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(Circulation. 1998;98:1892-1897.)
© 1998 American Heart Association, Inc.
Clinical Investigation and Reports |
Cardiovascular Outcome in White-Coat Versus Sustained Mild Hypertension
A 10-Year Follow-Up Study
From the Department of Cardiovascular Medicine, Northwick Park, and St Mark's Hospital NHS Trust and Institute for Medical Research, Harrow, Middlesex, UK.
Correspondence to Dr A. Lahiri, MB, BS, MSc, MRCP, FACC, FESC, Department of Cardiovascular Medicine, Northwick Park Hospital, Watford Rd, Harrow, Middlesex, HA1 3UJ, UK.
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Abstract |
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Background—The aim of this study was to compare the risk conferred by white-coat versus sustained mild hypertension for the development of cardiovascular disease.
Methods and Results—Patients (n=479) who underwent 24-hour intra-arterial ambulatory blood pressure monitoring on the basis of a persistently elevated clinic systolic blood pressure of 140 to 180 mm Hg were followed up for the development of subsequent cardiovascular events during a 9.1±4.2-year period. White-coat hypertension, defined as a clinic systolic blood pressure of 140 to 180 mm Hg associated with a 24-hour ambulatory systolic blood pressure <140 mm Hg and diastolic blood pressure <90 mm Hg, was present in 126 patients, and the remainder had sustained mild hypertension. A subgroup of patients without complications underwent follow-up echocardiography and carotid ultrasound. White-coat hypertensives were younger (44±12 versus 52±10 years, respectively; P<0.001) and had a significantly lower incidence of cardiovascular events (1.32 versus 2.56 events per 100 patient-years, respectively; P<0.001) than sustained hypertensives. Multivariate analysis revealed age (P=0.002), sex (P=0.007), race (P=0.001), smoking (P=0.005), and the presence of white-coat hypertension (hazard ratio, 0.29; 95% CI, 0.09 to 0.90; P=0.04) to be independent predictors of subsequent cardiovascular events. Subgroup analysis in patients without complications revealed a lower incidence of left ventricular hypertrophy and lesser degrees of carotid hypertrophy in the white-coat group.
Conclusions—These findings indicate a relatively benign outcome in white-coat hypertension compared with sustained mild hypertension.
Key Words: hypertension • prognosis • hypertrophy • cardiovascular diseases • carotid arteries
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Introduction |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Over the past 50 years, it has been increasingly recognized that isolated clinic blood pressure measurements taken by the physician may not be truly representative of the daily blood pressure load away from the medical environment.1 2 Twenty-four-hour ambulatory blood pressure monitoring offers a more valid assessment of an individual's true blood pressure level by taking frequent readings during routine daily activities.3 Application of this technique has allowed the identification of a subgroup of individuals with a persistently elevated clinic blood pressure but normal ambulatory blood pressure. The term "white-coat hypertension" has been used to describe this phenomenon, and it is thought to occur in
20% to 40%
of presumed mildly hypertensive patients.4 A
recently completed longitudinal study5 and
preliminary data from a large ongoing study6 have
shown white-coat hypertension to be associated with a lower risk of
subsequent cardiovascular events than sustained
hypertension. However, comparative cross-sectional data regarding
target-organ damage in patients with white-coat versus sustained
hypertension are conflicting.7 8 9 10 11 12 13 14 Left
ventricular hypertrophy, carotid wall
thickening, and atherosclerotic plaques are prognostically significant
forms of target-organ damage15 16 and may be
considered surrogate markers of overt cardiovascular
disease.17 The aim of this study was to compare the risk conferred by white-coat and sustained mild hypertension for the development of subsequent cardiovascular events and for the long-term development of surrogate markers of overt cardiovascular disease in an uncomplicated subgroup of patients.
