(Circulation. 2000;102:1139.)
© 2000 American Heart Association, Inc.
Clinical Investigation and Reports |
Response to Antihypertensive Therapy in Older Patients With Sustained and Nonsustained Systolic Hypertension
From the Hypertension and Cardiovascular Rehabilitation Unit (R.H.F., J.A.S., L.T., J.G.), Catholic University of Leuven, Leuven, Belgium; Imperial College (C.J.B.), Hammersmith Hospital, London, UK; Department of Cardiology (D.C.), University of Gent, Gent, Belgium; Department of Internal Medicine (P.W.d.L.), University of Maastricht, Maastricht, the Netherlands; Hypertension Division (J.D.), University Medical Center, Ljubljana, Slovenia; Department of Epidemiology and Health Promotion (M.J.), National Public Health Institute, Helsinki, Finland; Istituto Auxologico Italiano (G.L., G.P.), Ospedale San Luca, Milano, Italy; Beaumont Hospital (E.O.), Dublin, Ireland; Clinica Medica IV (P.P.), Universitá di Padova, Padova, Italy; Hospital "12de Octubre" (J.L.R.), Madrid, Spain; Department of Medicine (H.V.), Helsinki University Central Hospital, Helsinki, Finland; and Department of Medicine and Therapeutics (J.W.), University of Aberdeen, Aberdeen, UK.
Correspondence to R. Fagard, MD, PhD, Department of Medicine, U.Z. Gasthuisberg–Hypertensie, Herestraat 49 B-3000, Leuven, Belgium. E-mail robert.fagard{at}uz.kuleuven.ac.be
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Abstract |
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Background—The goal of the present study was to assess the effect of antihypertensive therapy on clinic (CBP) and ambulatory (ABP) blood pressures, on ECG voltages, and on the incidence of stroke and cardiovascular events in older patients with sustained and nonsustained systolic hypertension.
Methods and Results—Patients who were 
60 years old, with
systolic CBP of 160 to 219 mm Hg and
diastolic CBP of <95 mm Hg, were randomized into the
double-blind placebo-controlled Systolic Hypertension in Europe
(Syst-Eur) Trial. Treatment consisted of nitrendipine, with the
possible addition of enalapril, hydrochlorothiazide, or
both. Patients enrolled in the Ambulatory Blood Pressure Monitoring
Side Project were classified according to daytime systolic
ABP into 1 of 3 subgroups: nonsustained hypertension (<140
mm Hg), mild sustained hypertension (140 to 159 mm Hg), and
moderate sustained hypertension (160 mm Hg). At baseline,
patients with nonsustained hypertension had smaller ECG voltages
(P<0.001) and, during follow-up, a lower incidence of
stroke (P<0.05) and of cardiovascular
complications (P=0.01) than other groups. Active
treatment reduced ABP and CBP in patients with sustained hypertension
but only CBP in patients with nonsustained hypertension
(P<0.001). The influence of active treatment on ECG
voltages (P<0.05) and on the incidence of stroke
(P<0.05) and cardiovascular events
(P=0.06) was more favorable than that of placebo only in
patients with moderate sustained hypertension.
Conclusions—Patients with sustained hypertension had higher ECG voltages and rates of cardiovascular complications than did patients with nonsustained hypertension. The favorable effects of active treatment on these outcomes were only statistically significant in patients with moderate sustained hypertension.
