., body mass index [BMI], fasting glucose, cigarette smoking, alcohol intake, albumin to creatinine ratio [ACR] and estimated glomerular filtration rate [eGFR]) were measured at nine exams over 30 years. We analyzed 781 adults with a complete 24 hour ambulatory BP monitoring (ABPM) recording in year 30 at 48-60 years old. Sleep hypertension was defined as asleep SBP ≥ 120 mm Hg or diastolic BP (DBP) ≥ 70 mm Hg on ABPM. To assess the importance of earlier exposure to CVD risk factors on sleep SBP in middle age, a likelihood ratio test was used to compare nested multivariable adjusted linear regression models with CVD risk factors measured at all exams (Model 1) and year 30 only (Model 2). Poisson regression was used for the sleep hypertension outcome. Results: In year 30, the mean sleep SBP / DBP was 113 / 67 mm Hg; 41.1% of adults had sleep hypertension. Compared with CVD risk factors measured at year 30 only (Model 2), BMI, fasting glucose, cigarette smoking, alcohol intake, ACR and eGFR measured at all exams (Model 1) statistically significantly increased the explanatory value for higher sleep SBP in middle age (all p-values < 0.05; Table ). With the exception of ACR (p=0.057), results were consistent for sleep hypertension. Conclusion: Exposure to less healthy levels of CVD risk factors in young adulthood may independently contribute to higher sleep SBP and having sleep hypertension by middle age. Studies with repeated ABPM are needed to track determinants of higher sleep BP over the lifespan.

Association between sleep disturbance and nocturnal blood pressure profiles by a linear mixed model analysis: the Nagahama study

ObjectivesWe 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. MethodsThe 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. ResultsMean 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. ConclusionMore attention should be paid to sleep efficiency as a factor in maintaining circadian BP rhythm.

Absence Of Sympathetic Vasodilation During Mental Stress With Non‐Dipping Circadian Blood Pressure Pattern In Young White And Black Adults Could Be An Early Indicator Of Hypertension

People of Black African ethnicity (BA) have greater prevalence of hypertension compared with those of White European ethnicity (WE) and are at greater risk of developing hypertension‐associated cardiovascular disease (CVD). Older WE non‐dipper hypertensives show endothelial dysfunction. Endothelial dysfunction and higher prevalence of non‐dipping nocturnal blood pressure have been documented in Blacks relative to Whites. Novel environmental stress stimuli evoke sympathetic vasoconstriction in renal and splanchnic vasculature, but vasodilatation in limb muscle, which may habituate on repetition. In young adults altered response to novel stimuli is predictive of developing hypertension later on in life. However, It is not known whether non‐dippers also show endothelial dysfunction and altered responses to environmental stressors. Thus, we hypothesized that non dippers would show smaller muscle vasodilator or muscle vasoconstrictive responses on repetition of an environmental stressor and blunted reactive hyperaemia relative to dippers. Experiments were performed on 17 WEs (21±0.64 years) and 16 BAs (22±0.77 years) who were resident in the UK. Responses were recorded following release of arterial occlusion for 2 min (reactive hyperaemia) and by 5 sound stimuli (S1–5; 100 dB, 2 KHz). Continuous arterial blood pressure (ABP) was recorded by finger photoplethysmography. Forearm blood flow (FBF) was recorded by venous occlusion plethysmography; forearm vascular conductance (FVC) was calculated as FBF/ABP. 24 hour Ambulatory blood pressure monitoring was done. Relative to WES, BAs showed higher 24 hour systolic blood pressure (SBP)(110±1.33 vs 117±3.17 mmHg) and higher sleep‐time SBP (99±1.36 vs 108±3.05 mmHg) p&lt;0.05 as well as higher proportion of pre‐/hypertensives (7/16, 40%) compared with WE (1,5.8%). 40% BAs were non‐ dippers compared to 17.6 % WE. Six of the pre‐/hypertensive BAs were nocturnal dippers. Relative to normotensive BA dippers, BA non‐dippers showed higher sleep SBP (93±4.65 vs 108±3.01 mmHg) and heart rate (59±4.69 vs 72±3.11 bpm) p&lt;0.05. Relative to WE dippers, the WE non dippers showed higher day‐time and night time mean ABP (85.25±1.14 vs 91.57±2.39 mmHg) ; (71.55±0.88 vs 81.25±1.71 mmHg) p&lt;0.05. During reactive hyperaemia, there was no difference between dippers and non‐dippers in the two ethnic groups ( WE: +0.39± 0.03 vs +0.45± 0.08; BA : +0.41± 0.05 vs +0.34± 0.05 p&gt;0.05 ). During S1–5, WE and BA dippers showed a net increase in FVC indicating forearm vasodilatation (WE, +0.005±0.002 CU; BA, +0.007±0.002 CU) whilst WE and BA non‐dippers showed a net decrease in FVC indicating forearm vasoconstriction, (WE − 0.007±0.004 CU; BA −0.007±0.003 CU). These results indicate that in young normotensive non‐dippers, sympathetic vasoconstriction to mental stress precedes development of endothelial dysfunction and could serve as an early indicator of cardiovascular disorder. Thus, we propose that exaggerated sympathetic vasoconstrictor response to environmental stressors contributes to the development of hypertension and CVD in non‐dippersThis abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Carotid atherosclerosis and the association between nocturnal blood pressure dipping and cardiovascular events