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Methods |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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The hypertension database in our institution consists of 502 patients with mild hypertension, defined as a clinic systolic blood pressure of 140 to 180 mm Hg, who had undergone 24-hour intra-arterial ambulatory blood pressure monitoring within the period January 1, 1979, to January 1, 1993.18 The diagnosis of hypertension was based on persistently elevated clinic blood pressures taken over a period of weeks to months in a primary-care setting. At the initial hospital visit, a single blood pressure measurement was taken by a nurse or technician, with the patient resting for 5 to 10 minutes in the supine position. Those in whom clinic blood pressure remained elevated were requested to undergo 24-hour ambulatory intra-arterial blood pressure monitoring within 2 months. Antihypertensive medication either had not been started or had been withdrawn in the 8 weeks preceding intra-arterial blood pressure monitoring. Baseline clinic blood pressure was taken as the mean of 2 or more readings at separate visits in the 4 weeks before or after the intra-arterial study. Secondary causes of hypertension were excluded, and informed consent was obtained before intra-arterial ambulatory blood pressure monitoring. General practitioners were informed of the results of the test, and antihypertensive therapy was generally recommended if 24-hour ambulatory systolic blood pressure was
140 mm Hg or diastolic blood pressure 90
mm Hg. The treatment of lower ambulatory blood pressure readings was
more conservative and discretionary. Subsequent assessment of blood
pressure control and treatment was largely left to the individual
general practitioners and was based on clinic blood
pressure measurements.
White-coat hypertension was defined as an elevated clinic
systolic blood pressure of 140 to 180 mm Hg associated
with a 24-hour ambulatory systolic blood pressure <140
mm Hg and diastolic blood pressure <90 mm Hg; those
with sustained hypertension had a 24-hour ambulatory systolic
blood pressure 140 mm Hg or diastolic blood
pressure 90 mm Hg.
Follow-Up
The study patients have been intermittently reviewed over the
years to record clinic blood pressure, drug therapy, and the
occurrence of interim cardiovascular events. The most
recent follow-up was performed during an 18-month period from 1994 to
1996 (Figure 1
). Of the 502 study
patients, 50 patients had died (dates and certified causes of death
obtained from the National Health Service Central Register, Southport,
UK), and 244 attended follow-up reevaluation in 1994 to 1996,
consisting of a full history, physical examination, clinic blood
pressure measurement on usual medication, risk factor profile, blood
urea, serum electrolytes and creatinine estimation, total
cholesterol level, echocardiography,
and carotid ultrasonography. In the remaining 208 patients who failed
to respond to 2 written communications, a minimum of 2 years of
follow-up data were obtained on 185 of these patients from departmental
and hospital records of previous visits. Adequate follow-up data
were not available for the remaining 23 patients, which restricted the
analysis to 479 of the 502 patients. The racial composition of
the group, reflecting the local population of the London boroughs of
Harrow, Brent, and Ealing, consisted of 361 white, 86 South Asian
(Indian subcontinent), and 32 black subjects.
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Documentation of Events
Departmental and hospital records of all patients were
scrutinized before follow-up. Events were classified as
noncardiovascular death, coronary events, and
cerebrovascular events. Coronary events consisted of fatal and
nonfatal myocardial infarction, arrhythmic death, congestive heart
failure death, and coronary
revascularization. Cerebrovascular events included
fatal and nonfatal stroke. A history of myocardial infarction, stroke,
coronary artery bypass graft surgery,
percutaneous transluminal coronary angioplasty,
or peripheral revascularization
volunteered by the patient was accepted if documented in the hospital
records or if confirmed by the general
practitioner.
Intra-Arterial Blood Pressure Monitoring
The methodology of intra-arterial blood pressure
recording used in this laboratory has been well
documented.19 20 Blood pressure was recorded
from a fine brachial artery cannula with a specially designed
transducer/perfusion unit and an Oxford Medilog Mark I tape
recorder. The equipment was designed so that patients were fully
ambulant and able to carry out their normal daily activities. The
24-hour tape recordings were analyzed on a custom-built
hybrid computer using a program that calculated mean hourly blood
pressure and heart rate. Mean systolic and
diastolic intra-arterial blood pressures were
calculated by averaging the 24-hour systolic and
diastolic readings.
