Nocturnal Blood Pressure Fall Research Articles

Symmetrical Ambulatory Arterial Stiffness Index: Relationship with Serum Cystatin C Levels

Objective: Increased central arterial stiffening is the consequence of many disease states such as diabetes, atherosclerosis, and chronic renal disease. Symmetrical Ambulatory Arterial Stiffness Index (Sym-AASI) may provide a simple clinical approach to evaluate arterial stiffness. This study has tried to evaluate the relationship of Sym-AASI with cystatin C levels. Design and methods: The sample subjects were 53 males and 34 females (mean age = 59.3 ± 13.5 years). Kidney function was evaluated by measuring serum cystatin C and estimated glomerular filtration rate (eGFR). The ambulatory BP was measured noninvasively for 24 h. Results: Patients in the highest quartile showed an older age ( p < 0.001) and worse eGFR (p < 0.001). Pulse pressure (PP) increased as cystatin C was higher. Mean Sym-AASI showed an increase from the first to the last cystatin C quartile. Correlation test showed a significant relationship of Sym-AASI with age (r = 0.573), serum creatinine (r = 0.237), eGFR (–0.323), cystatin C (r = 0.427), systolic blood pressure (r = 0.525), and PP (r = 0.647). Multivariate regression analysis showed that age, cystatin C, nocturnal systolic blood pressure reduction, and nocturnal diastolic blood pressure fall were independently related to Sym-AASI. There was not any independent association between eGFR and Sym-AASI or between cystatin C and PP. Conclusions: Increased Sym-AASI seems to be independently associated with serum cystatin C levels. Sym-AASI seems to be better than PP to detect changes in the arterial wall. This could be a simple and easy method to evaluate arterial stiffness in hypertensive patients without needing more complex devices.

INFLUENCE OF CHRONOTHERAPY WITH DIFFERENT ANTIHYPERTENSIVE DRUGS ON CIRCADIAN BLOOD PRESSURE PATTERN

Aim. To determine the value of different blood pressure (BP) measurement methods for arterial hypertension (HT) chronotherapy efficacy assessment. Material and methods. Two similar open, randomized, cross-over studies (morning vs evening intake) were carried out. Duration of the initial wash-out period was 2 weeks; duration of both treatment courses — 3 weeks; the interval between courses — 1 week. Only patients with stable HT (mean day-time BP>135/85 mm Hg) were included. Ambulatory BP monitoring (ABPM) was carried out prior to treatment and at the end of both treatment courses. The patients performed home BP monitoring (HBPM) throughout the study. Pharmacokinetics of verapamil (n=14, mean daily dose — 240.0±16.3 mg) was studied to assess compliance with verapamil therapy. In ramipril trial (n=30) its mean daily dose was 8.9±0.7 mg. The following main ABPM variables were analyzed: ABPM means and variability, maximal and minimal values, nocturnal BP fall, parameters of Fourier transformation and smoothness index. The morning and evening BP means and morning BP surge (morning – evening BP) were assessed by HBPM. Student’s t-value and Mahalanobis distance were used to evaluate individual value of each variable (“morning” vs “evening” effect). This analysis was first done separately for each trial. After that, combined data were analyzed. Results. Overall antihypertensive effect was more intense with morning ramipril (p<0.05) intake and evening verapamil intake. The t-values ranged 2.2-2.3 for nocturnal BP fall; 2.0-2.1 for night-time BP variability; 3.8-4.3 for morning BP surge. The t-values of office and 24-hour BP were low (0.2-1.7). Conclusion. Morning BP surge based on HBPM is a good instrument for chronotherapy effect assessment. Evening administration of antihypertensive drugs causes nocturnal BP fall shift towards “dipper” status.

Nondipping in Parkinson's Disease

Objective. The aim of this study was to identify patients with Parkinson's disease who showed loss or decrease of nocturnal blood pressure fall (nondipper patients) as a marker of autonomic dysfunction. Presence or absence of orthostatic hypotension was considered to investigate whether alterations in circadian blood pressure pattern are associated with posture-related dysregulation of blood pressure. Methods. 40 patients with Parkinson's disease underwent 24-hour blood pressure monitoring. 21 patients were diagnosed with arterial hypertension and received anti-hypertensive drugs. Nondipper patients were defined as having nocturnal decrease of mean systolic and diastolic blood pressure less than 10%. Presence or absence of orthostatic hypotension was determined by Schellong's test. Results. We identified 35 nondipper patients (88%). Nondipping was detected in 20 patients with orthostatic hypotension (95%) and in 15 patients without orthostatic hypotension (79%). 18 patients with hypertensive and 22 patients with normal blood pressure values were detected. Conclusions. In conclusion 24-hour blood pressure monitoring showed a high prevalence of nondipping in 40 patients with Parkinson's disease with and without orthostatic hypotension independent of coexisting arterial hypertension and antihypertensive treatment. 24-hour blood pressure monitoring may be useful to identify non-dipping as a marker of autonomic dysfunction in patients with Parkinson's disease.

