24-hour aortic blood pressure variability showed a stronger association with carotid damage than 24-hour brachial blood pressure variability: The SAFAR study.

We aim to compare 24-hour aortic blood pressure variability (BPV) with brachial BPV in relation to carotid damage as estimated by carotid intima-media thickness (CIMT) and cross-sectional area (CCSA). Four hundred and forty five individuals received brachial and aortic 24-hour ambulatory BP monitoring with a validated device (Mobil-O-Graph). Systolic BPV was estimated by average real variability (ARV) and time-weighted standard deviation (wSD). In multiple logistic regression analysis, CIMT > 900 µm was significantly and independently associated with aortic ARV (OR = 1.38; 95% CI: 1.04-1.84), aortic wSD (OR = 1.65; 95% CI: 1.19-2.29) and brachial ARV (OR = 1.53; 95% CI: 1.07-2.18), but not with brachial wSD. CCSA > 90th percentile was significantly and independently associated with aortic ARV (OR = 1.50; 95% CI: 1.07-2.10) and wSD (OR = 1.70; 95% CI: 1.12-2.56), but not with brachial BPVs. In receiver operator characteristics curve analysis, aortic wSD identified CCSA > 90th percentile better than brachial wSD (AUC: 0.73 vs 0.68, P < .01). In conclusion, aortic 24-hour systolic BPV showed a slightly stronger association with carotid damage than brachial BPV.

Non-invasive vascular biomarkers in patients with Behçet's disease: review of the data and future perspectives.

Vascular inflammation in small to large veins and arteries contributes substantially to mortality above that of the general population in Behçet's disease. Recent data verified also the presence of accelerated classical subclinical arterial damage (atheromatosis, arteriosclerosis, arterial hypertrophy) even in patients free of overt vascular complications, and may be complementary to that of vasculitis. Early detection of such vascular damage might provide helpful pathophysiological insight and potentially even guide treatment management. Herein, we review the existing literature for each one of the most widely applied non-invasive vascular biomarkers (assessing endothelial dysfunction, atheromatosis/hypertrophy, arteriosclerosis and central haemodynamic parameters) that are clinically used in primary cardiovascular prevention. We aim to: (i) identify early pathophysiological vascular pathways, complementary to vasculitis, in the development of vascular complications and (ii) identify gaps in knowledge and suggest future research topics. We identified evidence of proof of concept for some of the widely applied non-invasive vascular biomarkers (carotid plaques, pulse wave velocity, flow mediated dilatation). Yet, several steps in their clinical validation process are lacking. Extensive vascular phenotyping of a large prospective observational patient cohort with the application of these easy-to-use, low-cost, free of any adverse effect, non-invasive methods should be performed in order to test their ability to provide clinically meaningful guidance regarding the prognosis and treatment of Behçet's disease.

Albuminuria in Association with Cognitive Function and Dementia: A Systematic Review and Meta-Analysis.

OBJECTIVES: Cerebral microvascular disease is considered to contribute to cognitive dysfunction. We opted to explore whether albuminuria, a marker of systemic microangiopathy, is associated with cognitive impairment, dementia, and cognitive function. DESIGN: Systematic review; independent reviewers screened 2359 articles, derived through the search strategy, for identification of observational studies quantifying an association of albuminuria with the outcomes of interest, abstracted data on study characteristics and results and evaluated studies on quality using the Newcastle-Ottawa scale. SETTING: Community. PARTICIPANTS: Adults. MESUREMENTS: Cognitive impairment and dementia, defined by validated neuropsychological tests or clinical guidelines, respectively, and cognitive function, assessed by validated instruments. RESULTS: Thirty-two eligible studies were identified. Albuminuria was associated with cognitive impairment (Odds Ratio (OR): 1.35, 95% Confidence Interval (CI): 1.19-1.53; 7,852 cases), dementia (OR: 1.35, 95% CI: 1.10-1.65; 5,758 cases), clinical Alzheimer's disease (OR: 1.37, 95% CI: 1.11-1.69; 629 cases) and vascular dementia (OR: 1.96, 95% CI: 1.16-3.31; 186 cases); the effect remained significant among longitudinal, population-based and high quality studies. Time-to-event analysis on prospective studies of non-demented at baseline individuals also showed a significant association with incident dementia (Risk Ratio: 1.52, 95% CI: 1.16-1.99; 971 cases). Worse global cognitive performance (Hedge's g: -0.13, 95% CI: -0.18, -0.09; 68,348 subjects) and accelerated cognitive decline (g: -0.20, 95% CI: -0.34, -0.07; 31,792 subjects) were noted among subjects with albuminuria, who also scored lower in executive function, processing speed, verbal fluency, and verbal memory. CONCLUSIONS: Albuminuria was independently associated with cognitive impairment, dementia and cognitive decline. The stronger effects for vascular dementia and cognitive performance in domains primarily affected by microvascular disease support that the association could be mediated by shared microvascular pathology in the kidney and the brain.

