Ambulatory Blood Pressure In Relation Research Articles

S-32-3: RECENT IDACO ANALYSIS ON THE RISK OF PROGRESSION TO SUSTAINED HYPERTENSION FROM WHITE-COAT HYPERTENSION OR MASKED HYPERTENSION

In the general population, the cardiovascular risk is increased in patients with masked hypertension (MH), whereas in individuals with white-coat hypertension (WCH) it is virtually the same as in the normotensive individuals. However, no conclusive evidence exists as to whether WCH and MH are accompanied by a greater rate of development of a sustained hypertensive state, i.e. hypertension both in and outside the clinical environment. We investigated the risk of progression to sustained hypertension in initially untreated participants of cohort studies included in the International Database on Ambulatory blood pressure in relation to Cardiovascular Outcome (IDACO) study. Within the IDACO, 5 populations comprising 1081 individuals had ambulatory (ABP) and conventional (CBP) blood pressure measured at baseline and at follow up. We excluded from the analysis subjects on BP-lowering treatment at baseline (n = 252) and individuals with untreated sustained hypertension at baseline (n = 80), leaving 749 subjects included in the current analysis. The cut-off value for elevated CBP was > = 140/90 mm Hg and for daytime ABP > = 135/85 mm Hg. At baseline, 110 individuals (14.7%) was defined as MH, 64 subjects as WCH (8.5%), and 575 (76.8%) as normotensives. MH patients were older (50 vs 45 years compared to normotensives, P < 0.01) and more frequently male (50.9 vs 31.5% compared to normotensives, P < 0.01). During median follow-up of 9.7 years, there were 264 incident cases of sustained hypertension. In the analyses adjusted for cohort, sex, age, body mass index, smoking and drinking, both MH (HR 2.23, 95%CI 1.57 to 3.17) and WCH (HR 1.84, 95%CI 1.37 to 2.47) significantly increased risk of progression to sustained hypertension. In conclusion, long-term risk of progression to sustained hypertension is 2-fold higher in individuals with masked hypertension or white coat hypertension at baseline as compared to normotensive subjects at baseline. However, this observation might be due to more frequent initiation of antihypertensive therapy in both groups.

Isolated diastolic hypertension in the IDACO study.

Background: The prognostic implications of isolated diastolic hypertension (IDH), as defined by 2017 American College of Cardiology (ACC)/ American Heart Association (AHA) guidelines, have not been tested using 24-h ambulatory BP monitor (ABPM) thresholds. Methods: We analyzed data from 11,135 participants in the International Database on Ambulatory Blood Pressure in Relation to Cardiovascular Outcomes (IDACO). Using either 24-h mean ABPM values or mean nighttime ABPM values, we performed Cox regression to test the independent associations of IDH with death or cardiovascular events. Analyses were conducted in the cohort overall, as well as after stratification by age (<50 years vs ≥50 years). Results: The median age at baseline was 54.7 years and 49% were female. Over a median follow-up of 13.8 years, 2,836 participants died and 2,049 experienced a cardiovascular event. Overall, irrespective of age, IDH on 24-h ABPM defined by 2017 ACC/AHA criteria was not significantly associated with death (Hazard Ratio [HR] 0.95 [95% CI 0.79-1.13]) or cardiovascular events (HR 1.14 [95% CI 0.94-1.40]), compared with normotension. However, among the subgroup <50 years old, IDH was associated with excess risk for cardiovascular events (2.87 [95% CI 1.72-4.80]), with evidence for effect modification on the basis of age (P-interaction <0.001). Conclusions: Using ABPM data, this study suggests that IDH defined by 2017 ACC/AHA criteria is not a risk factor for cardiovascular disease in adults aged 50 years or older but is a risk factor among younger adults. Thus, age is an important consideration in the clinical management of adults with IDH.

A comprehensive risk score incorporating 24-hour ambulatory blood pressure.