The impact of a nondipping blood pressure (BP) pattern, defined as (awake systolic BP - sleep systolic BP)/awake systolic BP<0.1, on cardiovascular events in populations with different degrees of carotid atherosclerosis is uncertain. The authors hypothesized that a nondipping BP pattern would show differential predictive power for cardiovascular events, including total cardiovascular death, sudden death, nonfatal cardiovascular events, and nonfatal stroke, between populations with and without carotid atherosclerosis. To test this hypothesis, the authors analyzed 493 patients (mean age 67.9years, 47.5% men) from the J-HOP (Japan Morning Surge-Home Blood Pressure) study for whom ambulatory BP monitoring and carotid intima-media thickness data were available. Twenty-nine cardiovascular events occurred during follow-up (1867 person-years). A nondipping BP pattern was independently associated with cardiovascular events in the population without carotid atherosclerosis, defined as carotid intima-media thickness <1.1mm after adjustment for other cardiovascular risk factors including age, sex, diabetes mellitus, chronic kidney disease, and 24-hour systolic BP (hazard ratio, 8.15; 95% confidence interval, 1.76-37.78 [P<.01]). This association was not found in the population with carotid intima-media thickness ≥1.1mm. Therefore, in the hypertensive population without carotid atherosclerosis, physicians should consider ambulatory BP monitoring to determine the nocturnal BP pattern as an alternative approach to assessing cardiovascular events.

Abstract 131: Racial Differences in Nocturnal Hypertension and Non-dipping Blood Pressure: The Coronary Artery Risk Development in Young Adults (CARDIA) Study

Risk factors for nocturnal hypertension are more common among blacks compared with whites. We hypothesized nocturnal hypertension and nocturnal non-dipping BP are more common among blacks compared with whites. We analyzed data for 781 participants of the population-based Coronary Artery Risk Development in Young Adults (CARDIA) study who completed ambulatory blood pressure (BP) monitoring (ABPM) in 2015-2016. Awake and sleep periods were defined using actigraphy and self-report. Nocturnal hypertension was defined as mean sleep systolic BP (SBP)/diastolic BP (DBP) ≥ 120/70 mm Hg. Non-dipping SBP and DBP, separately, were defined as a decline in mean sleep BP, relative to mean awake BP &lt; 10%. The mean age of participants was 54.7 years, 21.1% were white women, 38.5% were black women, 16.8% were white men and 23.6% were black men. The prevalence of nocturnal hypertension was 18.2% and 44.5% among white and black women, respectively, and 35.9% and 59.8% among white and black men, respectively. After multivariable adjustment, the prevalence of nocturnal hypertension was higher among black women, white men and black men, each compared with white women (Table). The prevalence of non-dipping SBP was 21.2% and 40.9% among white and black women, respectively, and 19.8% and 37.5% among white and black men, respectively. After multivariable adjustment, non-dipping SBP was more common among black women and black men compared with white women. There were no statistically significant differences in non-dipping DBP across race-gender after multivariable adjustment. Nocturnal hypertension and non-dipping SBP are more common among blacks compared with whites even after adjustment for mean BP.