A marked fall in nocturnal blood pressure is associated with the stage of primary open-angle glaucoma in patients with arterial hypertension

Introduction. The aim of this study was to assess blood flow in the vessels of the eyeball and changes in the optic nerve in patients with arterial hypertension and primary open-angle glaucoma. Material and Methods. The patients were divided into groups: 1 (night blood pressure, BP, fall, NBPF, not more than 10%; non-dippers); 2 (NBPF 10–15%, dippers) and 3 (NBPF>15%; extreme dippers). Results. In the group of dippers and extreme dippers, perfusion pressure was significantly lower than that in the non-dippers group, there was reduced thickness of the nerve fibers and a greater decrease in the visual field. Significant relationships between peak systolic, end-diastolic flow in the ophthalmic and central retinal arteries and night perfusion pressure, thickness of nerve fibers, and a loss of visual field were observed. Conclusion. In patients with glaucoma and well-controlled hypertension, a nocturnal BP fall of more than 10% is associated with a greater visual field defect and greater degeneration of the optic nerve fibers. Low minimum diastolic pressure and the level of nocturnal BP fall, but not the absolute value of average arterial BP at night, should be included in the group of specific risk factors in patients with hypertension and open-angle glaucoma. These findings also suggest avoiding excessive lowering of BP at night in this group.

Negative Influence of HIV Infection on Day-Night Blood Pressure Variability

An attenuation of the physiological day-night blood pressure (BP) reduction is an important predictor of cardiovascular (CV) events and death. We compared circadian BP profile in treatment-naive HIV-infected patients and in healthy control subjects. Fifty-two antiretroviral therapy-naive HIV-infected patients (85% men, age 39 ± 11 years, BP 125/78 ± 11/9 mm Hg) and 156 age- and BP-matched HIV-negative controls (85% men, age 39 ± 10 years, BP 125/78 ± 9/7 mm Hg) underwent 24-hour BP monitoring. Subjects with a nocturnal reduction of systolic BP <10% were defined as "nondippers." Nighttime BP was higher in HIV-infected subjects (113/69 ± 11/9 vs 109/67 ± 8/6 mm Hg, P = 0.008/0.005). Nocturnal systolic/diastolic BP reduction was 8.8/13.2% in HIV-positive patients and 11.7/17.2% in HIV negative (P = 0.002/0.001). The prevalence of "nondippers" was 35% and 15%, respectively (P = 0.003). In multivariate analysis, nocturnal systolic BP fall was negatively associated to HIV infection (β = -0.22, P = 0.001). HIV viral load, low CD4 cell count, and AIDS progression risk were all related with a flattened day-night BP profile (P < 0.01). HIV infection per se negatively affects circadian BP rhythm. These findings, obtained in subjects without major CV risk factors and antiretroviral naive, suggest that day-night BP changes may play a role in the HIV-related increase in CV risk.

Morning Surge in Blood Pressure and Cardiovascular Risk

Hypertension is the most powerful risk factor for the cardiovascular diseases, including stroke, coronary artery disease, heart failure, chronic kidney disease, and aortic and peripheral arterial diseases. There is a significant variability in BP level among hypertensives; however, the diagnosis of hypertension and the therapeutic target of BP are based on the average of each BP measured. There is marked diurnal variation in the onset time of cardiovascular events, with the peak being exhibited in early morning. Blood pressure (BP) also exhibits a similar diurnal variation, with a decrease during sleep and a surge in the morning.1,2 In addition to the persistent pressor stress (averaged throughout a 24-hour period), dynamic diurnal variation in pressor stress from the nadir to the peak in the morning, that is, the morning surge in BP, would be expected to progress target organ damage and trigger cardiovascular events, particularly those occurring in the morning.3,4 Because my group first demonstrated that exaggerated morning surge in BP constitutes a risk for stroke independent of 24-hour BP,5 there has been a steady increase in cross-sectional and prospective evidence supporting the idea that morning BP surge is an independent risk factor for cardiovascular disease. Here I review the recent evidence and the remaining unresolved issues on this topic. ### Prospective Findings on Cardiovascular Events Normal morning BP surge is a physiological phenomenon, but an exaggerated morning BP surge is a cardiovascular risk. Thus, the association between the degree of morning BP surge and cardiovascular risk is not linear but rather has a threshold. There have been 6 prospective studies demonstrating that the morning surge in BP is a risk for cardiovascular events (Table 1).5–10 These studies have used 3 different definitions of the morning BP surge as follows (Figure 1): (1) a sleep-trough surge defined as the morning BP (2-hour …