Key Words: blood pressure monitoring • aging • hypertrophy, left ventricular • prognosis • hypertension, white coat • trials
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Introduction |
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TopAbstractIntroductionMethodsResultsDiscussionAppendix 1References |
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Ambulatory blood pressure (ABP) may be normal in patients with elevated clinic pressure (CBP). This subgroup of so-called white coat, isolated clinic or nonsustained hypertensives composes
25% of the hypertensive population.1 2 3 This
phenomenon has been extensively studied in hypertensives in general but
not in isolated systolic hypertension (ISH), which is
present in 10% of the elderly in the seventh decade of life and
in even 25% of octogenarians.4 With regard to target
organ damage, left ventricular mass appeared to be lower in
white coat hypertensives than in patients with sustained
hypertension,5 6 7 8 9 and prognostic stud- ies in hypertensives in general8 10 and in patients
with refractory hypertension11 revealed that the morbidity
or mortality risk was less in patients with low ABP than in patients in
whom hypertension was sustained during ambulatory monitoring. On the
other hand, when the initiation12 13 or
intensification14 of antihypertensive therapy was based on
CBP measurements in patients with elevated CBP and low ABP, CBP was
significantly reduced, whereas ABP hardly changed. The latter finding
together with the contention of some investigators that white coat
hypertension may not be innocuous9 15 might favor the
initiation of drug treatment in these patients. To obtain a better
insight into the cardiovascular consequences of
nonsustained systolic hypertension in the elderly and the
impact of antihypertensive therapy, we analyzed the data from
the Ambulatory Blood Pressure Monitoring Side
Project16 17 of the Systolic Hypertension in
Europe (Syst-Eur) Trial,18 an outcome trial of
antihypertensive treatment in older patients with ISH. To the best of
our knowledge, the Syst-Eur Trial is the only randomized
placebo-controlled trial available that included ABP monitoring in its
design.16 |
Methods |
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Trial Design
The protocol of the Syst-Eur Trial18 was approved by the ethics committees of the University of Leuven and of the participating centers; all subjects gave informed consent. Eligible patients had to be
60 years old. During the run-in period on placebo
treatment, patients were seen at 3 baseline visits 1 month apart. CBP
was measured twice in the sitting position at each visit by use of
standard sphygmomanometry. Patients could be admitted to the
double-blind phase of the trial when they had an average run-in
systolic blood pressure (BP) of 160 to 219 mm Hg with
diastolic BP of <95 mm Hg. After stratification by
center, sex, and previous cardiovascular complications,
the patients were randomized to double-blind treatment with active
medication or matching placebo. Active treatment consisted of
nitrendipine (10 to 40 mg/d), which could be combined with or replaced
by enalapril (5 to 20 mg/d), hydrochlorothiazide (12.5
to 25 mg/d), or both drugs, to reduce the sitting systolic BP
by 20 mm Hg or to <150 mm Hg. At each 3-monthly visit,
CBP was measured twice in the sitting position, and the 2 BPs were
averaged. ECG was performed yearly. ECG left ventricular
mass was estimated as the sum of the S wave in lead
V1 and the R waves in leads aVL and
V5 and is expressed in millivolts.19
Biochemical measurements included serum cholesterol
(mmol/L) and serum creatinine (µmol/L).
ABP Monitoring
Of the 198 Syst-Eur centers, 46 agreed to enroll all of their
patients in the substudy on ABP monitoring, which involved
recordings at entry, at 6 and 12 months, and annually
thereafter with properly validated and calibrated monitors and
appropriate cuff size.16 17 All monitors were programmed
to record BP during an entire 24-hour period at intervals of 
30
minutes. At least 80% of the required recordings had to be
available for inclusion in the analysis. Editing criteria
encoded in the monitor were disabled or set at limits as wide as
possible. No further editing was performed after data acquisition. Mean
values of ambulatory measurements were weighted by the time interval
between consecutive readings. Day and night were defined with short
fixed clock time periods that ranged from 10 AM to 8
PM and from midnight to 6
AM.20
Because there is no consensus on the cutoff values for ABP in ISH, we
arbitrarily defined 3 subgroups on the basis of the average daytime
systolic ABP. In accordance with cutoff values for conventional
systolic BP,21 22 patients were classified as
having moderate sustained hypertension (MoSH), mild sustained
hypertension (MiSH), or nonsustained hypertension (Non-SH) when daytime
systolic ABP averaged 160 mm Hg, 140 to 159
mm Hg, or <140 mm Hg, respectively.