Phenotypes of office systolic blood pressure according to both brachial and aortic measurements: frequencies and associations with carotid hypertrophy in 1861 adults.

BACKGROUND/AIM: Aortic SBP (aSBP) associates with arterial damage more consistently than brachial SBP (bSBP). However, it is unknown how often aSBP is normal in the presence of elevated bSBP, and vice versa; if SBP phenotyping on the basis of bSBP and aSBP cut-off values improves cardiovascular risk stratification. We tested the frequency of four office SBP phenotypes: type I (both normal bSBP and aSBP); type II (high bSBP but normal aSBP); type III (normal bSBP but high aSBP), and type IV (both high bSBP and aSBP), the probability of each phenotype to be associated with increased arterial damage, using type Ia (i.e. normal bSBP and low-normal aSBP) as reference. METHODS: In 1861 participants (age: 54 years, 49.1% men), we measured simultaneously bSBP, aSBP, and carotid cross-sectional wall area with ultrasound. RESULTS: Depending on the applied cut-off values, type II and type III phenotypes represented together 5-11% of the population (0.9-3.4 and 1.8-10.3%, respectively) and type IV around 20%. Subgroups with phenotypes, Ib (i.e. normal bSBP and high-normal aSBP), II, III, and IV had gradually significantly higher probability (by 1.37-1.91, 2.3-3.3, 3.3-8.9 times, and 4.18-6.25, respectively) to present elevated carotid artery cross-sectional wall area compared with the reference group, even after adjustment for DBP and other confounders. CONCLUSIONS: Type II (i.e. isolated high bSBP) and type III (i.e. isolated high aSBP) office SBP phenotypes were common and had intermediate level (between types I and IV) of arterial damage.

Ambulatory Aortic Stiffness Is Associated With Narrow Retinal Arteriolar Caliber in Hypertensives: The SAFAR Study.

BACKGROUND: Arterial stiffness measured under static conditions reclassifies significantly cardiovascular (CV) risk and associates with narrower retinal arterioles. However, arterial stiffness exhibits circadian variation, thus single static stiffness recordings do not correspond to the "usual" 24 hr, awake, and asleep average arterial stiffness. We aimed to test the hypothesis that ambulatory 24 hr, awake, and asleep aortic (a) pulse wave velocity (PWV) associate with retinal vessel calibers, independently of confounders and of static arterial stiffness, in hypertensive individuals free from diabetes and CV disease. METHODS: Digital retinal images were obtained (181 individuals, age: 53.9±10.7 years, 55.2% men) and retinal vessel calibers were measured with validated software to determine central retinal arteriolar and venular equivalents (CRAE and CRVE, respectively); ambulatory (24 hr, awake, asleep) and static office aPWV were estimated by Mobil-O-Graph; and static office carotid to femoral (cf) PWV by SphygmoCor. RESULTS: Regression analysis performed in 320 gradable retinal images showed that, after adjustment for confounders: (i) ambulatory aPWV was significantly associated with narrower retinal arterioles but not with venules; (ii) asleep aPWV had stronger associations with CRAE than awake aPWV; (iii) both ambulatory aPWV and cfPWV were associated mutually independently with narrower retinal arterioles; aPWV introduction in the model of cfPWV, improved model's R2 (P = 0.012). Similar discriminatory ability of 24 hr aPWV and of cfPWV to detect the presence of retinal arteriolar narrowing was found. CONCLUSION: Ambulatory aPWV, estimated by an operator-independent method, provides additional information to cfPWV regarding the associations of arterial stiffness with the retinal vessel calibers.