The Bedtime Administration Ameliorates Blood Pressure Variability and Reduces Urinary Albumin Excretion in Amlodipine-Olmesartan Combination Therapy

Chronotherapy has the potential to improve blood pressure (BP) variability and to decrease stroke and cardiovascular events. The present study examined the efficacy and safety of the bedtime administration in amlodipine-olmesartan combination therapy, as compared with the morning administration. The present study was an open-label, randomized crossover study of the effects of the morning vs. bedtime administration of amlodipine-olmesartan combination. The subject was 31 essential hypertensive patients. Morning BP surge (MBPS) and nocturnal BP pattern were analyzed from ambulatory BP data. Glucose and lipid profiles and cardiovascular-renal data were also collected. The bedtime administration reduced MBPS significantly (24.2 ± 13.5 mmHg vs. 32.3 ± 14.2 mmHg, p < 0.001) with no excessive nocturnal BP fall. In nondipper, the bedtime administration significantly improved nocturnal BP. On the other hand, it did not reduce nocturnal BP in dipper. Urinary albumin/creatinine ratio was lower in the bedtime administration than in the morning administration (42.5 ± 59.9 mg/g vs. 75.3 ± 26.4 mg/g, p = 0.044). In amlodipine-olmesartan combination therapy, the bedtime administration reduced better MBPS with correcting nocturnal BP fall and improved urinary albumin excretion. The bedtime dosing of amlodipine and olmesartan seems more apt than the morning dose to obtain the therapeutic goal.

Autonomic nervous system and endothelial peripheral dysfunction in normal tension glaucoma patients

Abstract Purpose To define parameters of autonomic nervous system activity and peripheral vascular reactive hyperemia in normal tension glaucoma patients. Methods Ambulatory 24‐hour electrocardiogram and blood pressure (BP) monitoring by using Lifecard CF and SpaceLab 90207‐30 combined with occlusion provocation test were carried out in 54 NTG patients (44 women, mean age 59.7) and 43 matched control subjects (34 women, mean age 57.0). Heart rate variability (HRV) time and frequency domain parameters [low‐frequency (LF), high‐frequency (HR) and LF/HF ratio], and blood pressure variability (BPV) were calculated and analyzed for both study groups. Postocclusive hyperemia response parameters (TM ‐ time to peak flow, TH –half‐time hyperaemia, TR –time to rest flow, BZ‐biological zero and MAX – maximum hyperemic response) were compared for patients with a nocturnal fall in mean BP (MPB) of less than 10% (non‐dippers), of 10‐20% (dippers) and of more than 20% (over‐dippers) Results NTG patients demonstrated higher LF and LF/HF values for 24‐hour period, day‐time and night time than control subjects. There was no difference in BPV between study groups (10.4 ± 1.9 vs. 10.5 ± 2.1, p=0.790). In NTG patients, TH was significantly higher (79.0 ± 80.9 s vs. 51.5 ± 35.3 s, p=0.028) and BZ was significantly lower (2.3 ± 1.0 vs. 3.1 ± 2.0, p=0.009) as compared to the control group. There was statistically significant difference between NTG non‐dippers, dippers and over–dippers in the BZ parameter (2.3 ± 0.9 vs. 2.7 ± 1.3 vs. 1.4 ± 0.4 p=0.024). Conclusion NTG patients exhibit abnormal ANS system activity and a different systemic hyperemia response as compared with healthy subjects.

