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Journal of Human Hypertension (2006) 20, 923931

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ORIGINAL ARTICLE

Prevalence and clinical implications of the


inter-arm blood pressure difference:
a systematic review
CE Clark1, JL Campbell1, PH Evans1 and A Millward2
1

Primary Care Research Group, Institute of Health & Social Care Research, Peninsula Medical School,
Exeter, Devon, UK and 2Institute of Biomedical and Clinical Science, Peninsula Medical School,
Derriford, Plymouth, Devon, UK

A blood pressure (BP) difference between arms was first


reported over 100 years ago. Knowledge of its prevalence and relevance to the accurate measurement of BP
remains poor. Current hypertension guidelines do not
emphasise it. The objectives of this study were to
establish the best estimate of prevalence of the interarm difference (IAD) in the population, to consider its
implications for accurate BP measurement and treatment, and to discuss its aetiology and potential as a risk
marker for cardiovascular disease. Systematic literature
review was carried out. The data sources were Medline
EMBASE and CINAHL databases, and Index of Theses.
Studies reporting prevalence rates of IAD were retrieved
and considered for inclusion against explicit methodological criteria. Point prevalence rates were extracted
and weighted mean prevalence rates calculated. The
main outcome measures were weighted mean preva-

lences of systolic IADX10 and X20 mm Hg and of


diastolic IADX10 mm Hg. Thirty-one studies were identified. Most had methodological weaknesses; only four
met the inclusion criteria. Pooled prevalences of the IAD
from these four studies were 19.6% systolic X10 mm Hg
(95% CI 18.021.3%), 4.2% systolic X20 mm Hg (95% CI
3.45.1%) and 8.1% diastolic X10 mm Hg (95%CI 6.9
9.2%). In conclusion, an IAD is present in a substantial
number of patients and should be looked for whenever
diagnosis and treatment depend on accurate measurements of BP. The importance of an IAD should be
better emphasised in current hypertension management
guidelines. There is evidence associating an IAD with
peripheral vascular disease, raising the possibility that
its presence may predict cardiovascular events.
Journal of Human Hypertension (2006) 20, 923931.
doi:10.1038/sj.jhh.1002093; published online 12 October 2006

Keywords: blood pressure measurement; interarm difference

Introduction
Patients are regularly encountered in the clinical
setting with a different systolic or diastolic
blood pressure (BP) in each arm. Comparisons
of arm pressures have been made ever since the
modern sphygmomanometer was introduced,1
yet the significance of this finding, which Cyriax
named the differential BP sign,2 is still poorly
appreciated today.
Hypertension is one of the major causes of
premature morbidity and mortality throughout the
developed and developing worlds.3 The vast majority of patients with hypertension are managed in
primary care4 and measurement of BP is the most
common investigation performed in this setting.5
Correspondence: Dr CE Clark, Primary Care Research Group,
Institute of Health & Social Care Research, Peninsula Medical
School, Smeall Building, St Lukes Campus, Magdalen Rd, Exeter,
Devon EX1 2LU, UK.
E-mail: christopher.clark@pms.ac.uk
Received 10 May 2006; revised 21 August 2006; accepted 25
August 2006; published online 12 October 2006

The management of hypertension is known to be


suboptimal;6 therefore, knowledge of the latest
guidelines, and the many factors known to influence
readings, is crucial.7 The prevalence of a systolic
(sIAD) or a diastolic (dIAD) inter-arm difference, its
importance for the management of hypertension, its
significance as a potential marker of peripheral
vascular disease (PVD) and predictor of cardiovascular disease (CVD) in hypertensive patients are the
subjects of this review.
Although recent ambulatory BP monitoring guidelines recommend routine bilateral assessment,8 the
latest British guidelines for the management of
hypertension merely state that BP should initially
be measured in both arms as patients may have large
differences (410 mm Hg) between arms. The arm
with the higher values should be used for subsequent measurements.9 This appears to be guidance
repeated almost verbatim through previous
versions1014 stretching back over 60 years.15 The
guidelines do not consider the prevalence of the IAD
and suggest that differences X20 mm Hg systolic
and/or 10 mm Hg diastolic warrant specialist