Echocardiography
M-mode and 2-dimensional echocardiography
were performed by the same investigator using a commercially available
machine (ATL Ultramark 9 HDI CV) with a 2- to 3-MHz broad-band
transducer. Left ventricular end-diastolic
dimensions were obtained from 2-dimensionally guided M-mode tracings
according to the recommendations of the American Society of
Echocardiography.21 Left
ventricular mass index was calculated as
follows22 :
LVMI={0.8x1.04[(LVID+PWT+IVST)3-LVID3]+0.6}/body
surface area (g/m2), where LVID is the left
ventricular internal diameter, PWT the posterior wall
thickness, and IVST the interventricular septal thickness.
Left ventricular hypertrophy was considered
present if LVMI was 125 g/m2 for men and
110 g/m2 for women.
Carotid Ultrasonography
Both carotid arteries were imaged with the high-resolution
Kontron Sigma 44 ultrasound system equipped with a mechanical sector
probe with a 7.5-MHz annular imaging transducer providing an axial
resolution of 0.15 mm. The mid and distal common carotid artery,
carotid bulb, and proximal portions of the internal and external
carotid arteries were systematically interrogated in short-axis and
long-axis views. Three end-diastolic measurements of
diffuse carotid intima-media thickness (IMT) were carried out on
the far wall of both common carotid arteries, 1 cm proximal to the
carotid bulb in the longitudinal view.23 The mean
of the 6 IMT measurements was used in the analysis.
Two-dimensionally guided M-mode tracings of the distal common carotid
artery were also obtained to determine lumen diameter (D). This was
used to calculate cross-sectional area (CSA) as follows:
(IMT+D/2)2-(D/2)2 .
Carotid IMT and arterial wall CSA were considered to be
markers of carotid hypertrophy. A plaque was defined as a
distinct area with an IMT 50% greater than that of the adjacent
wall,11 and the maximal IMT measurement
(IMTmax) was used as a semiquantitative score for
carotid atherosclerosis severity. In the absence of
atheroma, the greater of the IMT measurements from the far
wall of the distal common carotid artery and the carotid bulb were
taken as IMTmax.
Reproducibility of Left Ventricular and Carotid
Artery Measurements
To assess serial intraobserver reproducibility of LVMI and
carotid measurements, 30 patients underwent
echocardiography and carotid ultrasonography on 2
separate occasions within a period of 2 weeks. Coefficients of
variation for IMT, lumen diameter, IMTmax, and
LVMI were 1%, 2%, 11%, and 14%, respectively.
Statistical Analysis
The clinical variables analyzed included age, sex,
race, body mass index, serum cholesterol, smoking, and
years of follow-up. Echocardiographic
parameters consisted of the presence or absence of left
ventricular hypertrophy, and carotid
measurements included IMT, CSA, and IMTmax.
Continuous variables were tested for normality by the
Shapiro-Francia test. A log10 transformation was
used for IMT, CSA, and IMTmax to improve the
assumption of normality; all other continuous variables conformed
to a normal distribution. A comparison between the groups with
white-coat and sustained mild hypertension was made by use of 2 sample
t tests and Fisher's exact test for continuous and
categorical variables, respectively. Cox's survival
analysis was performed to determine the independent predictors
of time to the first cardiovascular event with
respective hazard ratios, 95% CIs, and P values. The
continuous variables included in the Cox model were age, body mass
index, initial clinic systolic blood pressure, and
cholesterol level; hazard ratios reflected the risk
associated with a unit increase in these variables. Categorical
variables consisted of sex, race, smoking, and white-coat
hypertension; hazard ratios represented the risk of a first
event in men relative to women, South Asians relative to whites,
smokers relative to nonsmokers, and white-coat hypertensives relative
to sustained hypertensives, respectively. Because Afro-Caribbeans
constituted only a small proportion of the study population, this group
was not included in the analysis of race.