Non-dipping pattern of hypertension and obstructive sleep apnea syndrome

There is growing recognition of cardiovascular consequences of obstructive sleep apnea (OSA). Recurrent episodes of airway obstructions result in hypoxia and hypercapnia increasing sympathetic neural tone, which in turn causes vasoconstriction and marked increases in blood pressure (BP). BP response to OSA may be important in understanding the absence of nocturnal BP fall in the subgroup of hypertensive patients termed 'non-dippers'. Even mild sleep apnea can increase nocturnal BP through different mechanisms including hypoxemia, sympathetic activation, mechanical changes and disruption of normal sleep. Sleep apnea may be an important factor in determining the increased cardiovascular risk in hypertensive non-dippers. Effective treatment of sleep apnea may attenuate neurohumoral and metabolic abnormalities, improve diurnal BP control and conceivably reduce cardiovascular risk. This review examines the evidence linking OSA to non-dipping pattern of hypertension, and discusses potential mechanisms underlying this link. We will review first, prognostic value of nighttime BP; second, the cardiovascular consequences of sleep apnea; third, the evidence for altered diurnal BP profile in sleep apnea; fourth, the mechanisms contributing to both nocturnal and daytime hypertension in sleep apnea; fifth, the benefits of sleep apnea treatment and finally implications for hypertension management.

Nocturnal blood pressure fall as predictor of diabetic nephropathy in hypertensive patients with type 2 diabetes.

BackgroundHypertensive patients with reduced blood pressure fall (BPF) at night are at higher risk of cardiovascular events (CVE).MethodsWe evaluated in hypertensive diabetic patients, if a reduced nocturnal BPF can precedes the development of diabetic nephropathy (DN). We followed 70 patients with normal urinary albumin excretion (UAE) for two years. We performed 24-hours ambulatory BP monitoring in baseline and at the end of the study.ResultsFourteen (20%) patients (GI) developed DN (N = 11) and/or CVE (n = 4). Compared to the remaining 56 patients (GII) in baseline, GI had similar diurnal systolic (SBP) and diastolic BP (DBP), but higher nocturnal SBP (138 ± 15 vs 129 ± 16 mmHg; p < 0.05) and DBP (83 ± 12 vs 75 ± 11 mmHg; p < 0,05). Basal nocturnal SBP correlated with occurrence of DN and CVE (R = 0.26; P < 0.05) and with UAE at the end of the study (r = 0.3; p < 0.05). Basal BPF (%) correlated with final UAE (r = -0.31; p < 0.05). In patients who developed DN, reductions occurred in nocturnal systolic BPF (12 ± 5 vs 3 ± 6%, p < 0,01) and diastolic BPF (15 ± 8 vs 4 ± 10%, p < 0,01) while no changes were observed in diurnal SBP (153 ± 17 vs 156 ± 16 mmHg, NS) and DBP (91 ± 9 vs 90 ± 7 mmHg, NS). Patients with final UAE < 20 μg/min, had no changes in nocturnal and diurnal BP.ConclusionsOur results suggests that elevations in nocturnal BP precedes DN and increases the risk to develop CVE in hypertensive patients with T2DM.

NOCTURNAL BLOOD PRESSURE FALL: DOES IT REALLY MATTERS: PP.14.39

Objective: Ambulatory blood pressure (ABP) permits blood pressure (BP) measurement during daytime and nighttime. In some patients, the nocturnal BP fall may be absent or reversed (non-dippers). We examined the incidence of cardiac arrhythmias and left ventricular hypertrophy (LVH) in untreated dipper and non-dipper (ND) hypertensive patients. Methods: Eighty newly diagnosed untreated hypertensive patients were enrolled. All patients underwent 24 hours BP monitoring using a noninvasive automatic ABP monitoring system, 48 hours continuous ECG recording and standard echocardiography. Patients were considered hypertensive if the mean BP was 135 or more for systolic, and/or 85 or more mmHg for diastolic BP on ABP monitoring. ND patients were identified by absence of significant (>10%) nocturnal BP fall. Results: Fifty patients (62.5%) of the study population were ND. No differences were noted in the mean 24 hour systolic and diastolic BP (137.4 ± 6.1 vs. 135.4 ± 3.7 and 81.4 ± 8.6 vs. 79.7 ± 3.3), or in diurnal systolic and diastolic BP (144 ± 9.3 vs. 145 ± 3.8 and 83.9 ± 8.2 vs. 84.9 ± 5.1 mmHg) in ND and dippers respectively, p = NS. However, mean nocturnal systolic and diastolic BP were significantly higher in the ND group (139.7 ± 13.2 vs.125.4 ± 5 and 79.4 ± 10.1 vs.74.6 ± 3.3 mmHg, p < 0.05). LVH was observed in 47 patients (58.7%): 42 (84%) in the ND group, compared to only 5 (16.6%) in the dipper group, P < 0.01. Mean septal and posterior wall thickness was 1.25 ± 0.12 and 1.22 ± 0.1 vs. 0.89 ± 0.16 and 0.91 ± 0.24 cm in ND and dippers respectively, P < 0.01. No lethal arrhythmias were observed, with more prevalent ventricular and supraventricular ectopics in the ND group (38(76%), vs. 5(16.6%) patients), of which ventricular ectopics were the most significant: 32(64%) vs. 4(13.3%) patients, P<0.01. Arrhythmias were more prevalent in patients who had LVH compared to those with normal LV wall thickness: 36(76.5%) vs. 8(24.2%) patients, P < 0.01. Conclusions: Non-dipper hypertensive patients are more prone to have ventricular arrhythmias and to develop LVH compared with dipper hypertensive patients. Significant correlation was observed between LVH and arrhythmia occurrence in this study.