The Keith-Wagener-Barker and Mitchell-Wong grading systems for hypertensive retinopathy: association with target organ damage in individuals below 55 years.

BACKGROUND: The usefulness of the hypertensive retinopathy classification by Keith-Wagener-Barker (KWB) in clinical practice remains controversial. The simplified Mitchell-Wong grading, combining the two initial KWB' grades in one stage, is proposed as an alternative method; both systems are poorly validated regarding their association with target organ damage. OBJECTIVE: In a population free of cardiovascular disease and diabetes, we aimed to investigate the interobserver and intraobserver agreement of both grading systems, their association with aortic stiffness, carotid hypertrophy or plaques and the role of age and sex on this association. METHODS: Digital retinal images were obtained and graded - according to both classifications - by two independent and blinded observers; aortic stiffness (carotid-femoral pulse wave velocity, m/s) and common carotid hypertrophy (cross-sectional area, mm) or plaques were assessed by tonometry and ultrasound, respectively. RESULTS: From the gradable retinal photos obtained by 200 eyes of 107 consecutive patients (age: 54 ±â€Š13 years, 51% men, 79% hypertensive patients) and after adjustments for confounders, the intraobserver and interobserver level of agreement was as following: KWB 88/64% and Mitchell-Wong 91/71%, respectively; exclusively in younger, not older, individuals aortic stiffness, carotid hypertrophy, but not plaques, were significantly associated with both systems, independently from confounders; no differences regarding target organ damage were found between stages 1 and 2 of KWB. CONCLUSION: Detecting early signs of hypertensive retinopathy may be of value in young individuals; the Mitchell-Wong seems preferable to the KWB classification system only for reasons of simplifying clinical practice.

Asleep home blood pressure monitoring in obstructive sleep apnea: a pilot study.

BACKGROUND: Obstructive sleep apnea (OSA) is known to be related to nocturnal blood pressure (BP) and nondipping hypertension. This pilot study evaluated night-time BP assessed using a home monitor in patients with OSA. PARTICIPANTS AND METHODS: Patients referred to a sleep clinic were subjected to polysomnography, clinic BP measurements, and home BP monitoring using a device that allows daytime (3 days, two duplicate readings per day) and automated night-time BP measurement (3 nights, three readings per night). RESULTS: Thirty-nine patients were included [72% men, mean age 48.7±10.8 years, clinic BP 131.2±19.6/84.1±11.9 mmHg, apnea-hypopnea index (AHI): 35.2±25.7]. All BP measurements were significantly correlated with the polysomnography indices. There was a consistent trend toward stronger correlations of the night-time diastolic home BP with the AHI (r=0.56), the duration of desaturation (0.53), and the maximum (-0.57) and minimum (-0.48) arterial oxygen saturation (all P<0.001). In stepwise multivariate analysis (independent variables age, sex, body weight, smoking status, and BP parameters), the AHI was associated independently with weight and night-time diastolic home BP (R=0.53). CONCLUSION: In patients with OSA, the assessment of night-time BP using a home monitor appears to be feasible and related to the severity of OSA. Given the wide availability of home BP monitoring in clinical practice, this method appears to be useful in the evaluation of BP in patients with OSA.

Assessment of the diurnal blood pressure profile and detection of non-dippers based on home or ambulatory monitoring.