Although ambulatory blood pressure (BP) monitoring is required for the proper diagnosis and management of hypertension, conventional office BP has not yet been replaced by ambulatory BP in the currently available risk charts. For the current analysis, we selected 9,024 participants from the International Database on Ambulatory blood pressure in relation to Cardiovascular Outcomes (IDACO) aged ≥40 to <80 years with a baseline ambulatory BP recording including ≥6 daytime and ≥3 nighttime reading. Given the age range of the analyzed participants, we focused on systolic BP as a risk factor. Time-to-event analysis was conducted using the Cox model, and the 5-year risk was computed using the established formula used in the Heart “OMics” in AGEing (HOMAGE) study (J Am Heart Assoc 2017:e005231). Age at enrolment averaged 59.0 years, 48.2% women, and average 24 h systolic BP was 125.8 mmHg. The median number of ambulatory readings recorded over 24 h and the median follow-up of the cohort was 55 (ranging across cohorts from 37 to 80) and 13.9 years (from 4.0 to 23.3 years), respectively. All endpoints—composite cardiovascular endpoints, cardiovascular mortality, and total mortality—were positively associated with 24-h systolic BP, being on antihypertensive drug treatment at baseline, age, male sex, smoking, a history of cardiovascular disease, having diabetes, and non-drinking alcohol (P≤0.0032). Total mortality was inversely associated with body mass index and total cholesterol, whereas the composite cardiovascular endpoint and cardiovascular mortality were not. None of the endpoints was associated with Non-Asian versus Asian ethnicity (P≥0.31). Based on these findings, we constructed a risk score for each endpoint. The reference category was assigned to young (40–44 years old), women, no smoker, body mass index between 25–29 kg/m2, total serum cholesterol between 5.17–6.20 mmol/L, no diabetes, no history of cardiovascular disease, drinker, and 24-h ambulatory BP of <110 mmHg. The relative risk of cardiovascular events among the quintile of the scores in the participants was clearly separated, and estimated versus observed outcomes across the quintile groups demonstrated similar trends with showing good agreement. Although replication has not yet been fully achieved, the current risk calculator can be a valuable tool for healthcare providers as well as people for introducing ambulatory BP monitoring to the early detection and intervention for the general population and treatment naïve patients with high BP.

AMBULATORY PULSE PRESSURE COMPONENTS AT AGE 18–40 YEARS CAN PREDICT OUTCOMES

Objective: Risk factors for young adults are of special interest. It has been previously shown that average 24-hour ambulatory pulse pressure (PP) can be expressed as a sum of two components: ‘elastic’ PP (elPP) and ‘stiffening’ PP (stPP) associated, respectively, with arterial stiffness at the diastolic blood pressure (BP) and the pressure dependence of stiffness during the systole. The study objective was to determine elPP and stPP (‘PP components’) from 24-hour ambulatory BP (24-hABP) monitoring and assess their prognostic value for selected types of events for the young age using the International Database of Ambulatory blood pressure in relation to Cardiovascular Outcomes (IDACO). Design and method: Longitudinal population-based study of young adults age 18–40 years from 9 cohorts; Europeans (6 cohorts), Asians (2 cohorts), and South Americans (1 cohort), with baseline observations that included 24-hABP records of adequate quality at baseline. Participants were followed up for events including the incidence of fatal and non-fatal coronary events and fatal and non-fatal heart failure (‘hard cardiac events’) and that of cerebrovascular death and non-fatal stroke (‘hard cerebrovascular events’). The PP components were determined from the individual 24-hABP record using a previously described procedure. For each PP component the hazard ratio (HR) per 1SD increase was determined using Cox regression model adjusted for cohorts (dummy variables) and the baseline characteristics given in Results. Results: Baseline characteristics of the 2635 participants were age 30 ± 5y, males 46%, average 24-hour ambulatory diastolic BP 70 ± 7 mmHg, and heart rate 75 ± 9 beats/min, body mass index 24 ± 4 Kg/m2, smoking 29%, drinking alcohol 43%, serum cholesterol 5.0 ± 1.1 mg/dL, history of cardiovascular disease 2.8%, diabetes mellitus 1.6%, and on antihypertensive drugs 2.1%. Hard cardiac and hard cerebrovascular events occurred during the 13.6 ± 6.2 years of follow up. The elPP and stPP were weakly correlated (r = 0.39). The table shows the calculated HR. Conclusions: For young adults 24-hour ambulatory elPP (but not stPP) shows protective power for hard cardiac events, while stPP (but not elPP) is a risk factor for hard cerebrovascular events.

Clinic and ambulatory blood pressure in relation to the interaction between plasma advanced glycation end products and sodium dietary intake and renal handling.