Relationship Between Exercise Heart Rate Recovery and Circadian Blood Pressure Pattern

The aim of the present cross-sectional study was to evaluate heart rate recovery (HRR) in normotensive and hypertensive individuals with either nondipper or dipper type circadian rhythm of blood pressure. Eighty-five patients were divided into 4 groups according to the presence of hypertension and pattern of circadian blood pressure as follows: (1) normotensive/dipper, n=20; (2) normotensive/nondipper, n=21; (3) hypertensive/dipper, n=22; and (4) hypertensive/nondipper, n=22. HRR indices were calculated by subtracting first, second, and third minute heart rates from the maximal heart rate obtained during stress testing and designated as HRR1, HRR2, and HRR3. Mean HRR1 values (29.7+/-4.0 vs 26.6+/-3.7, P=.016) were significantly higher in the normotensive/dipper group than the normotensive/nondipper group. Mean HRR1 values (28.6+/-4.0 vs 24.8+/-4.6 beats per minute, P=.007) were higher in the hypertensive/dipper group than the hypertensive/nondipper group. Spearman's correlation analyses revealed a positive correlation between degree of nighttime dipping and HRR1 (r=.600, P=.001). The correlation coefficient between degree of nighttime dipping and HRR1 was higher in the hypertensive group than the normotensive group (r=.676, P=.001 and r=.575, P=.001, respectively). Blunting of the nocturnal fall in blood pressure associates with a delayed recovery of heart rate after graded maximal exercise in both normotensive and hypertensive groups.

AMBULATORY ARTERIAL STIFFNESS INDEX AND BRACHIAL PULSE PRESSURE: THE INFLUENCE OF CIRCADIAN BLOOD PRESSURE RHYTHM IN NORMOTENSIVE ADOLESCENTS: PP.3.114

Background: The ambulatory arterial stiffness index (AASI) is a new index that reflects the dynamic relation between diastolic and systolic blood pressure though the circadian blood pressure rhythm. The purpose of this study was to investigate the association between AASI, dipping status and pulse pressure as a index of arterial stiffness in normotensive adolescents. Methods: This was a cross-sectional study conducted with 253 high school students (115 boys and 138 girls), aged between 12 to 18 years (14.89 ± 1.7). A 24 hours ambulatory blood pressure monitoring was carried out to all patients using a Spacelabs monitor. Normal dipping was defined as a > or equal 10% decline in mean systolic and diastolic ambulatory blood pressure from day to night. We determined the diurnal and nocturnal blood pressure and brachial pulse pressure values and computed AASI for each participant. Results: AASI was a strong predictor for systolic and diastolic nocturnal blood pressure fall (r = −0.369 and −0.305, respectively; P < 0.0001). No gender difference was apparent for these characteristics. Additionaly, AASI predicted the status of dipping/nondipping (P = 0.002). Nondippers showed significantly higher AASI than dippers (0.407 ± 0.17 vs. 0.295 ± 0.13; P < 0.0001). However, dipper and nondipper conditions were not affected the association between AASI and brachial pulse pressure (r = 0.176; P = 0.005). Conclusion: AASI is strongly correlated with nocturnal blood pressure fall and is increased in nondipping. Additionallly, we show that the association between brachial pulse as indicator of arterial stiffness and AASI is independent of the characterization of the dipping or notdipping status in normotensive adolescents.