Follow-Up
The analysis of the changes of BP during follow-up was
restricted to patients who had 1 repeat ABP monitoring within 2 years
after randomization and who were still on double-blind treatment and
not taking other antihypertensive drugs. If >1 monitoring was
performed within that period, that closest to 12 months after
randomization was used for the analysis. The ECG
analysis was also based on the recordings closest to
the 1-year visit.
The analyses on outcome were performed according to the intention-to-treat principle. Stroke was the primary end point of the Syst-Eur Trial and was defined as a neurological deficit with symptoms that continued for >24 hours or led to death with no apparent cause other than vascular. The incidence of all cardiovascular events was the second end point for the present study and included sudden death and fatal and nonfatal stroke, myocardial infarction, and heart failure, as described previously.18
Statistical Analysis
Database management and statistical analysis were
performed with SAS software, version 6.12 (SAS Institute Inc). Data are
reported as mean±SD or ±SEM values. Analyses of the data were
performed by Student’s paired and unpaired t tests or by
ANOVA and ANCOVA. Rates of events were calculated as the number of
events divided by the total follow-up time and are expressed as
events/1000 patient-y; these rates were compared between the active
treatment and placebo groups.23 All tests were
2-sided.
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Results |
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Patient Characteristics at Baseline
ABP monitoring was performed at baseline in a total of 717 patients, of whom 695 had successful measurements. The mean age was 70.0±6.3 years, the mean body mass index (BMI) was 26.6±4.0 kg/m2, and 38% were men. The mean of the 6 CBPs was 174±11/86±6 mm Hg, and 24-hour ABP averaged 147±16/80±9 mm Hg. Forty-three percent of the patients had received antihypertensive therapy in the past, and 9% were current smokers. Serum creatinine levels averaged 88.2±17.6 µmol/L, and serum cholesterol levels averaged 6.03±1.13 mmol/L. These baseline characteristics did not differ significantly between the 342 patients randomized to active treatment and the 353 patients randomized to the placebo group and were in general similar to the characteristics of the total Syst-Eur Trial population (n=4695).18
Daytime systolic ABP was <140 mm Hg in 167 patients,
between 140 and 159 mm Hg in 326 patients, and 160 mm Hg
in 202 patients. The Table 1
shows
the characteristics of the 3 subgroups. Age, sex, and BMI did not
differ between these groups. Diastolic daytime and
systolic and diastolic nighttime and clinic BPs
were higher in sustained than in nonsustained hypertensives, except for
diastolic CBP (P=0.36). Within each group,
baseline characteristics did not differ according to whether patients
were allocated to active or to placebo treatment.
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The sum of three ECG voltages averaged 3.23±1.0 mV at baseline and did
not differ according to treatment group. However, the voltages
increased from Non-SH to MiSH and MoSH (P<0.001) (Table 1
). The differences in voltages among the 3 groups remained
significant after adjustment for systolic CBP
(P=0.005) but not after control for daytime systolic
ABP (P=0.91).
Follow-Up
BP and Heart Rate
ABP was available in 465 patients on double-blind treatment after
an average of 11.7±3.4 months of follow-up, which was similar in the
various subgroups. Seven patients were taking open-label
antihypertensive medication, leaving 458 patients for further
analysis. Table 2 summarizes the
study treatment at the time of the repeat ABP monitoring in the 6
subgroups. More patients progressed to dual and triple antihypertensive
therapy in the sustained than in the nonsustained hypertensive groups.
Figures 1 and 2 illustrate the changes in
systolic and diastolic BPs, respectively. Within
the active treatment group, daytime and nighttime ABPs decreased
significantly in patients with sustained hypertension but not in
patients with nonsustained hypertension; by contrast, CBP was reduced
in all 3 subgroups. Active treatment reduced ABP and CPB more than
placebo in MiSH and MoSH. In Non-SH, however, there were no significant
differences between the treatment groups with regard to the changes in
ABP except for daytime systolic BP; the changes in both
systolic and diastolic CBPs were more pronounced in
the active treatment group than in the placebo group. Changes in
daytime, nighttime, and clinic heart rate from baseline to follow-up
averaged 0.1±8.5, -0.4±6.7, and -0.3±9.6 bpm, respectively, in all
patients combined (NS) and did not differ between the various
subgroups.