Advanced glycation end product (AGE) clearance may cause renal tubular injuries, such as changes in sodium reabsorption. We hypothesize that AGEs interact with sodium metabolism to influence blood pressure (BP). The study participants were outpatients who were suspected of having hypertension but had not been treated with antihypertensive medication. Clinic and ambulatory blood pressures were measured at baseline (n = 989) and during follow-up (median, 4.4 years, n = 293). Plasma AGE concentrations were measured by enzyme-linked immunosorbent assay. Twenty-four-hour urine was collected for measurements of creatinine, sodium and lithium. In a cross-sectional analysis (n = 989), subjects in the top quintile versus quintiles 1-4 of plasma AGE concentration had significantly (P ≤ 0.004) lower fractional excretion of lithium (18.3% vs. 21.6%) and fractional distal reabsorption rate of sodium (95.0% vs. 95.8%) but similar BP (P ≥ 0.25). However, there was an interaction between plasma AGE concentration and urinary sodium excretion in relation to diastolic BP (P ≤ 0.058). Only in participants with low urinary sodium chloride excretion (≤6 grams/day, n = 189), clinic (84.3 vs. 80.2 mmHg), 24-h (83.9 vs. 80.4 mmHg), daytime (87.8 vs. 84.8 mmHg) and nighttime (75.1 vs. 72.1 mmHg) diastolic BP at baseline were higher (P ≤ 0.05) in the top quintile than in quintiles 1-4 of plasma AGE concentration. In the longitudinal study (n = 383), similar trends were observed, with significant (P ≤ 0.05) differences in the increment in daytime diastolic BP (6.8 vs. -1.7 mmHg) and incidence of ambulatory and treated hypertension (hazard ratio 3.73) during follow-up. In conclusion, AGEs were associated with high BP, probably via enhanced proximal sodium handling and on low dietary sodium intake.

Isolated Diastolic Hypertension in the IDACO Study: An Age-Stratified Analysis Using 24-Hour Ambulatory Blood Pressure Measurements

[Figure: see text].

BLOOD PRESSURE IN RELATION TO INTERACTION BETWEEN DIETARY SODIUM INTAKE AND SERUM URIC ACID IN CHILDREN AND ADOLESCENTS WITH PRIMARY HYPERTENSION

Abstract Objective: We investigated ambulatory blood pressure in relation to interaction between dietary sodium intake and serum uric acid in children and adolescents with primary hypertension. Design and method: The study subjects were in the age range from 10 to 24 years, admitted in Ruijin Hospital because of hypertension. Ambulatory blood pressure monitoring was performed during hospitalization using SpaceLabs 90217 monitors. We collected 24-hour urine for measurements of sodium excretion. We measured serum uric acid concentration with a blood chemistry autoanalyzer, and defined hyperuricemia as a serum uric acid concentration of at least 5.5 mg/dl. Our analysis was restricted to those with primary hypertension (n = 580). Results: The prevalence of hyperuricemia was 48.7%, being higher in male (n = 252) than female (n = 31, 54.9% vs 25.4%) and in untreated (n = 84) than treated patients (n = 199, 56.4% vs 46.1%). Ambulatory blood pressure did not differ across the quartile distributions of urinary sodium excretion (P &gt; = 0.05), but was significantly (P &lt; = 0.04) higher in patients with hyperuricemia than those without for all components, except 24-hour and daytime systolic blood pressure (P &gt; = 0.15). In multivariable regression analysis adjusted for age, sex, body mass index, current smoking and alcohol intake, there was a significant (P &lt; = 0.03) interaction between urinary sodium excretion and serum uric acid in relation to 24-hour systolic and diastolic blood pressure. Indeed, in the presence of hyperuricemia, 24-hour systolic/diastolic blood pressure was 2.2/1.1 mm Hg higher with 100 mmol increase in urinary sodium excretion. Conclusions: Dietary sodium intake interacts with serum uric acid to be associated with ambulatory blood pressure.

Ambulatory blood pressure in relation to interaction between dietary sodium intake and serum uric acid in the young

Purpose We hypothesise that dietary sodium intake interacts with serum uric acid to influence blood pressure (BP) in children and adolescents. In the present study, we investigated ambulatory BP in relation to hyperuricaemia, dietary sodium intake and their interaction in children and adolescents with hypertension. Materials and methods A total of 616 study participants were 10–24 years old and had primary hypertension diagnosed after admission in a specialised inpatient ward. Ambulatory BP monitoring was performed during hospitalisation. 24-h urine was collected for measurements of electrolytes. Hyperuricaemia was defined as a serum uric acid of ≥327.25 μmol/L in patients <18 years old and of ≥420 and ≥360 μmol/L, respectively, in male and female patients ≥18 years old. Results In adjusted analyses, patients with hyperuricaemia (n = 283), compared with those with normal serum uric acid, had similar 24-h systolic BP (131.7 mmHg, p = 0.54) and a significantly (p ≤ 0.005) lower 24-h diastolic BP (77.5 vs. 80.9 mmHg) and higher 24-h pulse pressure (54.2 vs. 51.7 mmHg). In similar adjusted analyses, 24-h ambulatory pulse pressure, but not systolic/diastolic BP (p ≥ 0.12), significantly differed across the quartile distributions of urinary sodium excretion (p for trend ≤ 0.04). Further adjusted analyses showed significant (p ≤ 0.04) interaction between serum uric acid and urinary sodium excretion in relation to 24-h systolic BP. In patients with hyperuricaemia (p = 0.04), but not those with normal serum uric acid (p = 0.13), 24-h systolic BP was significantly associated with urinary sodium excretion, with a 6.5 ± 2.1 mmHg difference between quartiles 4 and 1. Similar results were observed for daytime and night-time BP and pulse pressure. Conclusions Both hyperuricaemia and higher dietary sodium intake were associated with higher pulse pressure, and their interaction further heightened systolic BP.