Race and sex differences in ambulatory blood pressure measures among HIV+ adults

Ambulatory blood pressure monitoring (ABPM) can identify phenotypes that cannot be measured in the clinic. Determining race and sex disparities in ABPM measures among HIV+ individuals may improve strategies to diagnose and treat hypertension in this high-risk population. We compared ABPM measures between 24 African-American and 25 white HIV+ adults (36 men and 13 women). Awake systolic blood pressure (SBP) and diastolic blood pressure (DBP) were similar in African-Americans and whites. After multivariable adjustment, sleep SBP and DBP were 9.7 mm Hg (95% confidence interval [95% CI]: 4.7, 14.8) and 8.4 mm Hg (95% CI: 4.3, 12.5) higher, respectively, among African-Americans compared with whites. After multivariable adjustment, SBP and DBP dipping ratios were 5.2% (95% CI: 1.7%, 8.7%) and 6.1% (95% CI 2.0%, 10.3%) smaller among African-Americans compared with whites. After multivariable adjustment, awake and sleep SBP and DBP were higher in men compared to women. There was no difference in SBP or DBP dipping ratios comparing men and women. The prevalence of awake masked hypertension was 42% in men versus 17% in women, and the prevalence of sleep masked hypertension was 57% among African-Americans versus 18% among whites. These data suggest that ABPM measures differ by race and sex in HIV+ adults.

Chronotherapy for hypertension in obstructive sleep apnoea (CHOSA): a randomised, double-blind, placebo-controlled crossover trial

BackgroundObstructive sleep apnoea (OSA) is an important cause of secondary hypertension. Nocturnal hypertension is particularly prevalent in OSA and is a strong predictor of cardiovascular mortality. Studies in patients with...

Sleep-Wake Concordance in Couples Is Inversely Associated With Cardiovascular Disease Risk Markers.

To determine whether interdependence in couples' sleep (sleep-wake concordance i.e., whether couples are awake or asleep at the same time throughout the night) is associated with two markers of cardiovascular disease (CVD) risk, ambulatory blood pressure (BP) and systemic inflammation. This community-based study is a cross-sectional analysis of 46 adult couples, aged 18-45 years, without known sleep disorders. Percent sleep-wake concordance, the independent variable, was calculated for each individual using actigraphy. Ambulatory BP monitors measured BP across 48 h. Dependent variables included mean sleep systolic BP (SBP) and diastolic BP (DBP), mean wake SBP and DBP, sleep-wake SBP and DBP ratios, and C-reactive protein (CRP). Mixed models were used and were adjusted for age, sex, education, race, and body mass index. Higher sleep-wake concordance was associated with lower sleep SBP (b = -.35, SE = .01) and DBP (b = -.22, SE = .10) and lower wake SBP (b = -.26, SE = .12; all p values < .05). Results were moderated by sex; for women, high concordance was associated with lower BP. Men and women with higher sleep-wake concordance also had lower CRP values (b = -.15, SE = .03, p < .05). Sleep-wake concordance was not associated with wake DBP or sleep/wake BP ratios. Significant findings remained after controlling for individual sleep quality, duration, and wake after sleep onset. Sleep-wake concordance was associated with sleep BP, and this association was stronger for women. Higher sleep-wake concordance was associated with lower systemic inflammation for men and women. Sleep-wake concordance may be a novel mechanism by which marital relationships are associated with long-term CVD outcomes.

AMBULATORY BLOOD PRESSURE PATTERNS IN PATIENTS WITH RETINAL VEIN OCCLUSION.

Failure of blood pressure (BP) to dip during sleep (nondipper pattern) is associated with cardiovascular disease and stroke. The prevalence and degree of nondipping and masked hypertension in patients with retinal vein occlusion (RVO), which is associated with stroke, has not been previously examined. We measured clinic and 24-hour ambulatory BPs in 22 patients with RVO and 20 control participants without known eye disease matched by age and sex. Mean BP dipping, defined as the ratio of difference in mean awake and sleep systolic BPs to mean awake systolic BP, and masked and nocturnal hypertension were compared between groups. Mean 24-hour ambulatory BP was 144/79 mmHg among those with RVO and 136/77 mmHg among controls. Patients with RVO had an almost 2-fold higher prevalence of nondipping pattern (80.8% [95% confidence interval, 52.8-94.1] vs. 50.4% [95% confidence interval, 26.1-74.5]; P = 0.008). Average sleep systolic BP dip in patients with RVO was 6.1% versus 11.9% in controls (P = 0.004). More patients with RVO had masked hypertension by ambulatory BPs than controls (71% vs. 50%), but this difference was not statistically significant. Our data suggest an association between RVO and nondipper BP pattern. Ambulatory BP monitoring may be useful in the evaluation of patients with RVO by identifying those who may benefit from more aggressive BP control.