Multivariate analysis was performed on a
subgroup of patients without complications with white-coat versus
sustained mild hypertension to assess whether there was a significant
difference in left ventricular and carotid artery
parameters between these 2 groups, after adjustment for
clinical variables. A value of P<0.05 was considered
significant.
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Results |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Demographic Data
Of the 479 patients analyzed, 126 were designated as having white-coat hypertension, and 353 had sustained mild hypertension. As shown in Table 1
, the white-coat
hypertension group were significantly younger than those with sustained
hypertension (44±12 versus 52±10 years, respectively;
P<0.001) but otherwise demonstrated similar demographic
characteristics. Details of preevent antihypertensive drug therapy were
available for 112 of 126 patients with white-coat hypertension and 317
of 353 patients with sustained hypertension. A significantly greater
proportion of patients with white-coat hypertension were not taking
antihypertensive medication at follow-up compared with those with
sustained hypertension, and fewer were on multiple therapy (Table 2).
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Hemodynamic Data
A comparison of the blood pressure data is given in Figure 2. In accordance with the definition,
24-hour ambulatory systolic and diastolic blood
pressures were considerably lower in the group with white-coat
hypertension than in those with sustained hypertension. Initial clinic
systolic and diastolic blood pressres, although
elevated, were also significantly lower in the white-coat hypertension
group, but follow-up clinic blood pressures were similar in both
groups.
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Comparison of Events
In the white-coat hypertension group, 15 first events were
recorded, consisting of 4 noncardiovascular deaths,
5 cardiovascular deaths, 3 myocardial infarctions, and
3 coronary revascularizations. These
occurred over a period of 9.0±4.0 years for the 126 patients, yielding
an event rate of 1.32 events per 100 patient-years. In comparison, 83
first events occurred in the 353 sustained hypertensives during a
9.2±4.3-year follow-up period, giving a significantly higher event
rate of 2.56 events per 100 patient-years (P<0.001) for the
latter group. These events included 13
noncardiovascular deaths, 16
cardiovascular deaths, 10 strokes, 31 myocardial
infarctions, 12 coronary
revascularizations, and 1 peripheral
revascularization. Figure 3 shows the frequency distribution of
noncardiovascular death, coronary events, and
cerebrovascular events in the 2 groups of patients. Whereas the
prevalence of noncardiovascular death in the 2 groups
was similar, those with sustained hypertension had approximately twice
the risk of coronary events and at least 4 times the risk of a
cerebrovascular event compared with white-coat hypertensives.
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Table 3 summarizes the
results of the Cox survival analysis for predicting the time to
a first event. Age (P=0.002), sex (P=0.007), race
(South Asians relative to whites, P=0.001), smoking
(P=0.005), and the presence of white-coat hypertension
(P=0.04) were independent predictors of subsequent
cardiovascular events.
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Target-Organ Status
Of the 244 patients who attended follow-up evaluation, 32 were
excluded because of a history of overt cardiovascular
disease, and 15 had suboptimal echocardiographic views.
Therefore, a subgroup of 197 patients without complications were
assessed for cardiovascular target-organ damage at a
mean follow-up period of 10.1±3.4 years; 65 had white-coat
hypertension, and 132 were sustained hypertensives. There was no
statistically significant difference in the demographic and blood
pressure data of the white-coat and sustained hypertensives in this
subgroup compared with the original study population.
As outlined in Table 4,
LVMI and the prevalence of left ventricular
hypertrophy were significantly lower in those with
white-coat hypertension. Similarly, IMT and CSA were significantly
lower in the latter group than in those with sustained hypertension.