BACKGROUND: A unique advantage of ambulatory blood pressure (ABP) monitoring is the assessment of nocturnal blood pressure (BP) and the detection of non-dippers. This study assessed nocturnal BP and non-dippers using a novel home BP (HBP) monitor. METHODS: Eighty-one hypertensives performed within 2 weeks ABP (24-h, Microlife WatchBP O3) and HBP monitoring (Microlife WatchBPN) during daytime (6 days, duplicate morning and evening measurements) and nighttime (automated asleep measurements, 3 nights, 3 readings/night). Patients' preference in using ABP or HBP was assessed by a questionnaire. RESULTS: Strong associations were found between ABP and HBP (intraclass correlation coefficients for awake systolic/diastolic 0.75/0.81; asleep 0.87/0.85). No statistically significant difference was found between HBP and ABP (mean difference ± SD awake systolic/diastolic 1.5 ± 10.1/-1.1 ± 6.0 mm Hg, P = 0.20/0.09; asleep -0.4 ± 7.8/-1.0 ± 5.3, P = 0.63/0.09). There was substantial agreement (74%, kappa 0.2) between ABP and HBP in the detection of non-dippers, which was similar to the previously reported test-retest reproducibility of repeated ABP monitoring in the diagnosis of non-dippers. Moderate to severe disturbance from ABP monitoring was reported by 18% of the participants and severe restriction of their daily activities by 9, vs. 3 and 1.5%, respectively for HBP (P < 0.001/ <0.01, for comparisons respectively). Nighttime BP monitoring and cuff discomfort were the main complaints for ABP (46 and 32%, respectively) and HBP (34 and 28%), whereas 89% reported more nighttime sleep disturbance by ABP than HBP (P < 0.001). CONCLUSIONS: HBP monitoring appears to be a reliable and well accepted by users alternative to ABP for the assessment of nocturnal BP and the detection of non-dippers.

Automatic office blood pressure measured without doctors or nurses present.

BACKGROUND: We evaluated the agreement between office blood pressure (OBP) measured by a mercury sphygmomanometer (Sphyg) and an automatic (Auto) device without any observers, and compared Auto and Sphyg OBP with ambulatory blood pressure (ABP) and home blood pressure (HBP). METHODS: OBP was measured in 75 hypertensive patients at two sites using an automatic monitor without a doctor or a nurse present and by Sphyg during three clinic visits. Between visits, monitoring of ABP and HBP was also performed. RESULTS: The mean Auto OBP was similar to that of Sphyg OBP and the values were closely correlated (intraclass correlation coefficient=0.84 for systolic OBP and 0.91 for diastolic OBP); however, the difference between Auto and Sphyg systolic OBP (1.6 ± 8.2 mmHg) varied by the first office visit, sex, and the site. Auto systolic OBP was lower than both systolic awake ABP (137.1 ± 14.7 mmHg) and HBP (139.2 ± 15.6 mmHg). Auto systolic OBP and Sphyg OBP were similarly correlated with systolic awake ABP (both r=0.59, P<0.001). The mean Auto diastolic OBP was similar to that of Sphyg OBP (81.1 ± 11.3 vs. 80.3 ± 13.3 mmHg, P=0.20, intraclass correlation coefficient=0.91), and diastolic awake ABP and HBP. Auto diastolic OBP and Sphyg OBP were related to diastolic awake ABP (both r>0.68, P<0.001). In multivariable analyses, neither OBP measure was a significantly stronger predictor of out-of-office blood pressure than the other. CONCLUSION: Auto systolic OBP measured without a doctor or a nurse present was lower than systolic awake ABP and HBP. Auto and rigorously assessed Sphyg OBP had similar means and were similarly related to awake ABP. Auto OBP might be an advantageous alternative to Sphyg measurements in the usual clinic setting.

Diagnostic accuracy of home vs. ambulatory blood pressure monitoring in untreated and treated hypertension.