Ambulatory Blood Pressure in Relation to Plasma and Urinary Manganese.

The association of blood pressure (BP) with manganese-an essential trace element required for human health-remains poorly studied. In 734 randomly recruited Swiss participants (mean age, 47.5 years; 51.4% women), we related ambulatory BP to 2 biomarkers, plasma manganese (pMn) and the urinary manganese (uMn) excretion. To allow for diurnal variation, we assessed BP and uMn over 24 hours and during wakefulness and sleep, using split urine samples. Twenty-four-hour, daytime, and nighttime systolic/diastolic BPs averaged 119.8/78.1, 123.8/81.2, and 107.0/68.3 mm Hg; the corresponding median uMn were 199.5, 83.0, and 51.5 μmol and median pMn, 0.52 μg/L. In analyses dichotomized by the median of the biomarkers, greater pMn was associated with higher 24-hour systolic/diastolic BP (+4.1/+2.3 mm Hg; P≤0.0003), greater daytime uMn with lower daytime BP (-3.5/-1.9 mm Hg; P≤0.0067), and greater nighttime uMn with higher nighttime BP (+2.9/+1.2 mm Hg; P≤0.046). In multivariable-adjusted analyses, significance (P≤0.030) was retained for the positive association of 24-hour and daytime diastolic BP with pMn and for systolic BP in relation to uMn at night. The association sizes for a 2-fold increment in the biomarkers amounting to 0.77 mm Hg (95% CI, 0.08-1.47 mm Hg), 0.97 (CI, 0.20-1.76) and 1.33 (CI, 0.20-2.50 mm Hg), respectively. In conclusion, there were positive associations between diastolic BP and pMn over 24 hours and during daytime and between systolic BP and uMn at night.

Early morning-Best time window of hourly 24-hour ambulatory blood pressure in relation to hypertensive organ damage: The Japan Morning Surge-Home Blood Pressure study.

The correlations between organ damage and hourly ambulatory blood pressure (BP) have not been established. The patients were 1464 participants of the Japan Morning Surge-Home Blood Pressure (J-HOP) study participants who underwent ambulatory BP monitoring. The hourly systolic BP (SBP) at xo'clock was defined as the average of SBP values measured at times x-30minutes, x, and x+30minutes. The mean age was 64.8±11.6years. The percentage of male participants was 47.8%. The left ventricular mass index (LVMI) was significantly associated with SBP at 6o'clock (r=0.166, P<0.001). The carotid intima-media thickness was significantly associated with SBP at 5o'clock (r=0.196, P<0.001). After adjustment for age, sex, smoking, hyperlipidemia, diabetes mellitus, antihypertensive drug use, clinic SBP, and 24-hour ambulatory SBP, the correlations of the LVMI and hourly SBP at 6o'clock remained significant (beta coefficient=0.125, P<0.01). In conclusion, morning ambulatory systolic BP especially at 5 and 6o'clock was independently associated with organ damage.

Evidence-based proposal for the number of ambulatory readings required for assessing blood pressure level in research settings: an analysis of the IDACO database

Background: Guidelines on the required number of ambulatory blood pressure (ABP) readings focus on individual patients. Clinical researchers often face the dilemma of applying recommendations and discarding potentially valuable information or accepting fewer readings.Methods: Starting from ABP recordings with ≥30/≥10 awake/asleep readings in 4277 participants enrolled in eight population studies in the International Database on Ambulatory Blood Pressure in Relation to Cardiovascular Outcomes (IDACO), we randomly selected a certain number of readings (from 30 to 1 awake and 10 to 1 asleep readings) at a time over 1000 bootstraps at each step. We evaluated: (i) concordance of the ABP level; (ii) consistency of the cross-classification based on office blood pressure and ABP; and (iii) accuracy in predicting cardiovascular complications. For each criterion, we fitted a regression line joining data points relating outcome to the number of readings covering the ranges of 30-20/10-7 for awake/asleep readings.Results: Reducing readings widened the SD of the systolic/diastolic differences between full (reference) and selected recordings from 1.7/1.2 (30 readings) to 14.3/10.3 mm Hg (single reading) during wakefulness, and from 1.9/1.4 to 10.3/7.7 mm Hg during sleep; lowered the κ statistic from 0.94 to 0.63, and decreased the hazard ratio associated with 10/5 mm Hg increments in systolic/diastolic ABP from 1.21/1.14 to 1.06/1.04 during wakefulness and from 1.26/1.17 to 1.14/1.08 during sleep. The first data points falling off these regression lines during wakefulness/sleep corresponded to 8/3 and 8/4 readings for criteria (i) and (iii) and to 5 awake readings for criterion (ii).Conclusions: 24-h ambulatory recordings with ≥8/≥4 awake/asleep readings yielded ABP levels similar to recordings including the guideline-recommended ≥20/≥7 readings. These criteria save valuable data in a research setting, but are not applicable to clinical practice.