The inter-arm blood pressure difference


CE Clark et al
924

referral.16 As only one in three measurements of BP


in practice are made according to guidelines,17,18 it is
unlikely that even this passing reference to an IAD
is acted upon. The latest Joint National Committee
guidelines (JNC VII) merely suggest BP verification
in the contralateral arm.19
Appreciation of the presence and implications of
an IAD is clearly vital for accurate diagnosis and
consistent management of hypertension. Following
an earlier small study of a mixed normotensive
and hypertensive cohort of primary care patients,
we proposed that the IAD may be caused by PVD.20
As PVD is itself a strong predictor of CVD,2126 the
recognition of the IAD as a sign of PVD would
suggest that the IAD may also have prognostic value
as a marker for predicting cardiovascular events in a
similar manner to a reduced ankle-brachial pressure
index (ABPI). ABPI measurement has been proposed
as a screening test,27 but is not routinely undertaken
in the general practice assessment of hypertensive
patients in the United Kingdom. It is time consuming and requires specialised equipment and a
degree of training, whereas bilateral brachial BP
measurements are easily taken and are in any case
recommended in the assessment of new hypertensive patients.9 In symptomatic chronic upper
limb ischaemia, where the IAD is marked,28 the
predominant cause is atherosclerosis (Table 1), and
this is associated with PVD.29 It therefore seems
logical that the causes of an asymptomatic IAD
should be similar. Consequently, the recognition of
an IAD could have value in providing a simple
screening test to apply in routine consultations
to identify patients potentially at the highest
risk of cardiovascular events and therefore in
need of further assessment. This would facilitate
more appropriate targeting of limited resources
in primary prevention, as required by the National
Service Framework for Coronary Heart Disease
(CHD).30

Methods

Table 1 Causes of chronic upper limb ischaemia

Results

K
K
K
K

K
K

Atherosclerosis
Vasculitis
e.g. polyarteritis nodosa, giant cell arteritis, Buergers disease
Fibromuscular hyperplasia
Connective tissue disorders
e.g. scleroderma, mixed connective tissue disease, systemic
lupus
Radiation arteritis
Thoracic outlet compression

Adapted with permission from Thompson and Kinsella.28

Identification of studies

The principal investigator searched Medline (1966


2006), Old Medline (19501965), EMBASE (1974
2006) and CINAHL (19822006) databases in May
2006 using the following MeSH, and full text terms:
blood pressure (restricted to analysis, instrumentation, classification or physiology) or hypertension
or arm and difference or differential. The result
set was limited to human and English language
results. Further references were identified from
specialist cardiovascular and hypertension journal
collections. The Index of Theses (19702006) was
searched and authors recently active in the field
were contacted. Further citations were identified
by hand searching of reference lists in retrieved
papers. Only English language papers were
reviewed, but some findings from foreign language
papers quoted in a previous review31 have been
cited in the Discussion.
Selection and quality assessment of studies

Cross-sectional or cohort studies reporting a prevalence figure for sIAD or dIAD were retrieved for
assessment. Reports meeting the predefined quality
criteria based on sample selection, sample size and
method of measurement of the IAD (Box 1) were
included in the analysis.
Data collection and synthesis

The principal investigator extracted data on


prevalence rates, study population and methods of
measurement from all studies reporting prevalences
of the IAD. Where possible data were combined to
derive pooled estimates of prevalences and magnitudes of sIAD and dIAD using weighted means and
standard errors.32

Searches identified 357 citations, from which 18


articles were retrieved. Hand searching of references
identified a further 19 older papers. After exclusion
of papers without prevalence data, only four papers
met the inclusion criteria (Figure 1).
Description of studies

All potential studies for inclusion were crosssectional studies reporting point prevalences of

Box 1 Inclusion criteria for studies


Sample size
Selection of subjects

n4100
Defined primary or secondary care population not selected individuals

Method of measurement

Simultaneous using automated sphygmomanometers


Crossover design, repeated measurements
Controlled setting

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CE Clark et al
925

Citations retrieved in search


(n=357)
Citations excluded from search
data (n=341)
Full text papers retrieved for potential
inclusion (n=18)
Additional papers identified from
references (n=19)
Full text papers considered for
inclusion (n=37)
Full text papers excluded: no
prevalence data (n=6)
Full text papers assessed against
inclusion criteria (n=31)
Papers not meeting inclusion
criteria (n=27)
Papers meeting inclusion criteria
(n=4)
Figure 1 QUORUM flow diagram (adapted from Moher et al
199980).