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Electrocardiography
Figure 3 shows that active
antihypertensive therapy significantly reduced the ECG voltages in
patients with sustained hypertension but not in those with Non-SH. The
difference between active treatment and placebo was significant only in
the group with MoSH.
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Cardiovascular Complications
In the placebo group, stroke incidence (P=0.03) and the
rate of cardiovascular events (P=0.01) were
significantly higher in patients with MoSH than in nonsustained
hypertensives, with intermediate results for those with MiSH. Active
treatment significantly reduced the rate of stroke (P=0.03)
and of all cardiovascular events (P=0.06)
only in patients with MoSH (Figure 4).
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Discussion |
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The Syst-Eur Trial included patients
60 years old whose
CBP averaged 160 mm Hg for systolic BP and <95
mm Hg for diastolic BP at 3 run-in visits while on
placebo.18 Of the patients enrolled in the Ambulatory
Blood Pressure Monitoring Side Project of the
trial,16 17 daytime systolic ABP was 160
mm Hg in 29% of the patients and between 140 and 159 mm Hg in
47%. Although normal values for ABP have not been definitely
established, it appears that about one fourth of the Syst-Eur Trial
patients had nonsustained, white coat or isolated clinic
systolic hypertension. In hypertensive populations in general,
echocardiographic left ventricular mass is
larger in patients with sustained hypertension than in white coat
hypertensives.5 6 7 8 9 The present study confirms with the
use of ECG voltages that the same holds true in older patients with
systolic hypertension; moreover, voltage differences among the
3 subgroups clearly depended on ABP. The incidences of stroke and of
cardiovascular events were, respectively, primary and
secondary end points in the Syst-Eur Trial. In the placebo group, the
rate of both end points was low in nonsustained hypertensives and was 3
to 4 times higher in patients with MoSH. These data fit with findings
in hypertensives in general,8 10 24 in refractory
hypertensives,11 or in the general
population25 that white coat hypertension is
associated with a better outcome8 10 11 or that the
predictive value of ABP persists after control for clinic or casual
BP.24 25 When the latter approach was applied to the
Syst-Eur Trial data,26 it was found that systolic
ABP was a significant predictor of cardiovascular
complications over and above CBP; diastolic CBP and ABP
were not associated with outcome in that analysis. The results
on surrogate and hard end points from the Syst-Eur Trial therefore
allow us to conclude that sustained systolic hypertension is
more harmful than white coat systolic hypertension in the
elderly, particularly when daytime systolic BP averages
160 mm Hg. It is unlikely that our results have been confounded
by other risk factors such as age, sex, relative weight, serum
cholesterol, and heart rate because they did not differ
among the 3 ABP subgroups, and the overall prevalence of smoking was
low in the study population. The Syst-Eur Trial data do not provide
information, however, on whether nonsustained systolic
hypertension is innocuous compared with true normotension, as suggested
by some,5 7 but not other,9 15 data on left
ventricular mass and by the results for morbidity and
mortality rates by Verdecchia et al10 in hypertensive
patients in general.