PS 11-08 Association of 24-hour urinary sodium excretion with ambulatory blood pressure parameter

Objective: As the important effects of sodium intake on blood pressure (BP) and on response to anti-hypertensive medication has been recognized for long times, it has been recommended that dietary sodium intake is restricted in hypertensive patients. However, the relationship between BP and salt is weak in most community studies. Moreover, a study in hypertensive Chinese patients showed that urinary sodium excretion is only related to diastolic BP (DBP) and not to systolic BP (SBP). Therefore, this study was to investigate whether the 24-hour urinary sodium excretion was associated with the ambulatory DBP and not with SBP. Design and Method: This study was composed of 121 patients who underwent coronary angiography or percutaneous coronary intervention. The 24-hour urine collection was usually performed at admission day 3 or 4. At the same admission day the ambulatory blood pressure monitoring (ABPM) was also performed. Additional ABPM was carried out in the uncontrolled blood pressure situations. Results: The mean serum creatinine was 0.96 ± 0.53, mean 24-hour sodium excretion 128.54 ± 170.76 and mean 24-hour potassium excretion 33.10 ± 13.99. The mean 24 hour urinary sodium/potassium excretion ratio was 3.62 ± 1.70 and mean 24 hour urinary sodium/creatinine excretion ratio 185.79 ± 523.82 and 24-hour micro-albuminuria 48.87 ± 152.57. The mean 24-hour sodium excretion was associated with sleep-SBP, sleep-DBP, sleep-pulse pressure (PP), wake-PP, 24-hour SBP, 24 PP, 24-hour potassium excretion, 24-hour sodium/potassium ratio and 24-hour sodium/creatinine ratio. After adjustment for age, gender, body mass index and urinary potassium excretion, only sleep-SBP was significantly associated with 24-hour urinary sodium excretion. Conclusions: Our study showed that 24-hour urinary sodium excretion was only associated with sleep SBP.

PP.37.20] THE RELATIONSHIP BETWEEN CENTRAL BLOOD PRESSURE AND LEFT VENTRICULAR MASS INDEX IN COMPARISON WITH CASUAL AND AMBULATORY BLOOD PRESSURES

Objective: Theoretically, it is postulated that the central blood pressure (BP) is more directly interact with the left ventricular mass index than casual blood pressure or ambulatory blood pressure which were measured more peripheral site. In some studies showed that central blood pressure or arterial stiffness iis more closely associated with left ventricular hypertrophy or function than others. But there is few study to compare the relationship in the general population in terms of the representative relation in healthy subjects Design and method: In the general population study for the middle aged subjects (30∼59 years) in the rural area in South Korea, 143 subjects undergone central blood pressure (BP) measurement using (HEM-9000AI: Omron Healthcare, Kyoto, Japan) and ambulatory blood pressure monitoring using TM2430, A&D in succession were analyzed. Casual blood pressure was measured six times random and alternative order using Omron 907 HEM and standard mercury sphygmomanometer. Left ventricular mass index (LVMI) was measured by echocardiography (Vivid-i, GE, USA) Results: Age was 47.9 ± 8.3 year and BMI was 25.3 ± 3.3 kg/m2. Casual systolic/diastolic BP was 123.2 ± 17.3 / 74.6 ± 12.6 mmHg by automated device (AD) and 123.2 ± 18.7/77.2 ± 11.5 mmHg by auscultation method (AM). Daytime BP was 131.5 ± 15.2/82.6 ± 9.7 mmHg and central systolic BP was 129.5 ± 19.9 mmHg. In simple and partially adjusted correlation coefficients for age sex, BMI, and 24 hour systolic BP, all of the correlation coefficients between LVMI and AD, AM, and central BPs were statistically significant. But when adjusted additionally for casual BP measured by AM, casual diastolic BPs by AD or AM and sleep systolic BP remained significant (beta = -0.15(p = 0.04), beta = -0.24 (p = 0.008), beta = -0.25(p = 0.007), respectively). But central BP or augmentation index were not independent factor for LVMI in the adjusted model (beta = -0.01, p = 0.68). And when additionally adjusted for casual systolic BP by AD, casual systolic BP by AM and nocturnal BPs remained significant. Conclusions: In terms of the relationship with LVMI, in our study done in a general population, central BP did not show additional benefit or superiority to casual or ambulatory BPs.