Although the proportion of patients with detectable carotid
atherosclerotic plaques in the 2 groups was similar,
IMTmax was significantly lower in those with
white-coat hypertension. After adjustment for clinical variables,
the prevalence of manifest left ventricular
hypertrophy was significantly lower in the white-coat
hypertension group (11% versus 38%, P<0.001; odds ratio,
0.45; 95% CI, 0.2 to 0.9; P=0.02). Similarly, IMT and CSA
were also significantly lower in the group with white-coat hypertension
(Table 5). A nonsignificant
trend toward a lower IMTmax in the white-coat
hypertension group was also observed.
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Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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The intra-arterial method of ambulatory blood pressure monitoring is a powerful research tool and remains the reference standard by which noninvasive monitors are validated.24 It provides beat-to-beat measurements of blood pressure over a 24-hour period in truly ambulant patients and therefore represents the most authentic measure of the daily hemodynamic burden imposed by blood pressure. In comparison, noninvasive auscultatory and oscillometric monitors rely on intermittent recordings at predetermined time intervals, and these may not be accurate during unrestricted physical activity. The present study provides the first longitudinal data on white-coat hypertension by the intra-arterial technique. Mild hypertension was defined on the basis of a clinic systolic blood pressure of 140 to 180 mm Hg and did not take into account the level of clinic diastolic blood pressure. The use of this definition was influenced by cross-sectional evidence showing systolic blood pressure to be more strongly correlated to target-organ damage than diastolic blood pressure25 and because of the increasingly more common view that systolic blood pressure, except possibly in younger patients, may play the predominant role in the development of cardiovascular morbidity and mortality.26 27
Our findings showed age, sex, race, smoking, and the presence of white-coat hypertension to be independent predictors of subsequent cardiovascular events in patients with mild hypertension based on conventional clinic blood pressure readings. South Asians were at a higher risk of cardiovascular complications than their white counterparts. This finding is consistent with epidemiological data from the United Kingdom showing that South Asians are particularly susceptible to coronary heart disease and also have a higher mortality from cerebrovascular disease than white subjects.28
White-coat hypertension was associated with a relatively benign outcome compared with sustained mild hypertension. This is substantiated by a significantly lower risk of subsequent cardiovascular events in the white-coat group and evidence of lesser degrees of prognostically significant target-organ damage compared with sustained hypertensives in the subset of patients without overt cardiovascular manifestations. Whereas the incidences of noncardiovascular deaths in the 2 groups were similar, sustained hypertensives had twice the incidence of subsequent coronary events and a >4-fold increased risk of cerebrovascular events compared with the white-coat hypertension group. It is notable, however, that the majority of patients with white-coat hypertension were being treated with antihypertensive drugs at follow-up. Blood pressure management during the interim period was based on clinic blood pressure readings as part of standard clinical practice and largely governed by the family practitioner. It is perhaps not surprising, therefore, that a large proportion of designated white-coat hypertensives received interim antihypertensive treatment because of persistently elevated clinic blood pressures. For ethical reasons, it was not possible to repeat intra-arterial ambulatory blood pressure monitoring to assess blood pressure control or influence further management.
Two previous longitudinal studies addressing the prognostic significance of white-coat hypertension, using intermittent noninvasive ambulatory blood pressure monitoring, have similarly found white-coat hypertension to be associated with a more benign outcome than ambulatory hypertension.5 6 It has also been observed that patients with a lower-than-predicted ambulatory blood pressure, derived from a regression line between ambulatory blood pressure and clinic blood pressure, have a lower risk of subsequent fatal or nonfatal cardiovascular events than patients with more elevated ambulatory blood pressure.29 These findings confirm the incremental prognostic value of ambulatory blood pressure monitoring for the stratification of cardiovascular risk in patients with presumed essential hypertension.