According to current guidelines,21 22 the management
of hypertension is mainly based on CBP. Before concluding that patients
with low or normal ABP should not be treated, it is of paramount
importance to assess the influence of antihypertensive therapy on BP,
surrogate end points, and cardiovascular complications
in such patients. The present placebo-controlled study confirms
previous uncontrolled observations12 13 14 that CBP
decreases and ABP hardly changes when treatment is guided by CBP in
patients with Non-SH. CBP also decreased in the placebo-treated
Syst-Eur Trial patients, probably due to further habituation to the
measurement conditions after the run-in period and to
regression-to-the-mean. However, both systolic and
diastolic CBPs were reduced more in the active treatment
group than in the placebo group, which suggests that part of the active
treatment effect on CBP can be ascribed to the treatment per se. This
could lend support to the initiation of antihypertensive therapy in
patients with white coat hypertension. However, a recent study
showed that antihypertensive therapy based on ABP led to similar BP
control, general well-being, and left ventricular mass as
treatment guided by CBP, and these results were achieved with a lesser
intake of drugs.27 Whereas the duration of that study was
limited to 6 months, the Syst-Eur Trial data show that the 1-year
changes in ECG voltages were not different between active treatment and
placebo in patients with Non-SH. By contrast, active treatment induced
a significant decrease in ECG left ventricular mass in
patients with MoSH. These results are compatible with the observation
that the treatment-induced changes in echocardiographic
left ventricular mass appear to be more closely related to
changes in ABP than to the changes in CBP.28 With regard
to outcome, active treatment reduced the incidence of
cardiovascular events and of stroke with statistical
significance only in the patients with MoSH. These findings on
surrogate and hard end points indicate that most of the benefit of
antihypertensive therapy in elderly patients with systolic
hypertension is seen in patients whose daytime systolic ABP is
160 mm Hg and that the benefit is less evident when this BP is
below that value.
A number of limitations have to be considered. The present findings are based on subgroups of patients from the Syst-Eur Trial, so the number of events was relatively small, particularly in the patients with Non-SH. Larger studies are therefore warranted to further clarify the effect of antihypertensive therapy on outcome in hypertensive patients with low or normal ABP. The patients of the present analysis were randomized to the active treatment and placebo groups but not within each stratum of ABP; nevertheless, the characteristics at baseline did not differ between the treatment groups. The classification of patients in subgroups according to ABP might have been different if >1 monitoring would have been used due to regression-to-the-mean.29 Finally, there is as yet no generally accepted definition of white coat hypertension and certainly not for isolated systolic white coat hypertension, so the results might differ if other cutoff values were used for the classification of patients according to ABP; the arbitrary cutoff values used in the present study should not be taken as an indication of what a normal reference ABP value might be.
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Acknowledgments |
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The Syst-Eur Trial was a concerted action of the BIOMED Research Program sponsored by the European Union. The trial was sponsored by Bayer AG (Wuppertal, Germany). The National Fund for Scientific Research (Brussels, Belgium) provided additional support. Study medication was donated by Bayer AG, Merck Sharp, and Dohme Inc (West Point, Pa). The trial was carried out in consultation with the World Health Organization, the International Society of Hypertension, the European Society of Hypertension, and the World Hypertension League.