Several studies with relatively small size and different design and end points have investigated the diagnostic ability of home blood pressure (HBP). This study investigated the usefulness of HBP compared with ambulatory monitoring (ABP) in diagnosing sustained hypertension, white coat phenomenon (WCP) and masked hypertension (MH) in a large sample of untreated and treated subjects using a blood pressure (BP) measurement protocol according to the current guidelines. A total of 613 subjects attending a hypertension clinic (mean age 53±12.4 (s.d.) years, men 57%, untreated 59%) had measurements of clinic BP (three visits, triplicate measurements per visit), HBP (6 days, duplicate morning and evening measurements) and awake ABP (20-min intervals) within 6 weeks. Sustained hypertension was diagnosed in 50% of the participants by ABP and HBP (agreement 89%, κ=0.79), WCP in 14 and 15%, respectively (agreement 89%, κ=0.56) and MH in 16% and 15% (agreement 88%, κ=0.52). Only 4% of the subjects (27/613) showed clinically significant diagnostic disagreement with BP deviation >5 mm Hg above the diagnostic threshold (for HBP or ABP). By taking ABP as reference, the sensitivity, specificity, positive and negative predictive value of HBP in detecting sustained hypertension were 90, 89, 89 and 90%, respectively, WCP 61, 94, 64 and 94% and MH 60, 93, 60 and 93%. Similar diagnostic agreement was found in untreated and treated subjects. HBP appears to be a reliable alternative to ABP in the diagnosis of hypertension and the detection of WCP and MH in both untreated and treated subjects.

Baseline predictors of resistant hypertension in the Anglo-Scandinavian Cardiac Outcome Trial (ASCOT): a risk score to identify those at high-risk.

BACKGROUND: Resistant hypertension is a well recognized clinical entity, which has been inadequately researched to date. METHODS: A multivariable Cox model was developed to identify baseline predictors of developing resistant hypertension among 3666 previously untreated Anglo-Scandinavian Cardiac Outcome Trial (ASCOT) patients and construct a risk score to identify those at high risk. Secondary analyses included evaluations among all 19 257 randomized patients. RESULTS: One-third (1258) of previously untreated, and one-half (9333) of all randomized patients (incidence rates 75.2 and 129.7 per 1000 person-years, respectively) developed resistant hypertension during a median follow-up of 5.3 and 4.8 years, respectively. Increasing strata of baseline SBP (151-160, 161-170, 171-180, and >180 mmHg) were associated with increased risk of developing resistant hypertension [hazard ratio 1.24 (95% confidence interval, CI 0.81-1.88), 1.50 (1.03-2.20), 2.15 (1.47-3.16), and 4.43 (3.04-6.45), respectively]. Diabetes, left ventricular hypertrophy, male sex, and raised BMI, fasting glucose, and alcohol intake were other significant determinants of resistant hypertension. Randomization to amlodipine ±â€Šperindopril vs. atenolol ±â€Šthiazide [0.57 (0.50-0.60)], previous use of aspirin [0.78 (0.62-0.98)], and randomization to atorvastatin vs. placebo [0.87 (0.76-1.00)] significantly reduced the risk of resistant hypertension. Secondary analysis results were similar. The risk score developed allows accurate risk allocation (Harrell's C-statistic 0.71), with excellent calibration (Hosmer-Lemeshow χ statistics, P = 0.99). A 12-fold (8.4-17.4) increased risk among those in the highest vs. lowest risk deciles was apparent. CONCLUSION: Baseline SBP and choice of subsequent antihypertensive therapy were the two most important determinants of resistant hypertension in the ASCOT population. Individuals at high risk of developing resistant hypertension can be easily identified using an integer-based risk score.

Morning hypertension assessed by home or ambulatory monitoring: different aspects of the same phenomenon?