IADs. In total, 31 English language series published


between 1915 and 2005 were assessed against the
inclusion criteria. Many studies exhibited selection bias in reporting selective or opportunistic
samples, or had unclear selection criteria,2,31,3340
and older studies tended to report highly selected
series.34,36,4145 Others suffered from bias in the selection of results for analysis37,46 or reported small sample
sizes (defined as o100 subjects).2,34,3436,41,43,4550
Studies reported one or more pairs of BP readings
measured either simultaneously or sequentially.
Simultaneous techniques used either two observers37,46 or a pair of automated sphygmomanometers41,51,52 to record BP in both arms at the
same time. Sequential methods involved measurement of BP in one arm and then the
other.2,20,29,33,35,36,38,39,4244,49,5359 Excluded studies,
with reasons for exclusion, are summarised in
Appendix A.
Reported prevalences

Only four studies met the inclusion criteria37,51,52,60


(Table 2). The mean prevalences of sIAD in these
studies were 19.6%X10 mm Hg (95% CI 18.0
21.3%) and 4.2%X20 mm Hg (95% CI 3.45.1%)
and for dIAD 8.1%X10 mm Hg (95% CI 6.99.2%).
The mean prevalences for excluded studies were
significantly higher (Table 3). One study presented
data for normotensive and hypertensive subjects,60
the prevalences of sIADX20 mm Hg and

Table 2 Characteristics of studies included in the review


Study (country of
origin)

Study population

Method of measurement

Sample
size

Prevalence of systolic
differences

Prevalence of diastolic
differences

Amsterdam and
Amsterdam (1943)60
(USA)

Normotensives

Repeated averaged
simultaneous
measurements

1000

31.2%X10 mm Hg
8.4%420 mm Hg

9.3%410 mm Hg

272

51%420 mm Hg

27.2%410 mm Hg

447

26.6%X10 mm Hg
7.2%X20 mm Hg
5.3%X10 mm Hg
0.1%X20 mm Hg
10%X10 mm Hg
indirect
6%X10 mm Hg direct
(difference NS)

15%X10 mm Hg

Hypertensives
Probably hospital, not
stated
Harrison et al. (1960)37 Patients attending
(USA)
clinic
Selected volunteers
with differences on
simultaneous indirect
measurement
Orme et al. (1999)52
(UK)

Staff, visitors and day


case surgery patients
at one DGH
No CVD
CVD

Lane et al. (2002)51


(UK)

Staff and patients in


one general hospital

Single sequential pair of


measurements
Simultaneous three pairs
of measurementsa
Simultaneous direct
intra-arterial

Automated simultaneous
2  2 crossover 4 pairs
readings averaged

447
53

4%X10 mm Hg
8%X10 mm Hg
indirect
1%X10 mm Hg direct
(difference NS)

462

8.2%X10 mm Hg
0X20 mm Hg

6.5%X10 mm Hg
0.4%X20 mm Hg

364

2.7%X10 mm Hg
0X20 mm Hg
19.4%X10 mm Hg
0X20 mm Hg

6.3%X10 mm
0.3%X20 mm
7.1%X10 mm
1.0%X20 mm

20%410 mm Hg
3.5%420 mm Hg

11.3%410 mm Hg
3.8%420 mm Hg

98
Simultaneous automated, 400
2 pairs of measurements

Hg
Hg
Hg
Hg

Abbreviation: CVD, cardiovascular disease.