OS 07-05 DETERMINANTS OF MORNING BLOOD PRESSURE SURGE IN NORMOTENSIVE SUBJECTS AND UNTREATED HYPERTENSIVE PATIENTS

Objective: Morning blood pressure (BP) surge has been regarded as a predictor of adverse cardiovascular events. However, its determinants remain controversial and no previous studies have evaluated whether or not there is a difference in the determinants of morning BP surge between normotensive and hypertensive subjects. Design and Method: We included 476 normotensive subjects (mean age 52.8 ± 15.4 years, 49.2% males) and 1028 untreated hypertensive patients (age 51.7 ± 13.9 years, 56.1% males) from the Korean Ambulatory Blood Pressure Registry. Sleep-trough morning BP surge was defined as the difference between mean systolic BP (SBP) during the 2 hours after awakening and the average of three readings centered on the lowest sleep SBP level. Results: Hypertensive patients had higher sleep-trough morning BP surge compared to normotensive subjects (27.6 ± 17.8 mmHg vs 25.7 ± 13.7 mmHg, p = 0.023). In multivariate linear regression analysis, 24-hour heart rate (24-h HR) variability (β = 0.397, p < 0.0001) was associated with MS in normotensive subjects. Meanwhile, in hypertensive patients, age (β = −0.113, p = 0.046), diabetes mellitus (β = −0.109, p = 0.043), daytime SBP (β = 0.301, p < 0.0001), night-time SBP (β = −0.375, p < 0.0001), 24-h SBP variability (β = 0.290, p < 0.0001) and night-time diastolic BP (DBP) variability (β = 0.185, p = 0.001) were found to be independent determinants of morning BP surge. Conclusions: Morning BP surge was more pronounced in hypertensive patients than in normotensive subjects, and its determinants were also different between them. These findings suggest that different pathogenic mechanism of morning BP surge may exist in normotensive subjects and hypertensive patients, respectively.

Uncontrolled hypertension in older patients: markers and associated factors to masked and white-coat effect.

BackgroundHypertension is the main risk factor for cardiovascular diseases, affecting more than half the elderly population. It is essential to know if they have proper control of hypertension. The aim of this study was to identify the associated factors to masked uncontrolled hypertension and false uncontrolled hypertension in older patients.MethodsTwo-hundred seventy-three individuals (70.1 ± 6.7 years-old) had blood pressure (BP) measured at the office and by ambulatory BP monitoring (ABPM), with the definition of controlled group (C), individuals with high office BP and adequate ABPM, called white-coat effect group (WCE), uncontrolled (UC), and subjects with appropriate office BP and elevated ABPM denominated masked effect group (ME). Age, body mass index, diabetes, pulse pressure (PP) and BP dipping during sleep were evaluated (Kruskal-Wallis test and logistic regression models).ResultsAge was higher in UC than in C and ME (P < 0.01), and 24-h ABPM PP was lower in C (48 ± 7 mmHg) and WCE (51 ± 6 mmHg) than in UC (67 ± 12 mmHg) and ME (59 ± 8 mmHg) (P < 0.01). Sleep systolic BP dipping was lower in ME than in C (P = 0.03). Female gender was associated with a greater chance of being of ME group, which showed a higher PP and lower BP dipping during sleep.ConclusionsIn older individuals, office BP measurements did not allow the detection of associated factors that would permit to differentiate WCE from UC group and C from ME group. ABPM favored the identification of a higher PP and a lower BP dipping during sleep in the masked effect and uncontrolled groups.

Amyloid burden and sleep blood pressure in amnestic mild cognitive impairment.