ADVERSE EFFECTS OF HIV INFECTION ON DAY-NIGHT BLOOD PRESSURE VARIABILITY: PP.14.29

Objective: An attenuation of the physiological day-night blood pressure (BP) reduction is an important predictor of cardiovascular events and death. Human immunodeficiency virus (HIV) infection has been linked with atherosclerotic cardiovascular complications, irrespective of antiretroviral therapy. It is unclear whether patients with HIV infection have an attenuated nocturnal BP reduction. Design: Cross-sectional case-control study, case:control matching ratio 1:3. Methods: Fifty-two antiretroviral therapy-naïve-HIV-infected patients (85% men, age 39 ± 11 years, BP 125/78 ± 11/9 mmHg) and 156 age- and BP-matched healthy controls (85% men, age 39 ± 10 years, BP 125/78 ± 9/7 mmHg) underwent 24-hour BP monitoring. Hypertension, diabetes, cardiovascular and renal disease, obesity, treatment with vasoactive drugs were exclusion criteria. Subjects with a nocturnal reduction of systolic BP <10% were defined as nondippers. Results: Average daytime BP did not differ in HIV and control subjects (124/80 ± 11/9 vs 124/79 ± 9/7 mmHg, p = n.s.). Nighttime BP was higher in HIV-infected subjects (113/69 ± 11/9 vs 109/67 ± 8/6 mmHg, p = 0.008/0.005). As shown in the Figure, nocturnal systolic/diastolic BP reduction was 8.8/13.2% in cases and 11.7/17.2% in controls (p = 0.002/0.001). The prevalence of nondippers was 35% in cases and 15% in controls (p = 0.003). In a multivariate analysis, nocturnal systolic BP fall was predicted by HIV infection (β=-0.22, p = 0.001). HIV viral load, low CD4 + cell count and AIDS progression risk were all related with a flattened day-night BP profile (p < 0.01). Conclusions: HIV infection per se influences negatively circadian BP rhythm. These findings, obtained in subjects without major cardiovascular risk factors and antiretroviral naive, suggest that day-night BP changes may play a role in HIV-related increase in cardiovascular risk.

ENDOTHELIAL DYSFUNCTION IN REFRACTORY HYPERTENSION: CORRELATION BETWEEN BLOOD PRESSURE LEVELS AND NOCTURNAL DIPPING BP IMPAIRMENT: PP.6.261

Introduction: There is marked association between hypertensive disease and the absence of the nocturnal blood pressure (BP) fall. There is also evidence of correlation between endothelial dysfunction and the non-dipping pattern which is associated with increased cardiovascular mortality. In this study we aimed to evaluate the influence of BP levels on endothelium dependent (Flow Mediated Dilation – FMD) and non-dependent (Nitroglycerin – NTG) vasodilation and on the presence of dipping profile (evaluated by ABPM) in resistant hypertensive patients controlled (CRH) or uncontrolled (UCRH). Methods: Refractory hypertensive (RH) patients (n = 76) were divided in 2 groups: CRH (n = 40; M14/ F26; 50,3 + 6,4 yrs) and UCRH (n = 36; M9/F27; 48 + 5,1 yrs). Normotensive individuals (NT, n = 29; M11/F17; 46,1 ± 10,2 yrs) constituted the third group. BP was measured by using ABPM in two occasions. FMD was performed and evaluated by non participating viewers. Statistics: Variables were compared by ANOVA test and Dunn's test was used for multiple comparisons. Pearson's coefficient was used to correlate variable. Results: The UCRH group presented the highest BP levels of the three groups. The FMD tests unveiled that the UCRH patients had a greater impairment of the endothelial function (6,9 + 0,5%) in comparison to the CRH patients (7,5 + 0,5%) (p < 0,05) and that also occurred when comparing the latter group to control subjects (12,0 + 1,4%) (p < 0.001). A positive correlation (Pearson) between 24 hour BP and endothelial dysfunction in the UCRH (p < 0,001; R = 63%) and CRH (p < 0,0001; r = 71%) groups was also noted. In addition, the data revealed nocturnal BP decline in UCRH subjects was less evident than in CRH (10,8 + 4,9 vs. 22,4 + 7,2 mmHg). Conclusions: We concluded that there is a direct correlation between BP levels and endothelial dysfunction both greater in UCRH patients than in CRH patients. The vascular function impairment probably determines the attenuated dipping blood pressure pattern in the hypertensive groups, especially the former.