In the representative subgroup of patients without overt cardiovascular disease, white-coat hypertension was associated with a significantly lower long-term prevalence of left ventricular hypertrophy and lesser degrees of carotid hypertrophy compared with the sustained hypertension group, even after adjustment for clinical variables. IMTmax was 13.6% lower in the white-coat hypertension group after adjusted analysis, indicating a tendency toward less advanced carotid atherosclerotic changes compared with sustained hypertension. However, this difference failed to reach statistical significance because of a wide 95% CI. This may be attributed in part to the relatively small sample size, the important influence of age, and other atherogenic factors not taken into account in this study, such as lipoprotein levels and hemostatic factors. Previous cross-sectional studies comparing target-organ status of white-coat hypertensives with sustained hypertensives have provided conflicting data.7 8 9 10 11 12 13 14 Nonetheless, in accordance with our findings, the only cross-sectional studies assessing both left ventricular and carotid artery structure found LVMI and carotid IMT to be lower in white-coat hypertensives than in sustained hypertensives.30 31 32
In the absence of universally accepted limits of normal ambulatory
blood pressure, the cutoff points used to dichotomize white-coat and
sustained hypertensives in previous studies have been largely
arbitrary. In the present study, we used a 24-hour ambulatory blood
pressure cutoff point of 140/90 mm Hg, for many reasons. First,
intra-arterial ambulatory blood pressure monitoring became
an established technique at our institution in the late 1970s, at a
time when there were few data on the normal range of ambulatory blood
pressure. Therefore, for clinical purposes, for those in whom 24-hour
ambulatory systolic blood pressure was 140 mm Hg or
diastolic blood pressure was 90 mm Hg,
antihypertensive treatment was generally advocated, whereas for those
with lower readings, the recommendations were more conservative.
Second, because intra-arterial monitoring allows the
continuous measurement of blood pressure in truly ambulant patients, it
has been suggested that average intra-arterial readings may
be higher than those obtained by intermittent, noninvasive
monitoring.33 Moreover, adopting this relatively
high ambulatory blood pressure cutoff point could only have served to
challenge the contention that white-coat hypertension is benign by
including higher levels of ambulatory blood pressure in the white-coat
group, thereby dampening any differences between those with white-coat
and sustained hypertension.
This study did not include a normotensive control group for comparison because an insufficient number of normotensives have undergone intra-arterial monitoring at our institution. Therefore, it was not possible to evaluate the clinical significance of white-coat hypertension in relation to normotension. However, it can be stated on the basis of our findings that in a group of individuals with mild hypertension as defined by clinic blood pressure measurement, the outcome in white-coat hypertension as presently managed is relatively benign compared with sustained hypertension.
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Acknowledgments |
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This study was supported by an educational grant from the Northwick Park Hospital Cardiac Research Fund. We gratefully acknowledge the guidance and support of the late Dr E.B. Raftery and the assistance of Christopher Kinsey and Ann Parsons during data collection.
Received May 13, 1998; revision received August 7, 1998; accepted August 11, 1998.
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 Authors/Task Force Members:, G. Mancia, G. De Backer, A. Dominiczak, R. Cifkova, R. Fagard, G. Germano, G. Grassi, A. M. Heagerty, S. E. Kjeldsen, et al. 2007 Guidelines for the Management of Arterial Hypertension: The Task Force for the Management of Arterial Hypertension of the European Society of Hypertension (ESH) and of the European Society of Cardiology (ESC) Eur. Heart J., June 11, 2007; (2007) ehm236v1. [Full Text] [PDF]