Ambulatory blood pressure in relation to oxygen desaturation index as simultaneously assessed by nighttime finger pulse oximetry at home.

We investigated the relationship between ambulatory blood pressure (BP) and oxygen desaturation index (ODI), while accounting for pulse rate and age. ODI was assessed by overnight finger pulse oximetry in 2342 participants on the day of ambulatory BP monitoring, and calculated as the number of desaturation episodes per sleeping hour. Both BP and pulse rate increased significantly (P≤.006) from normal (< 5events/h) to mildly (5-14), moderately (15-30), and severely (≥ 30events/h) elevated ODI. The association for BP was substantially attenuated by accounting for pulse rate (partial r² from .003-.012 to .002-.006). In adjusted analysis, the associations of 24-hour diastolic BP and 24-hour pulse rate with ODI were dependent on age (P≤.0001) and only significant in younger subjects (< 60years, P≤.0001). In conclusion, the association between ambulatory BP and ODI was partially mediated by pulse rate, a measure of sympathetic activity, and was more prominent in younger subjects.

Peripheral and central ambulatory blood pressure in relation to ECG voltage

BackgroundThe heart ejects in the central elastic arteries. No previous study addressed the question whether ECG voltages are more closely associated with central than with peripheral blood pressure (BP).MethodsUsing the oscillometric Mobil-O-Graph 24 h PWA monitor, we measured brachial, central BP and central hemodynamics over 24 hours in 177 men (mean age, 29.1 years), and linked to ECG voltages.ResultsFrom wakefulness to sleep, as documented by diaries, systolic/diastolic BP decreased by 11.7/13.1 mmHg peripherally and by 9.3/13.6 mmHg centrally, whereas pulse pressure (PP) increased by 4.3 mmHg. Over 24 hours and the awake and asleep periods, the peripheral-minus-central differences in systolic/diastolic BPs and pulse pressure averaged 11.8/−1.6, 12.7/−1.8 and 10.3/−1.2 mmHg and 13.4, 14.4 and 11.5 mmHg, respectively (P < 0.0001). Cornel voltage and index averaged 1.18 mV and 114.8 mV × ms. The Cornell voltages were 0.104/0.086 and 0.082/0.105 mV higher in relation to brachial 24-h and asleep systolic/diastolic BP (per 1-SD), respectively, and 0.088/0.90 mV and 0.087/0.107 mV higher in relation to central BP. The corresponding estimates for the Cornel indexes were 9.6/8.6 and 8.2/105 mV × ms peripherally and 8.6/8.9 and 8.8/10.7 mV × ms centrally. The regression slopes were similar for brachial and central BP (P ≥ 0.054). Associations of the ECG measurements with awake BP, PP, the augmentation ratio and pressure amplification did not reach significance.ResultsNIAGEN® safely and effectively raised circulating levels of NAD+ and related metabolites. Although no effect was observed on endothelial function, NIAGEN® significantly lowered PWV as well as systolic (SBP) and diastolic blood pressure (DBP) in all subjects (P < 0.05). When separated by baseline BP status, the BP-lowering effect of NIAGEN® was observed in pre-hypertensive (pHTN, n = 13) but not normotensive (N = 11) individuals (P < 0.01). Interestingly, NIAGEN® was lowered in all subjects regardless of baseline BP status.ConclusionChronic NIAGEN® supplementation lowers SBP in pHTN older adults and reduces aortic stiffness, independent of baseline blood pressure status.TableAssociation of ECG Cornell voltage and indexes with peripheral and central BP.Cornell voltage (SV3 + RaVL, mV)Cornell index (Cornell voltage × QRS duration, mV · ms)Peripheral BPCentral BPPeripheral BPCentral BPEstimate (95% CI)PEstimate (95% CI)PEstimate (95% CI)PEstimate (95% CI)PSystolic BP24-h0.104 (0.016 to 0.191)0.0210.088 (0.0003 to 0.177)0.0499.61 (0.65 to 18.57)0.0368.58 (−0.40 to 17.56)0.061Awake0.086 (−0.001 to 0.175)0.0540.062 (−0.026 to 0.151)0.177.69 (−1.30 to 16.69)0.0935.80 (−3.23 to 14.82)0.21Asleep0.082 (−0.006 to 0.170)0.0680.087 (−0.001 to 0.175)0.0538.17 (−0.82 to 17.16)0.0758.76 (−0.217 to 17.74)0.056Diastolic BP24-h0.086 (−0.002 to 0.174)0.0560.090 (0.002 to 0.178)0.0458.57 (−0.41 to 17.55)0.0618.93 (−0.04 to 17.90)0.051Awake0.056 (−0.032 to 0.145)0.210.060 (−0.029 to 0.149)0.185.62 (−3.42 to 14.65)0.225.97 (−3.06 to 15.00)0.19Asleep BP0.105 (0.017 to 0.192)0.0200.107 (0.019 to 0.194)0.01710.53 (1.60 to 19.47)0.02110.71 (1.78 to 19.64)0.019Pulse pressure24-h0.040 (−0.049 to 0.129)0.380.016 (−0.073 to 0.105)0.723.07 (−5.99 to 12.13)0.501.31 (−7.76 to 10.38)0.77Awake0.048 (−0.041 to 0.137)0.290.012 (−0.077 to 0.101)0.783.63 (−5.43 to 12.68)0.430.68 (−8.40 to 9.74)0.88Asleep0.001 (−0.091 to 0.088)0.980.001 (−0.087 to 0.090)0.98−0.29 (−9.37 to 8.78)0.950.21 (−8.86 to 9.28)0.96ECG refers to electrocardiography. BP stands for blood pressure. Cornell voltage is the voltage sum of S wave in precordial V3 lead (SV3) and R wave in limb aVL lead (ReVL), while Cornell index is the product of QRS duration multiplied by the Cornell voltage. The estimate (95% Confidence Interval, CI) of the association was unadjusted and expressed as 1-SD increase of BP. P value is for significance of the estimate. The association estimates of Cornell voltage (P ≥ 0.054) and index (P ≥ 0.079) with central BP were not significantly different from those estimates with peripheral measurements.ConclusionsThe diurnal rhythm of peripheral and central BP run in parallel. Central BP does not improve the association of Cornell voltage or index with peripheral BP.