a
Only this data set included in review.
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Table 3 Comparison of weighted mean prevalences of inter-arm differences for studies included and excluded
Inter-arm difference

sIADX10 mm Hg
sIADX20 mm Hg
dIADX10 mm Hg

Included studies

Excluded studies

Mean (%)

95% CI

Mean (%)

95% CI

19.6
4.3
8.1

18.022.3%
3.45.1%
7.09.2%

34.5
7.5
25.3

32.037.1%
4.910.0%
22.827.9%

Significance

Po0.001
Po0.001
Po0.001

Abbreviations: CI, confidence interval; dIAD, diastolic inter-arm difference; sIAD, systolic inter-arm difference.

dIADX10 mm Hg were significantly higher in the


presence of hypertension (sIADX20 mm Hg 8.4 vs
51%; OR 11.40, 95% CI 8.1216.01; Po0.0001 and
dIADX10 mm Hg 9.3 vs 27.2%; OR 3.64, 95% CI
2.555.20; Po0.0001). One study reported data for
subjects with or without CVD,52 and showed a
significantly higher rate of sIADX10 mm Hg in
patients with CVD (19.4% with CVD vs 2.7% without
CVD; OR 4.34, 95% CI 2.099.04; Po0.0001).

Discussion
The prevalence rates presented demonstrate that the
IAD is a common finding in clinical practice
whenever it is looked for. The majority of reports
and all included studies was from selected or
secondary care populations, the true general population or primary care prevalence is unknown.
Studies using sequential or single pair measurement
techniques appear to overestimate prevalence compared with studies meeting our inclusion criteria.
Strengths and weaknesses of the review

Published data on the prevalence of an IAD stretch


back to 1900.61 Thorough hand searching appears to
have yielded as full a set of papers as possible, but as
only English language papers were retrieved some
data may have been excluded. No foreign language
citations were identified after 1929;62 therefore, it
seems unlikely that our findings could have been
substantially altered by their inclusion. Data extraction was only carried out by one investigator but was
not a complex task, and the inclusion criteria were
clear and objective. The choices of inclusion criteria
were our own but based on a published critique32 of
the methodology of one of the studies.46
Implications for BP measurement in practice

Failure to recognise the IAD and to standardise


readings to the higher arm runs the risks of
inadequate treatment of hypertensive patients, false
diagnosis of hypotension due to over treatment
(pseudohypotension36), a delay in the diagnosis of
hypertension,63 or physician confusion creating the
potential for clinical inertia.64 The Health Survey
of England states that if systolic BP were lowered by
X10 mm Hg among the 71.5% of hypertensive
subjects uncontrolled (in the survey), we estimate
Journal of Human Hypertension

that 44000 fatal and nonfatal coronary events and


46000 fatal and nonfatal strokes could be prevented
each year in England.6 Given our estimate of the
prevalence of a sIADX10 mm Hg of 19.6%, there is
a one in 10 risk that a BP measurement could be
underestimated by this amount if the IAD has not
been excluded. We suggest that it is vital to undertake measurements of BP in a consistent manner in
both arms for all subjects, to record the findings
accurately, and to record measurements taken from
the higher arm to guide subsequent assessments.
This approach should be more clearly emphasised
in future hypertension guidelines, and given the
prevalence figures that we have presented, the
advice to refer subjects with a sIAD X20 mm Hg or
dIAD X10 mm Hg for specialist assessment is seen
to be impractical and should be revised.
Pathophysiology of the IAD