OBJECTIVE: There is increasing interest in morning hypertension assessed using out-of-office blood pressure (BP) measurement methods. This study compared morning BP taken by home (mHBP) versus morning ambulatory BP (mABP) monitoring. METHODS: A total of 588 hypertensives were included [mean age 53 +/- 12.4 (SD) years, 57% men, 59% untreated]. Average mHBP (6 days, duplicate morning measurements) was compared with mABP (first 1, 2 or 3 h after arising, readings at 20-min intervals). Morning 'hypertensives' were defined as individuals with mHBP or mABP at least 135/85 mmHg and morning 'reactors' as those with a difference between mHBP and average home BP or mABP and average awake ambulatory BP at the upper quartile of the respective distribution. RESULTS: Average mABP (2 h) was the closest to mHBP with mean difference 0.4 +/- 14.0/1.2 +/- 8.6 mmHg, 95% confidence intervals -0.8, 1.5/0.5, 1.9, P NS < 0.01, for systolic/diastolic and was strongly correlated with mABP (r = 0.60/0.68, P < 0.001). There was moderate agreement between mHBP and mABP in detecting morning 'hypertensives' (agreement 72%, kappa 0.44, for systolic BP and 75%, kappa 0.51, for diastolic) and slight agreement in detecting morning 'reactors' (agreement 68%, kappa 0.15, for systolic BP and 67%, kappa 0.13, for diastolic). These findings did not change when mABP of 1 or 3 h after arising were used or when untreated and treated individuals were analyzed separately. CONCLUSION: Despite their methodological differences, there seems to be considerable similarity between mHBP and mABP. Thus, both home and ambulatory BP monitoring appear to be interchangeable methods for the assessment of morning hypertension.

Arterial stiffness index based on home (HASI) vs. ambulatory (AASI) blood pressure measurements.

Ambulatory arterial stiffness index (AASI) is a novel index derived from the linear relationship between 24-h ambulatory systolic and diastolic blood pressure (BP) measurements. This study investigated whether 'home arterial stiffness index' (HASI) based on self-home BP measurements is similar to AASI. A total of 483 hypertensive subjects underwent 24-h ambulatory and 6-day home BP monitoring. AASI and HASI were defined as one minus the respective regression slope of diastolic on systolic BP. Mean HASI (0.66+/-0.17) was higher than 24-h (0.33+/-0.15) daytime (0.50+/-0.18) and nighttime AASI (0.37+/-0.19, P<0.001 for all comparisons vs. HASI) and was weakly correlated with 24-h (r=0.14, P<0.01) daytime (r=0.14, P<0.01) and nighttime AASI (r=0.09, P=0.05). Compared to 24-h AASI, HASI was less closely associated with age (r=0.46 and 0.10 respectively, P<0.001 for difference), systolic home BP (r=0.30 and 0.09, P<0.001) and pulse pressure (r=0.52 and 0.20, P<0.001), as well as with 24-h ambulatory systolic BP (r=0.21 and 0.05, P<0.05) and pulse pressure (r=0.56 and 0.25, P<0.001). No satisfactory agreement was observed between HASI and 24-h (agreement 63%, kappa 0.02) daytime (agreement 65%, kappa 0.1) or nighttime AASI (agreement 63%, kappa 0.03) in detecting subjects at the top quartile of the respective distributions. HASI appears to be similar but also has important differences from AASI and is less closely associated with markers of arterial stiffness. These data do not support the view that home BP measurements can replace ambulatory monitoring in the assessment of the arterial stiffness index.

Do proton pump inhibitors attenuate the effect of aspirin on platelet aggregation? A randomized crossover study.