Correction

HomeHypertensionVol. 64, No. 2Correction Free AccessCorrectionPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessCorrectionPDF/EPUBCorrection Originally published1 Aug 2014https://doi.org/10.1161/HYP.0000000000000012Hypertension. 2014;64:e1This article corrects the followingBlood Pressure Load Does Not Add to Ambulatory Blood Pressure Level for Cardiovascular Risk StratificationIntroductionIn the Hypertension article by Li et al (Li Y, Thijs L, Boggia J, Asayama K, Hansen TW, Kikuya M, Björklund-Bodegård K, Ohkubo T, Jeppesen J, Torp-Pedersen C, Dolan E, Kuznetsova T, Stolarz-Skrzypek K, Tikhonoff V, Malyutina S, Casiglia E, Nikitin Y, Lind L, Sandoya E, Kawecka-Jaszcz K, Filipovský J, Imai Y, Ibsen H, O’Brien E, Wang J, Staessen JA, on behalf of the International Database on Ambulatory blood pressure in relation to Cardiovascular Outcomes [IDACO] Investigators. Blood Pressure Load Does Not Add to Ambulatory Blood Pressure Level for Cardiovascular Risk Stratification. Hypertension. 2014;63:), a correction was needed.In Table 1, in the column “Characteristics,” the last two rows were mislabeled. Blood glucose, mg/dL should have been Serum cholesterol, mg/dL, and Serum cholesterol, mg/dL should have been Blood glucose, mg/dL.The authors apologize for this error.This correction has been made to the current online version of the article, which is available at http://hyper.ahajournals.org/content/63/5/925.full. Previous Back to top Next FiguresReferencesRelatedDetailsRelated articlesBlood Pressure Load Does Not Add to Ambulatory Blood Pressure Level for Cardiovascular Risk StratificationYan Li, et al. Hypertension. 2014;63:925-933 August 2014Vol 64, Issue 2 Advertisement Article InformationMetrics © 2014 American Heart Association, Inc.https://doi.org/10.1161/HYP.0000000000000012 Originally publishedAugust 1, 2014 PDF download Advertisement