To determine whether cortical β-amyloid (Aβ) deposition is associated with circadian blood pressure (BP) profiles and dynamic cerebral blood flow (CBF) regulation in patients with amnestic mild cognitive impairment (aMCI). Forty participants with aMCI were included in this study. Cortical Aβ depositions were measured by (18)F-florbetapir PET and expressed as the standardized uptake value ratio (SUVR) relative to the cerebellum. Circadian BP profiles were measured by 24-hour ambulatory monitoring during awake and sleep periods. The dipping status of sleep BP (i.e., the percent changes from the awake BP) was calculated and dichotomized into the dipper (≥10%) and nondipper (<10%) groups. Dynamic CBF regulation was assessed by a transfer function analysis between beat-to-beat changes in BP and CBF velocity measured from the middle cerebral artery during a repeated sit-stand maneuver. Age was positively correlated with a greater Aβ deposition in the posterior cingulate, precuneus, and mean cortex. Accounting for the age effect, attenuated reductions in sleep systolic BP were associated with higher levels of posterior cingulate SUVR. Consistently, the nondippers exhibited a higher SUVR in the posterior cingulate than the dippers. Transfer function gain between changes in BP and CBF velocity was diminished in the nondippers, and moreover those individuals with a lower gain exhibited a higher SUVR in the posterior cingulate. Attenuated reductions in sleep BP are associated with a greater Aβ burden in the posterior cingulate and altered dynamic CBF regulation in patients with aMCI.

Abstract 13181: Characteristics of Diurnal Change of Pulse Rate in Resistant Hypertension

Introduction: Sympathetic hyperactivity is one of the most important causes of resistant hypertension. Ambulatory blood pressure monitoring (ABPM) allows measurement of blood pressure (BP) and pulse rate (PR) throughout the day, as well as measurement of diurnal variations in BP and PR, which are controlled by the autonomic nervous system. Hypothesis: We hypothesized that abnormal diurnal change of BP and PR are associated with resistant hypertension. Methods: We evaluated 1003 patients with hypertension who were enrolled in the Japan Morning Surge Home Blood Pressure Study and were using ABPM. Resistant hypertension was defined as clinic BP≧140/90 mmHg despite the use of optimal doses of 3 classes of antihypertensive drugs, including a diuretic. BP or PR dipper status was defined as (awake systolic BP (SBP) or PR-sleep SBP or PR)/awake SBP or PR ≧0.1. BP or PR nondipper status was defined as (awake SBP or PR-sleep SBP or PR)/awake SBP or PR &lt;0.1 and ≧0. BP and PR riser status were defined as awake SBP or PR &lt; sleep SBP or PR. Results: The numbers of PR nondippers and PR risers in the resistant hypertensive groups were significantly greater than those in the non-resistant hypertensive groups (x2=9.35, p=0.009), but there were no significant differences in the diurnal variation of BP between the resistant hypertensive and non-resistant hypertensive groups (x2=3.10, p=0.21). In the resistant hypertensive groups, the proportion of PR risers was approximately three-fold greater than that in the non-resistant hypertensive groups after adjustment for age, gender, 24-h BP, PR, and BP variation (Hazard ratio 2.94, 95%Cl 1.25-6.91, p=0.013), but there were no significant differences in the proportion of PR nondippers (Hazard ratio 1.36, 95%Cl 0.82-2.26, p=0.23). Conclusions: A riser pattern of PR was associated with resistant hypertension. ABPM may be useful to identify resistant hypertensive patients who have autonomic nervous system dysfunction.

Short-term blood pressure variability in hypertensive patients with obstructive sleep apnea syndrome

Short-term blood pressure (BP) variability is an important cardiovascular risk factor. Whether patients with obstructive sleep apnea syndrome (OSAS) indeed display increased short-term BP variability and, if so, what is its underlying mechanism remain unclear. We compared the short-term BP variability between hypertensive patients with OSAS (OSAS group; n= 212) and those without OSAS (control group; n = 82) by examining data of 24-h ambulatory BP monitoring (ABPM) and investigated the effects of continuous positive airway pressure (CPAP) therapy on short-term BP variability in 37 hypertensive patients with OSAS. Short-term BP variability was calculated with the average real variability (ARV) of awake and sleep BP. ARVs of sleep systolic BP (SBP) and diastolic BP (DBP) were significantly higher in the OSAS group than in the control group. There was no significant difference in ARVs of awake SBP and DBP between the two groups. In the OSAS group, multiple regression analyses revealed that the body mass index (BMI) was an independent determinant for ARV of sleep DBP and that the lowest SpO2 was an independent determinant for ARVs of sleep SBP and sleep DBP. CPAP therapy decreased ARVs of sleep SBP and DBP. These results suggested that higher short-term BP variability during sleep is a characteristic feature of hypertensive patients with OSAS and that obesity and hypoxemia play essential roles in increasing short-term BP variability during sleep. CPAP therapy may improve exaggerated short-term BP variability during sleep in patients with OSAS.