Although the ability of arteriosclerosis to affect BP


has long been recognised65 and the presence of an
IAD is used to help diagnose symptomatic upper
limb ischaemia,28 in health it has historically been
dismissed as a normal variant. Anatomical explanations have been proposed31,39,49,53,60,66 but there is
now evidence for an association with PVD, suggesting a pathological rather than a physiological
aetiology.
Initially the IAD was described as a sign of aortic
aneurysm67 or vascular disease,68,69 and the earliest
report dismissed its magnitude in health as negligible, with differences of 10 mm Hg being unusual.61
The earliest series of 36 patients reported a pressure
difference of 10 mm Hg or more in 20%, leading to
the conclusion that the difference between the right
and left brachial arteries is by no means diagnostic
of aneurysm.70 Another early series of 100 healthy
subjects found only 10% to have equal BPs71 and
the argument against arteriosclerosis as a cause
ever since has been that these differences are too
frequent,37 and therefore represent a spectrum of
normality. Consequently, anatomical explanations were advanced, which considered the angulation and anatomy of the aortic arch and its
branches.31,39,49,53,60,66 The high prevalence of an
IAD in war victims with unilateral injuries seemed
to support this explanation.35 But normal anatomy
alone cannot explain the higher left arm pressures
noted.36,51 It is our contention that the IAD may be due

The inter-arm blood pressure difference


CE Clark et al
927

to occult PVD59 and one recent study of subclavian


artery stenosis has shown such an association.29
If indeed such an observation was confirmed, one
would predict that factors associated with PVD
should have a higher prevalence in patients with an
IAD. CHD is one common condition strongly associated with PVD, as defined by a reduced ABPI.2125,72
No study has set out to compare the prevalence of an
IAD in patients with or without CHD; however, data
extracted from one study meeting our inclusion
criteria showed a significantly higher prevalence of
sIADX10 mm Hg in patients with CVD than without
(19.4 vs 2.7%; OR 4.34, 95% CI 2.099.04;
Po0.0001).52 Arteriosclerosis was also more common
in subjects with an IAD in Kay and Gardners study,38
whereas although Singer and Hollander found no
relationship between coronary risk factors and an
IAD, they did find the mean sIAD to be significantly
higher in patients with known coronary artery
disease than without (14.5 vs 10.4 mm Hg;
P 0.05).55 Another smaller study reported higher
prevalence of IAD in patients with PVD compared to
both CHD patients and controls.36 Thus, there is a
body of indirect evidence to support our hypothesis.
There is also direct evidence from vascular studies.
In one angiographic series, 83% of patients undergoing vascular surgery with a difference in systolic
BPs had evidence of innominate or subclavian artery
stenosis on the side with the lower BP.73 IAD
prevalence is also high (7888%) in subclavian steal
syndrome,74,75 and the severity of the stenosis has
been associated with the size of the BP difference.76
In another large series of patients presenting for coronary angiography, the non-simultaneously measured
IAD had a low sensitivity and positive predictive
value, but high specificity (85% for 410 mm Hg and
94% for X20 mm Hg) and negative predictive value
(99% for 410 mm Hg and 98% for X20 mm Hg) for
predicting subclavian stenosis,77 and aortic arch
angiography in a series of subjects with PVD showed
a measurable stenosis of at least one brachiocephalic
artery in 42% of 48 subjects studied.78
Thus, there is evidence of an association of the
IAD with symptomatic PVD. We propose that there
is a similar underlying aetiology of asymptomatic
arterial disease causing the IAD reported in these
studies. As the risk of cardiovascular events is
similarly high for subjects with symptomatic and
asymptomatic PVD in primary care,79 the recognition of the IAD, assuming our hypothesis to be
correct, could become an important part of the risk
assessment of hypertensive patients. This would
facilitate the focusing of finite resources for primary
prevention onto those at highest risk, as demanded
by the National Service Framework for Coronary
Heart Disease.30 To justify this approach, evidence
from prospective survival studies is needed. To date,
only the authors have reported a correlation of
reduced event-free survival with the IAD in a
general20 and hypertensive (Clark CE, MSc Dissertation, Peninsula Medical School, 2006) primary care

population. Larger studies using careful and standardised bilateral assessments of BP are needed to
confirm this important observation, and to examine
the additional contribution as a risk factor that
recognition of the IAD can make to cardiovascular
risk assessment. Thus, Cyriaxs words from 1921:
Neglect to exclude the presence of the differential
blood-pressure sign may easily lead to totally
erroneous conclusions as to the state of the circulation33 remain just as relevant now.