Correction

HomeHypertensionVol. 63, No. 5Correction Free AccessCorrectionPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessCorrectionPDF/EPUBCorrection Originally published1 May 2014https://doi.org/10.1161/HYP.0000000000000008Hypertension. 2014;63:e128In the Hypertension article by Gu et al (Gu Y-M, Thijs L, Li Y, Asayama K, Boggia J, Hansen TW, Liu Y-P, Ohkubo T, Björklund-Bodegård K, Jeppesen J, Dolan E, Torp-Pedersen C, Kuznetsova T, Stolarz-Skrzypek K, Tikhonoff V, Malyutina S, Casiglia E, Nikitin Y, Lind L, Sandoya E, Kawecka-Jaszcz K, Imai Y, Mena LJ, Wang J, O’Brien E, Verhamme P, Filipovský J, Maestre GE, Staessen JA, on behalf of the International Database on Ambulatory blood pressure in relation to Cardiovascular Outcomes (IDACO) Investigators. Outcome-Driven Thresholds for Ambulatory Pulse Pressure in 9938 Participants Recruited From 11 Populations. Hypertension. 2014;63:229–237), a correction was needed.The affiliation for Christian Torp-Pedersen was incorrectly listed as: Copenhagen University Hospital, Copenhagen, Denmark. The correct affiliation is as follows: Department of Health Science and Technology, Aalborg University, Aalborg, Denmark.The authors apologize for the error.This correction has been made to the current online version of the article, which is available at http://hyper.ahajournals.org/content/63/2/229.full. Previous Back to top Next FiguresReferencesRelatedDetails May 2014Vol 63, Issue 5 Advertisement Article InformationMetrics © 2014 American Heart Association, Inc.https://doi.org/10.1161/HYP.0000000000000008 Originally publishedMay 1, 2014 PDF download Advertisement

Interpretation of Ambulatory Blood Pressure Profile for Risk Stratification

See related article, pp 925–933 A solid body of evidence supports the contention that cardiovascular morbidity and mortality are better predicted by ambulatory blood pressure (BP) than by BP measured in the physician’s office.1 Compared with office BP, the main advantage of ambulatory BP monitoring (ABPM) is the number of readings obtained throughout a 24-hour period. Frequent readings during wakefulness and sleep enable clinicians to obtain a more precise estimation of a patient’s BP, to assess BP levels in the outpatient setting, and to study BP variability and circadian profile. However, the clinical use of ABPM to refine cardiovascular risk stratification seems not so simple and immediate. Many numeric techniques exist for describing the features of ambulatory readings, and several ABPM-derived measures have been assessed as potential prognostic factors.1 These include average 24-hour, daytime (awake) and night-time (asleep) BP, dipping pattern, morning surge, pulse pressure, ambulatory arterial stiffness index, BP variability, and BP load.1 Despite the large number of studies addressing the prognostic value of these measures, some conclusions are based on samples with short follow-up duration, narrow age range, and insufficient power. Thus, controversy exists as to which components do have independent prognostic significance.1 In such a context, the new analysis of the International Database on Ambulatory BP in relation to Cardiovascular Outcomes (IDACO) study published in the current issue …

White-Coat Hypertension

> Two statisticians meet . > > -How do you do? > > -How do I do? Compared to whom? > > — Anonymous Thomas Pickering coined the term white-coat hypertension to denote individuals who were not on treatment for hypertension but who had elevated office blood pressure and normal daytime blood pressure measured with ambulatory blood pressure monitoring (ABPM). Clearly, these individuals would be at low cardiovascular risk.1 The traditional definition of white-coat hypertension is based, therefore, on an elevated office blood pressure with a normal blood pressure during the awake period with ABPM. However, because of the contribution of asleep blood pressure as a predictor of outcome, it seems counterproductive to exclude this period from consideration. The most recent European guidelines2 propose, therefore, an alternative definition of white-coat hypertension, which encompasses subjects with office systolic/diastolic blood pressure readings of ≥140/90 mm Hg and a 24-hour blood pressure <130/80 mm Hg. The purpose of this review is to provide new insights into the characteristics, definitions, and cardiovascular risk assessment in persons with white-coat hypertension, and it will be limited primarily to ABPM with a primary focus on prospective studies. ### Prevalence and Diagnosis White-coat hypertension occurs in 15% to 30% of subjects with an elevated office blood pressure,2,3 and the phenomenon is reasonably reproducible.2,4 Although there are no pathognomonic diagnostic features of white-coat hypertension, this condition occurs more frequently in women, older adults, nonsmokers, recently diagnosed patients with hypertension with a limited number of conventional blood pressure measurements in the office setting who have mild hypertension, pregnant women, and subjects without evidence of target organ damage.2,5,6 The misdiagnosis of subjects with white-coat hypertension as being truly hypertensive can result in them being penalized for employment and insurance rating, as well as being prescribed unnecessary lifelong treatment with potential side …