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 I. Z. Ben-Dov, J. D. Kark, D. Ben-Ishay, J. Mekler, L. Ben-Arie, and M. Bursztyn Predictors of All-Cause Mortality in Clinical Ambulatory Monitoring: Unique Aspects of Blood Pressure During Sleep Hypertension, June 1, 2007; 49(6): 1235 - 1241. [Abstract] [Full Text] [PDF]
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 M. Kikuya, T. W. Hansen, L. Thijs, K. Bjorklund-Bodegard, T. Kuznetsova, T. Ohkubo, T. Richart, C. Torp-Pedersen, L. Lind, H. Ibsen, et al. Diagnostic Thresholds for Ambulatory Blood Pressure Monitoring Based on 10-Year Cardiovascular Risk Circulation, April 24, 2007; 115(16): 2145 - 2152. [Abstract] [Full Text] [PDF]
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 D Erdogan, H Gullu, M Caliskan, I Yildirim, D Tok, and H Muderrisoglu Coronary flow reserve is preserved in white-coat hypertension Heart, August 1, 2006; 92(8): 1109 - 1112. [Abstract] [Full Text] [PDF]
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 T. G. Pickering, D. Shimbo, and D. Haas Ambulatory blood-pressure monitoring. N. Engl. J. Med., June 1, 2006; 354(22): 2368 - 2374. [Full Text] [PDF]
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 T. Ugajin, A. Hozawa, T. Ohkubo, K. Asayama, M. Kikuya, T. Obara, H. Metoki, H. Hoshi, J. Hashimoto, K. Totsune, et al. White-Coat Hypertension as a Risk Factor for the Development of Home Hypertension: The Ohasama Study Arch Intern Med, July 11, 2005; 165(13): 1541 - 1546. [Abstract] [Full Text] [PDF]
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T. G. Pickering, J. E. Hall, L. J. Appel, B. E. Falkner, J. Graves, M. N. Hill, D. W. Jones, T. Kurtz, S. G. Sheps, and E. J. Roccella Recommendations for Blood Pressure Measurement in Humans and Experimental Animals: Part 1: Blood Pressure Measurement in Humans: A Statement for Professionals From the Subcommittee of Professional and Public Education of the American Heart Association Council on High Blood Pressure Research Circulation, February 8, 2005; 111(5): 697 - 716. [Abstract] [Full Text] [PDF]
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T. G. Pickering, J. E. Hall, L. J. Appel, B. E. Falkner, J. Graves, M. N. Hill, D. W. Jones, T. Kurtz, S. G. Sheps, and E. J. Roccella Recommendations for Blood Pressure Measurement in Humans and Experimental Animals: Part 1: Blood Pressure Measurement in Humans: A Statement for Professionals From the Subcommittee of Professional and Public Education of the American Heart Association Council on High Blood Pressure Research Hypertension, January 1, 2005; 45(1): 142 - 161. [Abstract] [Full Text] [PDF]
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 S. J. Howell, J. W. Sear, and P. Foex Hypertension, hypertensive heart disease and perioperative cardiac risk{dagger} Br. J. Anaesth., April 1, 2004; 92(4): 570 - 583. [Abstract] [Full Text] [PDF]
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 G. Bobrie, G. Chatellier, N. Genes, P. Clerson, L. Vaur, B. Vaisse, J. Menard, and J.-M. Mallion Cardiovascular Prognosis of "Masked Hypertension" Detected by Blood Pressure Self-measurement in Elderly Treated Hypertensive Patients JAMA, March 17, 2004; 291(11): 1342 - 1349. [Abstract] [Full Text] [PDF]
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 H. O. Ventura and M. R. Mehra White Coat Hypertension and Sleep Apnea: Is There a Link? Chest, March 1, 2004; 125(3): 805 - 807. [Full Text] [PDF]
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F. Garcia-Rio, J. M. Pino, A. Alonso, M. A. Arias, I. Martinez, D. Alvaro, and J. Villamor White Coat Hypertension in Patients With Obstructive Sleep Apnea-Hypopnea Syndrome Chest, March 1, 2004; 125(3): 817 - 822. [Abstract] [Full Text] [PDF]
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 L. Poulsen Blood pressure and cardiac autonomic function in relation to risk factors and treatment perspectives in Type 1 diabetes Journal of Renin-Angiotensin-Aldosterone System, December 1, 2002; 3(4): 222 - 242. [Abstract] [PDF]