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Footnotes |
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A list of all Syst-Eur Trial participants is given in the Appendix, which may be found Online at www.circulationaha.org
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Appendix 1 |
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TopAbstractIntroductionMethodsResultsDiscussionAppendix 1References |
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Trial Coordinators
Robert Fagard, MD, and Jan A. Staessen, MD; Coordinators of the Project on Ambulatory Blood Pressure Monitoring: Denis Clement, MD; Eoin T. O’Brien, MD; Giuseppe Mancia, MD; Gianfranco Parati, MD; Jan A. Staessen, MD; and Lutgarde Thijs, BSc; Regional Coordinators: Guramy G. Arabidze, MD (Bellorussia and the Russian Federation); Willem H. Birkenhäger, MD (the Netherlands); Christopher J. Bulpitt, MD (United Kingdom); Manuel Carrageta, MD (Portugal); Hilde Celis, MD (Belgium); Françoise Forette, MD (France); Jozef Kocemba, MD (Poland); Gastone Leonetti, MD (Italy); Choudamir Nachev, MD (Bulgaria); Eoin T. O’Brien, MD (Ireland); Eberhard Ritz, MD (Germany); José L. Rodicio, MD (Spain); Joseph Rosenfeld, MD (Israel); Jaakko Tuomilehto, MD(Finland, Estonia, and Lithuania); Steering Committee: Guramy G. Arabidze, MD; Paul De Cort, MD; Robert Fagard, MD; Françoise Forette, MD; Kalina Kawecka-Jaszcz, MD; Gastone Leonetti, MD; Choudomir Nachev, MD; Eoin T. O’Brien, MD; José L. Rodico, MD; Joseph Rosenfeld, MD; Jaakko Tuomilehto, MD; John Webster, MD; and Yair Yodfat, MD; Data Monitoring Committee: Christopher J. Bulpitt, MD; Astrid E. Fletcher, PhD; Jan A. Staessen, MD; and Lutgarde Thijs, BSc; End Point Committee: Peter W. de Leeuw, MD; Robert Fagard, MD; Gastone Leonetti, MD; and James C. Petrie, MD; Ethics Committee: Willem H. Birkenhäger, MD; Collin T. Dollery, MD; and Robert Fagard, MD; Publication Committee: Willem H. Birkenhäger, MD; Christopher J. Bulpitt, MD; Jan A. Staessen, MD; and Alberto Zanchetti, MD; Coordinating Office: Nicole Ausseloos; Veerle Boon; Hilde Celis, MD; Elly Den Hond, DSc; Lut De Pauw, RN; Paul Drent, RN; Dimitri Emelianov, MD; Robert Fagard, MD; Jerzy Gasowski, MD; Heng Fan; Tatiana Kuznetsova, MD; Yvette Piccart; Jan A. Staessen, MD; Yvette Toremans; Lutgarde Thijs, BSc; Sylvia Van Hulle, RN; Ji G. Wang, MD; and Renilde Wolfs.
Clinical Centers
The following investigators took part in the side
project on Ambulatory Blood Pressure Monitoring: in Belgium: L.
Bienasewski, H. Celis, R. Fagard, J. Staessen, R. Van Hoof, W. Vinck
(Leuven), P. De Cort (Kumtich), D. Staessen, and J. Staessen
(Mechelen); in Bulgaria: S.T. Braianova, E.G. Goshev, K.G.
Kirilov, T.R. Poriazova, B. Shahov, and V. Stoyanovsky (Sofia);
in Estonia: T. Laks (‘I’allinn); in Finland:- M.
Jääskivi, C. Sarti, P. Tiitto-Wiht, J. Tuomilehto
(Vantaa), T. Hakamäki, A. Lelitonen (Turku), P. Kivinen
(Kuopio), E. Lehtomäki (Tampere), R. Tilvis, H. Vanhanen, and K.
Halonen (Helsinki), E. Karonen (Kouvala), P.S. Kohonen-Jalonen (Espoo),
H. Wallinheimo (Kuusankoski); in Germany: S. Matthias, and E. Ritz
(Heidelberg); in Greece: A. Efstratopoulos (Athens); in Ireland: L.
Bradley, J. Duggan, and E. O’Brien (Dublin); in Israel: C.
Bott-Kanner, I. Kruchin, J.B. Rosenfeld, S. Zerapha (Givataim), B.
Boner, J. Rosenfeld, and J. Zabludowski (Petha Tiqva); in Italy: A.
Bossini, V. Cagli, C. Diveroli, G. Germano (Rome), R. Fogari, G.
Malamani, F. Tettamanti (Pavia), M. Antivalle, M. Baroni, S.
Lattuada, F. Leali, A. Libretti, M. Paravicini, M. Rindi (Milan), E.
Agostinacchio, G. Barracchia, A. Longo, G. Maiorano, E. Dolce, M.
Merlo, R. Pieri, N. Pietro, A. Pirrelli, V. Vulpis (Bari), M. Del
Torre, P. Palatini, E. Roman (Padova), B. Abdel-Haq, A. Salvetti, M.
Simi (Pisa), M. Fastidio, G. Leonetti, A. Ravogli, L. Terzoli (Milan),
and A. Vaccarela (Casatenovo); in the Netherlands: P. de Leeuw
(Maastricht), M.A.D.H. Schalekamp, A.J. Man in’t Veld, J.M.J. Van der
Cammen, A. van den Meiracker (Rotterdam), and A. Woittiez (Almelo); in
Poland: D. Czarnecka, K. Kawecka-Jaszcz, M. Rajzer, T. Grodzicki, B.