Blood Pressure in Relation to Interactions Between Sodium Dietary Intake and Renal Handling

There is abundant evidence that sodium intake is related to blood pressure. However, the relationship varies between individuals and is probably determined by renal sodium handling. We investigated clinic and ambulatory blood pressure in relation to interactions between sodium dietary intake and renal handling, as assessed by 24-hour urinary sodium excretion and endogenous lithium clearance, respectively. We calculated fractional excretion of lithium and fractional distal reabsorption rate of sodium, as markers of proximal and distal sodium handling, respectively. The 766 subjects included 379 men and 478 ambulatory hypertensive patients. They were never treated (n=697) or did not take antihypertensive medication for ≥2 weeks (n=69). In adjusted analyses, none of the associations of urinary sodium excretion, fractional excretion of lithium, and fractional distal reabsorption rate of sodium with clinic or ambulatory blood pressure were statistically significant (P≥0.09). However, there was significant (P=0.01) interaction between urinary sodium excretion and fractional excretion of lithium in relation to nighttime diastolic blood pressure. In tertile 3 but not tertiles 1 and 2 of fractional excretion of lithium, nighttime diastolic pressure was positively associated with urinary sodium excretion (P=0.03). However, nighttime diastolic pressure was higher in tertile 1 than tertile 3 of fractional excretion of lithium (+2.0 mm Hg; P=0.01), especially in the bottom tertile of urinary sodium excretion (+4.9 mm Hg; P<0.001). Similar trends were observed for nighttime systolic pressure and clinic and 24-hour diastolic pressure. In conclusion, sodium dietary intake and proximal tubular handling interact to be associated with blood pressure.

Is Masked Hypertension Related to Diabetes Mellitus?

We recently read with interest the article by Franklin et al1 concerning the prevalence of masked hypertension (MH) in diabetes mellitus. Analyzing data from the IDACO (The International Database of Ambulatory Blood Pressure in relation to Cardiovascular Outcome) project, the authors revealed that 42.5% of the antihypertensive-treated diabetics had MH (normal clinic blood pressure [BP] and daytime BP within the hypertensive range) and 29.3% of the untreated hypertensive diabetic population had MH. The equivalent cardiovascular risk for the latter patients was higher than the risk for stage 1 of hypertension, but less when compared with stage 2 of hypertension.1 While reading this article, some …

Masked Hypertension in Diabetes Mellitus

Although distinguishing features of masked hypertension in diabetics are well known, the significance of antihypertensive treatment on clinical practice decisions has not been fully explored. We analyzed 9691 subjects from the population-based 11-country International Database on Ambulatory Blood Pressure in Relation to Cardiovascular Outcomes. Prevalence of masked hypertension in untreated normotensive participants was higher ( P &lt;0.0001) among 229 diabetics (29.3%, n=67) than among 5486 nondiabetics (18.8%, n=1031). Over a median of 11.0 years of follow-up, the adjusted risk for a composite cardiovascular end point in untreated diabetic-masked hypertensives tended to be higher than in normotensives (hazard rate [HR], 1.96; 95% confidence interval [CI], 0.97–3.97; P =0.059), similar to untreated stage 1 hypertensives (HR, 1.07; CI, 0.58–1.98; P =0.82), but less than stage 2 hypertensives (HR, 0.53; CI, 0.29–0.99; P =0.048). In contrast, cardiovascular risk was not significantly different in antihypertensive-treated diabetic-masked hypertensives, as compared with the normotensive comparator group (HR, 1.13; CI, 0.54–2.35; P =0.75), stage 1 hypertensives (HR, 0.91; CI, 0.49–1.69; P =0.76), and stage 2 hypertensives (HR, 0.65; CI, 0.35–1.20; P =0.17). In the untreated diabetic-masked hypertensive population, mean conventional systolic/diastolic blood pressure was 129.2±8.0/76.0±7.3 mm Hg, and mean daytime systolic/diastolic blood pressure 141.5±9.1/83.7±6.5 mm Hg. In conclusion, masked hypertension occurred in 29% of untreated diabetics, had comparable cardiovascular risk as stage 1 hypertension, and would require considerable reduction in conventional blood pressure to reach daytime ambulatory treatment goal. Importantly, many hypertensive diabetics when receiving antihypertensive therapy can present with normalized conventional and elevated ambulatory blood pressure that mimics masked hypertension.