Hypertension in chronic kidney disease: the influence of renal transplantation.

Hypertension is one of the most prevalent cardiovascular risk factors in chronic kidney disease (CKD) and kidney transplants. The contribution of transplantation to hypertension in comparison to patients with CKD and similar renal function has not been characterized. Ninety-two transplants and 97 CKD patients with an estimated glomerular filtration rate less than 60 mL/min/1.73 m not receiving dialysis were enrolled. At entry, office blood pressure (BP) and 24-hr ambulatory blood pressure monitoring (ABPM) were obtained. Office BP was not different between transplants and CKD patients (139.5±14.3 vs. 135.2±19.3, P=1.00, respectively). ABPM 24-hr systolic blood pressure (SBP) (133.9±14.3 vs. 126.2±16.1, P=0.014), awake SBP (135.6±15.2 vs. 128.7±16.2, P=0.042), and sleep SBP (131.2±16.2 vs. 120.2 ±17.9, P=0.0014) were higher in renal transplants. When patients were classified according to BP patterns associated with highest cardiovascular risk, the proportion of patients with both nocturnal hypertension and non-dipper pattern was higher in transplants (68.5% vs. 47.4%, P=0.03). In the multivariate regression analysis, transplantation was an independent predictor of 24-hr, awake, and sleep SBP. Office BP is similar in kidney transplants and CKD patients with similar renal function. On the contrary, hypertension is more severe in kidney transplants when evaluated with ABPM mainly as a result of increased sleep systolic BP. Thus, precise evaluation of hypertension in kidney transplants requires ABPM.

Effects of nighttime single-dose administration of vasodilating vs sympatholytic antihypertensive agents on sleep blood pressure in hypertensive patients with sleep apnea syndrome.

Obstructive sleep apneas syndrome (OSAS) is associated with nocturnal hypertension with higher sleep blood pressure (BP) and its variability, both of which increase cardiovascular risk. In this crossover design study, the effect of nighttime single-dose administration of vasodilating (nifedipine 40 mg) vs sympatholytic (carvedilol 20 mg) antihypertensive agents on sleep BP in 11 hypertensive OSAS patients was evaluated. The authors recently developed a trigger sleep BP monitor with an oxygen-triggered function that initiates BP measurement when oxygen desaturation falls. The BP-lowering effects of nifedipine on the mean (P<.05) and minimum sleep systolic BPs (SBPs) (P<.01) were stronger than those of carvedilol. Sleep SBP surge (difference between the hypoxia-peak SBP measured by oxygen-triggered function and SBPs within 30 minutes before and after the peak SBP) was only significantly reduced by carvedilol (P<.05). The nighttime dosing of both vasodilating and sympatholytic antihypertensive drugs is effective to reduce sleep BP but with different BP-lowering profiles.

Effect of an exercise program on blood pressure, body mass index and abdominal circumference in elderly hypertensive patients