Gryglewska, J. Kocemba (Krakow), M. Kazmirowicz, B.
Krupa-Wojciechowska, and K. Rachon (Gdansk); in Portugal: A. Caetano,
H. Conçalves, A. Costa, G. Leira, A. Martinez, A. Mederios, S.
Pereira (Faro); in Slovenia: R. Accetto, B. Bucic, J. Dobovisek, P.
Dolenc, B. Kolsek, Z. Lapanja, M. Mihelic-Bricie, J. Petrin, 0.
Perc-Cercek, and A. Zemva (Ljubljana): in Spain: G.C. Barrionuevo, B.
Gil-Extremera, L.G. Gomez, J.M.B. Garcia, A.H. Herrera, A.
Maldonado-Martin (Granada), V. Cuesta, R. Marin, N. Navarro, F.
Vega (Oviedo), J. Mora-Macia, J. Pujadas (Barcelona), J. Michauila, J.
Redon (Sagunto), J.L. Rodicio, and L.M. Ruilope (Madrid); in the UK:
S.G. Armstrong, M. Beevers (Birmingham), C. Davidson, N.
Gainsborough, G. Kingswood, G. Mankikar, M. O’Neal, P.
Sharpstone (Brighton), P. Gunawardena, P.J. Luce, I.D. Starke, C.J.
Bulpitt, T. O’Brien, R. Unwin, M. Wilkins (London), L. Gates, J.C.
Petrie, J. Webster (Aberdeen).
Received March 8, 2000; revision received April 12, 2000; accepted April 14, 2000.
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References |
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TopAbstractIntroductionMethodsResultsDiscussionAppendix 1References |
|---|
1. Staessen J, O’Brien ET, Atkins N, et al, on behalf of the Ad-Hoc Working Group. Short report: ambulatory blood pressure in normotensive compared with hypertensive subjects. J Hypertens. 1993;11:1289–1297.[Medline] [Order article via Infotrieve]
2. Mancia G, Zanchetti A. White-coat hypertension: misnomers, misconceptions and misunderstandings: what should we do next? J Hypertens. 1996;14:1049–1052.[Medline] [Order article via Infotrieve]
3. Pickering TG. White coat hypertension. Curr Opin Nephrol Hypertens. 1996;5:192–198.[Medline] [Order article via Infotrieve]
4. Staessen J, Amery A, Fagard R. Editorial review: isolated systolic hypertension. J Hypertens. 1990;8:393–405.[Medline] [Order article via Infotrieve]
5.
Cavallini MC, Roman MJ, Pickering TG, et al. Is
white coat hypertension associated with arterial disease or
left ventricular hypertrophy?
Hypertension. 1995;26:413–419.
6. Cuspidi C, Marabini M, Lonati L, et al. Cardiac and carotid structure in patients with established hypertension and white coat hypertension. J Hypertens. 1995;13:1707–1711.[Medline] [Order article via Infotrieve]
7. Verdecchia P, Schillaci G, Borgioni C, et al. White coat hypertension and white coat effect: similarities and differences. Am J Hypertens. 1995;8:790–798.[Medline] [Order article via Infotrieve]
8.
Khattar RS, Senior R, Lahiri A.
Cardiovascular outcome in white-coat versus sustained
mild hypertension: a 10-year follow-up study. Circulation. 1998;98:1892–1897.
9.
Palatini P, Mormino P, Santonastaso M, et al.
Target-organ damage in stage I hypertensive subjects with white coat
and sustained hypertension: results from the HARVEST study.
Hypertension. 1998;31:57–63.
10.
Verdecchia P, Porcellati C, Schillaci G, et al.
Ambulatory blood pressure: an independent predictor of prognosis in
essential hypertension. Hypertension. 1994;24:793–801.
11.
Redon J, Campos C, Narciso ML, et al. Prognostic
value of ambulatory blood pressure monitoring in refractory
hypertension: a prospective study. Hypertension. 1998;31:712–718.