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J. Gomez-Cerezo, J. J. Rios Blanco, I. Suarez Garcia, P. Moreno Anaya, P. Garcia Raya, E. Vazquez-Munoz, and F. J. Barbado Hernandez Noninvasive Study of Endothelial Function in White Coat Hypertension Hypertension, September 1, 2002; 40(3): 304 - 309. [Abstract] [Full Text] [PDF]
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A. M. Grandi, R. Broggi, S. Colombo, R. Santillo, D. Imperiale, A. Bertolini, L. Guasti, and A. Venco Left Ventricular Changes in Isolated Office Hypertension: A Blood Pressure-Matched Comparison With Normotension and Sustained Hypertension Arch Intern Med, December 10, 2001; 161(22): 2677 - 2681. [Abstract] [Full Text] [PDF]
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R. Sega, G. Trocino, A. Lanzarotti, S. Carugo, G. Cesana, R. Schiavina, F. Valagussa, M. Bombelli, C. Giannattasio, A. Zanchetti, et al. Alterations of Cardiac Structure in Patients With Isolated Office, Ambulatory, or Home Hypertension: Data From the General Population (Pressione Arteriose Monitorate E Loro Associazioni [PAMELA] Study) Circulation, September 18, 2001; 104(12): 1385 - 1392. [Abstract] [Full Text] [PDF]
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 K. Kario, K. Shimada, J. E. Schwartz, T. Matsuo, S. Hoshide, and T. G. Pickering Silent and clinically overt stroke in older Japanese subjects with white-coat and sustained hypertension J. Am. Coll. Cardiol., July 1, 2001; 38(1): 238 - 245. [Abstract] [Full Text] [PDF]
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T.E Strandberg and V Salomaa White coat effect, blood pressure and mortality in men: prospective cohort study Eur. Heart J., October 2, 2000; 21(20): 1714 - 1718. [Abstract] [PDF]
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R. H. Fagard, J. A. Staessen, L. Thijs, J. Gasowski, C. J. Bulpitt, D. Clement, P. W. de Leeuw, J. Dobovisek, M. Jaaskivi, G. Leonetti, et al. Response to Antihypertensive Therapy in Older Patients With Sustained and Nonsustained Systolic Hypertension Circulation, September 5, 2000; 102(10): 1139 - 1144. [Abstract] [Full Text] [PDF]
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 J. A Staessen, E. T O'Brien, L. Thijs, and R. H Fagard Modern approaches to blood pressure measurement Occup. Environ. Med., August 1, 2000; 57(8): 510 - 520. [Abstract] [Full Text]
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M. F. Muldoon, P. Nazzaro, K. Sutton-Tyrrell, and S. B. Manuck White-Coat Hypertension and Carotid Artery Atherosclerosis: A Matching Study Arch Intern Med, May 22, 2000; 160(10): 1507 - 1512. [Abstract] [Full Text] [PDF]
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K. Kario, S. Hoshide, K. Shimada, T. G. Pickering, R. S. Khattar, R. Senior, and A. Lahiri White-Coat Hypertension Versus Sustained Hypertension in Japan • Response • Response Circulation, December 21, 1999; 100 (25): e157 - e158. [Full Text] [PDF]
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J. A. Staessen, L. Thijs, R. Fagard, E. T. O'Brien, D. Clement, P. W. de Leeuw, G. Mancia, C. Nachev, P. Palatini, G. Parati, et al. Predicting Cardiovascular Risk Using Conventional vs Ambulatory Blood Pressure in Older Patients With Systolic Hypertension JAMA, August 11, 1999; 282(6): 539 - 546. [Abstract] [Full Text] [PDF]
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 White-Coat Hypertension: A Benign Disorder? Journal Watch Cardiology, January 15, 1999; 1999(115): 1 - 1. [Full Text]
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 Benign Long-Term Outcome in White-Coat Hypertension Journal Watch (General), November 13, 1998; 1998(1113): 7 - 7. [Full Text]
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T. G. Pickering White Coat Hypertension: Time for Action Circulation, November 3, 1998; 98(18): 1834 - 1836. [Full Text] [PDF]
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