Nocturnal nondipping and left ventricular hypertrophy in hypertension: an updated review

The classification of hypertensive subjects according to circadian blood pressure (BP) variations (i.e., dipping vs nondipping) is a useful means for reliable individual risk stratification and effective therapeutic decision-making. Increasing evidence, although not univocal, suggests that a reduced nocturnal BP fall relates to an excess of cardiovascular complications. The association between nondipping status with left ventricular hypertrophy (LVH) and its therapeutic implications are still debated; in this article we examined the studies published in the last decade on this controversial issue. The studies identified by a PubMed search were eligible for the analysis if they fulfilled the following criteria: full articles in English, published from 1 January 2000 to 31 December 2009, and inclusion of adult or elderly subjects. According to these criteria, 26 studies encompassing 3877 participants have been selected. A total of 17 studies for a total of 2497 subjects were positive for a link between nondipping and LVH, whereas the remaining nine studies were negative. Notably, three studies that accurately defined the nondipping status on the basis of two consistent ambulatory blood pressure monitoring sessions over a short time interval showed a significant association of this pattern with LVH; this suggests that a persisting nondipping pattern is associated with a more pronounced cardiac involvement. Preliminary data support the view that nondipping may be reverted to dipping by chronotherapy and by diuretics in salt-sensitive patients. Whether restoring the normal nocturnal BP dip in hypertensives with LVH regresses cardiac damage at present remains an untested hypothesis.

EFFECTS OF ROSUVASTATIN ON BLOOD PRESSURE IN HYPERTENSIVE SUBJECTS WITH DYSLIPIDEMIA: 5D.06

Background and Aims: Blood pressure lowering effects of statins remains controversial, although it has been reported endothelium-dependent vasodilation wich is reduced in dyslipidemic subjects. The objective of the present study was to assess the effects of rosuvastatin on ambulatory blood pressure in hypertensive subjects with dyslipidemia. Subjects and Methods: 57 subjects with essential hypertension were included, 54.5 ± 9.3 years old (31 women). All of them were previously treated with ACEI, ARB or calcium channel blockers. As they were hypercholesterolemic, they were allocated to receive either dietary therapy or a dose of 10 mg of rosuvastatin (qd) at bedtime administration for 8 weeks. 24-hour ambulatory blood pressure monitoring was used to analyse effects on 24-hour blood pressure before and after treatment. Results: Neither 24-hour blood pressure nor lipid profile changes were detected on those subjects after 8 weeks with dietary therapy. On the opposite, those who received rosuvastatin 10 mg(qd) at bedtime (n: 30), systolic and diastolic ambulatory blood pressure decreased 5.3 and 4.1 mmHg. Also daytime and nighttime blood pressure decreased (4.7/5 mmHg at daytime and 7.6/4.5 at nighttime) p < 0.0001. Higher nocturnal blood pressure fall was evident with rosuvastatin (2.64%, p < 0.05). Total and LDL-cholesterol reduced and lipid goals were achieved at 73.3% of those subjects receiving rosuvastatin. Conclusions: Rosuvastatin reduces ambulatory blood pressure and increases nocturnal blood pressure decline when administered at bedtime apart from its lipid lowering effects. This blood pressure lowering effect may be related to improved endothelium dysfunction that use to be common at dyslipidemic subjects.

IMPACT OF AMBULATORY BLOOD PRESSURE MONITORING ON SLEEP QUALITY AND BLOOD PRESSURE: PP.3.127

Objective: During nocturnal non-invasive ambulatory blood pressure monitoring (ABPM), inevitably an undesirable external stimulus due to pump noise and pressure produced by cuff inflation may affect the quality of sleep, influence the physiological nocturnal blood pressure fall and consequently affect dipping status. We sought to investigate whether blood pressure monitoring provokes awakenings and changes in sleep quality, blood pressure and/or heart rate. Design and Method: The study population consisted of 108 consecutive subjects with stage I-II essential hypertension (aged 54 ± 9 years, 59 male, office BP = 148/97 mm Hg). Participants were divided into two groups according to whether they underwent ambulatory blood pressure monitoring (group A, n = 60), or not (group B, n = 48). Repeated measurements of blood pressure were registered with non-invasive automatic blood pressure monitors (Spacelabs 90207, Welch Allyn 6100S devices) every 20 min. Self-reported data regarding the quality of sleep, numbers and duration of arousal were obtained via standardized questionnaire. Results: Group A compared to group B demonstrated a small but significant increase in the number of nocturnal awakenings (2.8 vs 1.2, p = 0.045), although their duration did not significantly differ (p = NS). However, the two groups exhibited similar mean values of nocturnal blood pressure and heart rate (121/73 vs 119/71 mm Hg, 67 vs 65 beats/min, p = NS in both cases). The reported sleep quality did not differ between the two groups but both sleep quality and higher numbers of awakenings (>3) were associated with non-dipping status (p < 0.05, in both cases). Conclusions: Our findings indicate that even though ambulatory blood pressure monitoring induces modest sleep disturbances, it can accurately evaluate night time blood pressure profile and heart rate, without affecting sleep efficiency and quality. Sleep evaluation may be particularly useful in essential hypertension, as poor quality of nocturnal sleep was associated with non-dipping status.