Conclusions
The IAD has been repeatedly shown to occur in
substantial numbers of patients studied in primary
and secondary care, and needs to be looked for in all
patients whose diagnosis and treatment depend on
accurate BP measurements. Many studies have
overestimated prevalence due to poor design, and
our estimate of prevalence from good quality studies
is 19.6% sIADX10 mm Hg, 4.3%X20 mm Hg and
8.1%X10 mm Hg dIAD. The prevalence in coronary
heart disease and hypertensive patients appears to
be much higher. This fact, and the importance of
measuring both arms during assessment, should be
better emphasised in current hypertension management guidelines.
There is a body of evidence associating the IAD with
PVD, suggesting a pathological rather than physiological cause. This raises the possibility that the
presence of the IAD may have a prognostic value in
predicting cardiovascular events. There is preliminary
evidence for this but further large, carefully controlled
studies are needed to confirm it, and to establish what
independent contribution to cardiovascular risk assessment the detection of an IAD may make.

Acknowledgements
CEC was supported by a Clinical Academic Fellowship from Plymouth tPCT and a grant from Mid
Devon Research Group. We owe thanks to Ginny
Newton and her colleagues at Exeter Medical
Library for their persistence in obtaining so many
historic papers and books for this review.
Conflict of interests
None to declare.

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CE Clark et al
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Journal of Human Hypertension

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Journal of Human Hypertension

Appendix A
Summary of excluded studies
Study population

Reason for exclusion

Phipps (1915)34 (USA)

Mixed in-patients

Sequential measurements

Cyriax (1918)35 (UK)

War wounded

Cyriax (1920)2 (UK)

Cyriax (1921)33 (UK)

Sample
size

Prevalence of systolic differences

Prevalence of
diastolic differences

36

20%X10 mm Hg

Not stated

Sequential measurements

36

72%45 mm Hg

Not stated

Post-Surgical in-patients
Many war trauma.
Mainly with unilateral wounds

Sequential measurements

73

83%X10 mm Hg
20%X20 mm Hg

81%X10 mm Hg
12%X20 mm Hg

Private practice (93) and in-patients (35):


Unilateral or bilaterally unequal surgical
cases
Bilaterally equal and constitutional
disorders

Sequential measurements

128
56

Confirmed previous findings

Kay and Gardner (1930)38 (USA)

General medical practice, opportunistic


sample

Korns and Guinand (193l)31


(USA)

78

35%X10 mm Hg
7%X20 mm Hg

Confirmed previous
findings
45%X10 mm Hg
4%X20 mm Hg

Sequential measurements

125

12% 420 mm Hg

13% 410 mm Hg

Healthy University students, 73% male,


mean age 20

Simultaneous but single


pair of measurements

1000

22.2%X10 mm Hg

21.7%X10 mm Hg

Southby (1935)53 (Australia)

Patients attending one general practice

Sequential measurements

516

Differences above 20 mm systolic or


10 mm diastolic in 60% of cases

Israel (1944)39

Hypertensives, population not defined

Sequential measurements

125

18.4% 420 mm Hg

2.4% 410 mm Hg

Office patients

Sequential measurements

755

50%410 mm Hg
13.6% 420 mm Hg

33.7% 410 mm Hg

Swallow (1975)(letter)50 (UK)

General practice, 5054 year old males

Measurement technique
not stated

33

76%X10 mm Hg

Kristensen and Kornerup


(1982)43 (Denmark)

Highly selected normotensive patients


without signs of CVD
Unselected normotensive in-patients

Sequential measurements

55

34.5%X10 mm Hg
3.4%X20 mm Hg
60.9%X10 mm Hg
26.1%X20 mm Hg
49.1%X10 mm Hg
15.8%X20 mm Hg
5.2%X30 mm Hg
59.7%X10 mm Hg
25.8%X20 mm Hg
8.1%X30 mm Hg

14.5%X10 mm Hg

20%X10 mm Hg
3.4%X20 mm Hg

9.7%X10 mm Hg

Rueger (1951)

54

(USA)

23

Hypertensive out-patients

57

Hypertensive out-patients

62

Hashimoto et al. (1984)42 (USA)