12. Fagard R, Bielen E, Staessen J, et al. Response of ambulatory blood pressure to antihypertensive therapy guided by clinic pressure. Am J Hypertens. 1993;6:648–653.[Medline] [Order article via Infotrieve]
13. Pickering TG, Levenstein M, Walmsley P, for the Hypertension and Lipid Trial Study Group. Differential effects of doxazosin on clinic and ambulatory pressure according to age, gender and presence of white coat hypertension. Am J Hypertens. 1994;7:848–852.[Medline] [Order article via Infotrieve]
14. Waeber B, Scherrer U, Petrillo A, et al. Are some hypertensive patients overtreated? Lancet. 1987;2:732–734.[Medline] [Order article via Infotrieve]
15. Owens PE, Lyons SP, Rodriguez SA, et al. Is elevation of clinic blood pressure in patients with white coat hypertension who have normal ambulatory blood pressure associated with target organ changes? J Hum Hypertens. 1998;12:743–748.[Medline] [Order article via Infotrieve]
16. Staessen J, Amery A, Clement D, et al. Twenty-four hour blood pressure monitoring in the Syst-Eur Trial. Aging Clin Exp Res. 1992;4:85–91.
17. Emelianov D, Thijs L, Staessen JA, et al. Conventional and ambulatory blood pressure measurements in older patients with isolated systolic hypertension: baseline observations in the Syst-Eur Trial. Blood Press Monit. 1998;3:173–180.[Medline] [Order article via Infotrieve]
18. Staessen JA, Fagard R, Thijs L, et al. Randomized double-blind comparison of placebo and active treatment for older patients with isolated systolic hypertension. Lancet. 1997;350:757–764.[Medline] [Order article via Infotrieve]
19. Fagard R, Staessen J, Amery A. Exercise blood pressure and target organ damage in essential hypertension. J Hum Hypertens. 1991;5:69–75.
20. Fagard R, Brguljan J, Thijs L, et al. Prediction of the actual awake and asleep blood pressures by various methods of 24-h pressure analysis. J Hypertens. 1996;14:557–563.[Medline] [Order article via Infotrieve]
21.
The Joint National Committee on Prevention, Detection,
Evaluation, and Treatment of High Blood Pressure. The Sixth Report of
the Joint National Committee on Prevention, Detection, Evaluation and
Treatment of High Blood Pressure. Arch Intern Med. 1997;157:2413–2446.
22. Guidelines Subcommittee. World Health Organization–International Society of Hypertension Guidelines for the Management of Hypertension. J Hypertens. 1999;1999:17:151–183.
23. Gardner MJ, Altman DG. Statistics With Confidence. London, UK: BMI; 1989:28–33.
24. Perloff D, Sokolow M, Cowan RM, et al. Prognostic value of ambulatory blood pressure measurements: further analysis. J Hypertens. 1989;7(suppl 3):S3–S10.
25. Ohkubo T, Imai Y, Tsuji I, et al. Prediction of mortality by ambulatory blood pressure monitoring versus screening blood pressure measurements: a pilot study in Ohasama. J Hypertens. 1997;15:357–364.[Medline] [Order article via Infotrieve]
26.
Staessen JA, Thijs L, Fagard R, et al. Predicting
cardiovascular risk using conventional and ambulatory
blood pressure in older patients with systolic hypertension.
JAMA. 1999;282:539–546.
27.
Staessen JA, Byttebier G, Buntinx F, et al,
for the APTH Investigators. Antihypertensive treatment based on
conventional or ambulatory blood pressure measurement: a randomized
controlled trial. JAMA. 1997;278:1065–1072.
28. Fagard RH, Staessen JA, Thijs L. Relationship between changes in left ventricular mass and in clinic and ambulatory blood pressure in response to antihypertensive therapy. J Hypertens. 1997;15:1493–1502.[Medline] [Order article via Infotrieve]
29. Palatini P, Dorigatti F, Roman E, et al. White coat hypertension: a selection bias? J Hypertens. 1998;16:977–984.[Medline] [Order article via Infotrieve]
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