SERUM PHOSPHATE IN WHITE COAT HYPERTENSIVE PATIENTS: FOCUS ON DIPPING STATUS AND METABOLIC SYNDROME: 5B.05

Objective: Recent studies indicate an association of serum phosphate levels with blood pressure in hypertensive patients. A growing body of evidence suggests that white coat hypertension (WCH) is associated with target organ damage. Furthermore, metabolic syndrome (MS) and non-dipping pattern are also associated with increased cardiovascular risk. The purpose of this study was to explore the nocturnal blood pressure fall in WCH patients according to their serum phosphate, calcium levels and MS components. Design and Methods: The study comprised 2600 patients with WCH who attended our outpatient clinics. All patients underwent repeated office blood pressure measurements, 24-h ambulatory blood pressure monitoring, full clinical and laboratory evaluation. The diagnosis of MS was made according to the Adult Treatment Panel III criteria. Dipping pattern was defined as ‘dippers’ with nocturnal systolic blood pressure (NSBP) fall greater than or equal to 10% but less than 20%,‘non-dippers’ with NSBP fall greater than or equal to 0% but less than 10%, ‘extreme dippers’ with NSBP fall greater than or equal to 20%, and ‘reverse dippers’ with NSBP increase. Results: ‘Extreme dippers’ were 413, ‘dippers’ 1337, ‘non-dippers’ 734 and ‘reverse dippers’ 116. ‘Reverse dippers’ presented with significantly lower levels of serum phosphate, while ‘extreme dippers’ had significantly higher levels (3.39 ± 3.29 vs 3.58 ± 3.52 mg/dl, p < 0.0001). Grouping the patients according to the number of MS components, the main observation was the inverse relationship of serum phosphate to MS components (3.53 ± 0.36 to 3.50 ± 0.38 to 3.49 ± 0.38 to 3.44 ± 0.36 to 3.35 ± 0.31 mg/dl, p = 0.003). Conclusions: WCH patients with low phosphate levels appear to have impaired metabolic profile and higher incidence of non dipping profile. This observation may be important for the stratification of cardiovascular risk in WCH patients.

Serum phosphate in white-coat hypertensive patients: focus on dipping status and metabolic syndrome

Recent studies indicate an association between serum phosphate levels and blood pressure in hypertensive patients. A growing body of evidence suggests that white-coat hypertension (WCH) is associated with target organ damage. Furthermore, metabolic syndrome (MS) and a non-dipping pattern are associated with increased cardiovascular risk. The purpose of this study was to explore the nocturnal blood pressure fall in patients with WCH according to their serum phosphate levels and number of MS components fulfilled. The study included 2600 patients with WCH who attended our outpatient clinics. All patients underwent repeated office blood pressure measurements, 24-h ambulatory blood pressure monitoring and full clinical and laboratory evaluation. The diagnosis of MS was made according to the Adult Treatment Panel III criteria. Dipping pattern was defined as follows: 'dippers' had a nocturnal systolic blood pressure (NSBP) fall > or =10% but <20%; 'non-dippers' had an NSBP fall <10%; 'extreme dippers' had an NSBP fall > or =20% and 'reverse dippers' had an NSBP increase. There were 314 extreme dippers, 1337 dippers, 734 non-dippers and 116 reverse dippers. Reverse dippers presented with significantly lower levels of serum phosphate, whereas extreme dippers had significantly higher levels (3.39+/-3.29 vs. 3.58+/-3.52 mg per 100 ml, P<0.0001). The patients were classified according to the number of MS components and the main observation was the inverse relationship of serum phosphate with MS components (3.53+/-0.36, 3.50+/-0.38, 3.49+/-0.38, 3.44+/-0.36 and 3.35+/-0.31 mg per 100 ml, respectively, P=0.003). Patients with WCH and low serum phosphate levels appear to have a higher incidence of a non-dipping NSBP profile and an impaired metabolic profile. This observation may be important for the stratification of the cardiovascular risk in WCH patients.