Elderly residential home residents attending Sequential measurements


for BP checks. 50% were hypertensive

Gould et al. (1985)46 (UK)

Hypertensives

Simultaneous random zero


measurements with two
observers

174
91

Dismissed differences over 20 mm as


erroneous, found no apparent mean
differences over 10 mm systolic or
diastolic. Individual measured

43.5%X10 mm Hg
8.7%X20 mm Hg
29.8%X10 mm Hg
5.2%X20 mm Hg
1.8%X30 mm Hg
37.1%X10 mm Hg
12.9%X20 mm Hg
1.6%X30 mm Hg

The inter-arm blood pressure difference


CE Clark et al

Reference (country of origin)

differences were 8% readings 410 mm


Hg systolic and 3% diastolic. Concluded
that no bias is introduced by making
measurements in different arms
Goldhill (1986)47 (USA)

Not stated

One observer listening to


bilateral dopplers
Review of recordings of
dopplers and pressures

52
68

37%X6 mm Hg
13%X11 mm Hg
6%X6 mm Hg
None49 mm Hg

Yagi et al. (1986)45 (Japan)

Convalescent stroke in-patients

Simultaneous automated
measurements

47

Mean 131/83 in paretic arms, 129/78 in


intact arms, Po0.01/Po0.001

Frank et al. (1991)36 (USA)

Peripheral vascular disease in-patients

Sequential measurements

58

21%X20 mm Hg
41%X10 mm Hg
16%X10 mm Hg
3%X20 mm Hg
13%X10 mm Hg
0%X20 mm Hg

31%X10 mm Hg
4%X15 mm Hg
5%X10 mm Hg
3%X15 mm Hg
5%X10 mm Hg
3%X15 mm Hg
None

Coronary heart disease in-patients


Controls: orthopaedic & urology in-patients

38
38

Fotherby et al. (1993)41 (UK)

Elderly in & out-patients


Young in & out-patients

Simultaneous automated
measurements

40
40

10%410 mm Hg
None

Panayiotou et al. (1993)48 (UK)

Hemiplegic in-patients following acute


stroke

Simultaneous automated
measurements

15

No correlation with side of paresis, mean


inter-arm difference 4.4/4.7 mm Hg

Singer and Hollander (1996)55


(USA)

Ambulant patients over 5 years old


attending university hospital emergency
department

Sequential measurements
Single (not repeated)
simultaneous automated
indirect

300
310

OShea and Murphy (2000)49


(Ireland)

Patients attending for ambulatory BP


monitoring

Sequential measurements

39

33%X10 mm Hg

Clark (2001)59 (UK)

General practice

Sequential measurements

205

31%X10 mm Hg
4%X20 mm Hg

13%X10 mm Hg

Cassidy and Jones (2001)56 (UK)

General practice

Sequential measurements

237

23%X20 mm Hg

40%X10 mm Hg

Normotensive patients attending ER and


staff accepting BP screening

Sequential measurements

100

15%X10 mm Hg

Clark and Powell (2002)20 (UK)

General practice

Sequential measurements

280

40.7%X10 mm Hg
13.6%X20 mm Hg

Pesola et al. (2002)57 (USA)

Staff and visitors to an ER with history of


hypertension willing to be screened

Sequential measurements

100

18%X10 mm Hg

Shadman et al. (2004)29 (USA)

General population
Vascular patients

Sequential measurements

2975
1248

1.9%415 mm Hg
7.1%415 mm Hg

Not stated
Not stated

Arnett et al. (2005)58 (USA)

Random population sample


Hypertensive siblings

Sequential measurements

824

9.2%410 mm Hg
1.1%420 mm Hg
14.2%410 mm Hg
1.8%420 mm Hg

1.6%410 mm Hg
0420 mm Hg
2.8%410 mm Hg
0.1%420 mm Hg

(USA)

23.2%X10 mm Hg

931

Journal of Human Hypertension

2195

28%410 mm Hg
20.6% 410 mm Hg

The inter-arm blood pressure difference


CE Clark et al

Pesola et al. (2001)

44

13.3%420 mm Hg
11.6% 420 mm Hg