It is common practice to coadminister proton pump inhibitors with aspirin to diminish the risk of upper gastrointestinal bleeding. This is the first study that investigated the potential impact of a proton pump inhibitor on aspirin effects on platelet aggregation. Twenty-four hypertensive subjects eligible for treatment with low-dose enteric-coated aspirin (LDECA) for primary prevention of cardiovascular disease were randomized to receive 100 mg LDECA or 100 mg LDECA plus 30 mg lansoprazole for 4 weeks. Then, participants were crossed over to the alternative regimen for another 4 weeks. Salicylic, gastrin, and pepsinogen I blood level counting were used to ensure adherence to treatment. Platelet aggregation was evaluated by light transmittance aggregometry and PFA100. The LDECA administration reduced arachidonic acid (P < 0.001), collagen (P < 0.01), and epinephrine (P < 0.001) tests. These changes paralleled an increase in collagen/epinephrine duration (P < 0.001) but not in collagen/adenosine diphosphate duration and platelet count. No significant difference was found in any of these platelets' function tests with LDECA alone versus LDECA plus lansoprazole. A significant increase in salicylic levels was observed in patients on LDECA as well as in those on LDECA plus lansoprazole, whereas gastrin and pepsinogen I levels were increased only when lansoprazole was added. These data suggest that the concomitant use of the lansoprazole at 30-mg daily does not influence the long-term effect of LDECA on platelet aggregation. Furthermore, they might imply that an interaction of LDECA with other proton pump inhibitors on platelet aggregation is unlikely.

Long-term reproducibility of home vs. office blood pressure in children and adolescents: the Arsakeion school study.

This study compared the long-term reproducibility of home blood pressure (BP) in comparison with office BP in children and adolescents. Forty-eight subjects (27 boys, mean age 11.3+/-3.1 (s.d.) years) recruited from the Arsakeion school study because of elevated office and/or home BP were assessed with office (1 visit, mercury sphygmomanometer) and home BP measurements (3 days, electronic devices) in two assessments 17+/-4.9 months apart (range 10-26 months). Home and office BP were compared on the basis of the following criteria: (a) s.d. of mean BP; (b) s.d. of differences; (c) variation coefficient (CV); (d) concordance correlation coefficient (CCC); (e) test-retest correlations; (f) correlation with ambulatory BP. (a) The s.d. of mean home BP was lower than that of office BP in both the initial (home BP 9.1/7.1 mm Hg, systolic/diastolic; office BP 13.1/8.0 mm Hg) and the second assessment (9.2/6.0 and 14.9/11.5 respectively). (b) The s.d. of differences was lower for home BP (8.3/6.5 mm Hg, systolic/diastolic) than for office BP (13.9/10.7 mm Hg). (c) The CV of home BP (5.3/6.6, systolic/diastolic) was lower than that of office BP (8.2/10.9). (d) The CCC of home BP (0.54/0.50, systolic/diastolic) was higher than that of office BP (0.51/0.41). (e) Test-retest correlations were closer for home BP (r=0.58/0.52, systolic/diastolic) than for office BP (0.51/0.44). (f) Awake ambulatory BP was more closely associated with home (r=0.77/0.40, systolic/diastolic) than with office BP (0.65/0.24). These data suggest that in children and adolescents the long-term reproducibility of home BP is superior to that of office measurements.

Does dosing antihypertensive drugs at night alter renal or cardiovascular outcome: do we have the evidence?

PURPOSE OF REVIEW: Recent evidence suggests that blood pressure during nighttime and the early morning hours is associated with increased cardiovascular risk independently of the average 24 h blood pressure. The review aims to investigate whether nighttime administration of antihypertensive drugs alters the circadian blood pressure variation and prevents hypertension-induced target organ damage and cardiovascular or renal disease. RECENT FINDINGS: Several studies showed that nighttime administration of antihypertensive drugs has a larger blood pressure lowering effect during nighttime and the early morning hours. Some studies of intermediate endpoints, such as albuminuria, ventricular hypertrophy and carotid thickness suggested beneficial effects of nighttime administration of drugs. Few long-term outcome studies showed impressive cardiovascular protection using nighttime administration of antihypertensive drugs. Owing to methodological issues, however, these studies cannot prove whether, for the same 24 h blood pressure reduction, nighttime dosing provides greater cardiovascular and renal protection than the conventional morning dosing. SUMMARY: Whether nighttime dosing is superior to the conventional morning dosing in improving cardiovascular or renal outcome remains unclear. Randomized outcome studies comparing the same treatment administered in the morning versus at nighttime are needed. Until these data become available nighttime dosing of antihypertensive drugs cannot be recommended.