The study was approved by the Ethic Committee of the School of Medicine of Ribeirao Preto-University of S~ao Paulo Brazil. Objectives: To investigate and compare the effects of ten weeks of isolated aerobic and aerobic exercise associated with resistance exercise in blood pressure (BP), body mass index (BMI) and abdominal circumference (AC) older individuals with treated hypertension. Methods: 90 elderly volunteers aged from 65 to 75 years, on regular use of antihypertensive drugs (diuretics, ACE inhibitors, angiotensin receptor blockers or calcium channel blockers (diidropiridinic)) were selected. We excluded those with diabetes, BP greater than 160/100 mmHg, use of medications beta-blockers, obese grade II and III. Of the 90 seniors, 44 were able to perform the study protocols. Subjects were randomized into 3 groups : G1 (aerobic training, n 1⁄4 15 ), G2 ( aerobic training with anaerobic, n 1⁄4 15 ) and G3 (control, n 1⁄4 14 ). The aerobic sessions were held three times per week at intensity between 50% to 80% of maximum heart rate obtained by the maximum exercise test. The maximum load work was calculated by one-repetition maximum (1RM) and they exercised at 50 to 60% of 1RM. The ambulatory blood pressure monitoring (ABPM Space Labs Medical , 90207 ) was installed in the left arm, lasting for 24 hours, in before and after 10 weeks. The measurements of weight, height and abdominal circumference before and after training were also obtained. Statistics: We used the linear regression model with mixed effects and the Pearson correlation test. Results: Mean age was 68.5 5.1 years, with no diferences between groups (p 1⁄4 0:44), with a predominance of women (84 %) in the three groups (p 1⁄4 0:32 ). After 10 weeks of training, systolic BP (SBP) was reduced of 4.2 mmHg and 7.7 mmHg for G1 and G2, respectively. G3 had an increase of 5.7 mmHg during the 10 weeks. . Basal diastolic BP (DBP) was 75.4 mmHg in G1 , 75.8 mmHg in G2 and 72.8 mmHg in G3 , modifying these values to 72 mmHg, 72 mmHg and 73.7 mmHg, respectively. BMI values were reduced in G1 (p1⁄40.01) , G2 (p1⁄40.01) and increased in G3 (p1⁄40.01). Similarly, measures the abdominal circumference decreased in G1 (p <0.01) and G2 (p < 0.01), while the values of G3 tended to increase at the end of observation (p1⁄40.07). BMI values were correlated with: SBP 24 (p < 0.01, rho 0.6); waking SBP (p<0.001, rho 0.7) ;sleep SBP (p<0.001, rho 0.6 ); DBP 24 (p1⁄40.001; rho 0.47), DBP wake / sleep (p<0.001; 0:56 rho / p1⁄40.001, rho 0:45 ) and fat mass (p<.001, rho 0.74) . Conclusion: Ten weeks of isolated aerobic training and combined aerobic and resistance training were equally effective in reducing BP, in decreased abdominal circumference and body mass index. The weight loss achieved with the training may have influenced the drop in blood pressure.

The effect of ischemic stroke combined with obstructive sleep apnea syndrome on circadian blood pressure

Objective To investigate the effect of ischemic stroke combined with obstructive sleep apnea syndrome (OSAS) on circadian blood pressure. Methods Sixty-five ischemic stroke patients combined with OSAS (combined group), 51 ischemic stroke patients without OSAS (ischemic stroke group), and 76 healthy subjects (control group) were enrolled in this study. History of hypertension was inquired, and blood pressure and polysomnography (PSG) were monitored. All antihypertensive drugs were withdrawn. The morbidity rate of hypertension, and levels of pre-sleep and morning blood pressure were assessed. Results The morbidity rate of hypertension and refractory hypertension in combined group and ischemic stroke group were higher than control group ( P = 0.000, 0.000). The prevalence of simple high systolic blood pressure (SBP) in ischemic stroke group was higher than other 2 groups ( P = 0.000, 0.002), and the prevalence of simple high diastolic blood pressure (DBP) in combined group was higher than control group and ischemic stroke group (P = 0.002, 0.042), while the prevalences of high SBP and DBP in combined group and ischemic stroke group were all higher than control group ( P = 0.000, 0.045). The prevalence of pre-sleep hypertension and morning hypertension in combined group were all higher than control group ( P = 0.000, 0.000), and the prevalence of morning hypertension in combined group was also higher than ischemic stroke group ( P = 0.000), while only the prevalence of pre-sleep hypertension in ischemic stroke group was higher than control group ( P = 0.002). The difference of prevalence of pre-sleep hypertension between combined group and ischemic stroke group was not statistically significant ( P = 0.347). The pre⁃sleep SBP ( P = 0.000, 0.020) and morning SBP ( P = 0.000, 0.004) in combined group and ischemic stroke group were all higher than control group, but the difference between combined group and ischemic stroke group was not statistically significant ( P = 0.074, 0.100); the pre-sleep DBP ( P = 0.000, 0.000) and morning DBP ( P = 0.000, 0.000) in combined group were higher than the ischemic stroke group and control group, but the difference of pre⁃sleep DBP and morning DBP between ischemic stroke group and control group was not statistically significant ( P = 0.059, 0.054). The differences of pre⁃sleep SBP and morning SBP in combined group, ischemic stroke group and control group were not statistically significant ( P = 0.702, 0.329, 0.503), but the difference of pre⁃sleep DBP and morning DBP in combined group was statistically significant ( P = 0.000), while the differences of pre-sleep DBP and morning DBP in ischemic stroke group and control group were not statistically significant ( P = 0.058, 0.318). Conclusion Isolated systolic hypertension is the main manifestation of ischemic stroke patient. When the patient is combined with OSAS, SBP and DBP are liable to elevate, and the circadian rhythm of blood pressure may be affected.