Current Cardiology Reviews, 2008, 4, 101-106
101
Critical Review of the Ankle Brachial Index
Tahir H. Khan1,*, Falahat A. Farooqui2 and Khusrow Niazi3
1
Hospitalist / Instructor of Medicine, Emory University Dept of Medicine, Emory Crawford Long Hospital, 550 Peachtree St, MOT 6th Fl Rm 4307, Atlanta, GA 30308, USA; 2Dept of Medicine / Div of Cardiology, Emory University, 550
Peachtree St, MOT 6th Floor, Atlanta,GA 30308, USA; 3Emory University School of Medicine, Director of Peripheral
Intervention, Emory Crawford Long Hospital, 550 Peachtree St, MOT 6th Fl Rm 4307, Atlanta, GA 30308, USA
Abstract: Ankle brachial index (ABI) has been utilized in the management of peripheral arterial disease (PAD).ABI is a
surrogate marker of atherosclerosis and recent studies indicate its utility as a predictor of future cardiovascular disease and
all-cause mortality. Even so, this critical test is underutilized. The purpose of this review is to summarize available evidence associated with ABI methodology variances, ABI usage in the treatment of PAD, and ABI efficacy in predicting
cardiovascular disease. This review further evaluates how ABI is used in the prognosis and follow-up of lower extremity
arterial disease.We reviewed the most current American College of Cardiology guidelines for the management of PAD,
the Trans Atlantic Intersociety Consensus (TASC) working group recommendations, and searched the Medline for the following words: ankle brachial index, ABI sensitivity and specificity, and peripheral arterial disease.
The ABI is a simple, noninvasive clinical test that should not only be applied to diagnose PAD, but also to provide important prognostic information about future cardiovascular events. Although the ABI has been employed in clinical practice
for some time, our review of various studies reveals a lack of standardization regarding both the method of measuring ABI
and the cutoff point for abnormal ABI. It is extremely important that we understand all aspects of this crucial test, as it is
now being recommended as part of a patient’s routine health risk assessment.
Key Words: Peripheral arterial disease, Ankle Brachial index, ABI Sensitivity and Specificity, Atherosclerosis, Cardiovascular
morbidity and mortality.
INTRODUCTION
Peripheral arterial disease (PAD) of the lower extremities
is a common disease affecting approximately 12 million
people in the United States [1]. Atherosclerosis is the major
cause of PAD of lower extremities [2]. The prevalence of
PAD varies based on the population surveyed and the methodology of computing the ankle-brachial index (ABI) [3-5].
The ABI is the preferred initial screening test to help diagnose and grade the obstruction of peripheral arterial disease
(PAD) in the legs. Interval ABI results are used to monitor
the efficacy of revascularization procedures of lower extremities. Additional uses of ABI include predicting the
prognosis regarding the limb salvage, wound healing and
future cardiovascular related morbidity and mortality [6].
HISTORICAL PERSPECTIVE
Arterial measurements in lower extremities were first
described by Naumann in 1930 [7]. In 1950,Winsor was
first to use ABI measurements in patients with peripheral
arterial disease [8].
METHODS OF MEASURING ANKLE BRACHIAL
INDEX
The measurement of the ABI involves recording the systolic pressures in the brachial artery at each elbow and systolic pressures in the posterior tibial and the dorsalis pedis
arteries at each ankle. The result is reported as a ratio of the
*Address correspondence to this author at the Hospitalist / Instructor of
Medicine, Emory University Dept of Medicine, Emory Crawford Long
Hospital, 550 Peachtree St, MOT 6th Fl Rm 4307, Atlanta, GA 30308, USA;
Tel: 404- 686- 7478; Fax: 404-686-4824;
E-mail:
[email protected]
1573-403X/08 $55.00+.00
ankle systolic pressure in the numerator,over the higher brachial pressure in the denominator. The ABI is calculated for
each leg separately, and the lower of the two values is taken
as a result for the patient. Numerous methods of calculating
the ABI have been described based with variances in the
numerator taken in the ABI equation:
a) The current method recommended by the ACC/AHA involves using the higher of the two ankle systolic arterial
pressures, termed high ankle pressure (HAP) (Fig. 1) as the
numerator in the ABI equation [2,6,9-12].
b) A second method reported in the literature uses the lower
of the two ankle systolic arterial pressures,termed low ankle
pressure (LAP) as the numerator when calculating the ABI
[5,13,14].
c) A calculation applied in some epidemiological studies
uses the average of the two ankle systolic pressures as the
numerator in the ABI equation [15,16].
d) A few studies have used the posterior tibial artery systolic
pressure to calculate ABI [17,18].
INTERPRETATION OF ABI RESULTS
The patient is diagnosed with PAD when the ABI is < 0.9
[2,19]. PAD is graded as mild to moderate if the ABI is between 0.4 and 0.9, and an ABI less than 0.40 is suggestive of
severe PAD [19]. An ABI value greater than 1.3 is also considered abnormal, suggestive of non-compressible vessels.
CORRELATION OF ABI WITH LOWER EXTREMITY FUNCTION AND OUTCOMES
Patients with mild to moderate PAD are likely to experience lower extremity pain with exercise (claudication). Pa©2008 Bentham Science Publishers Ltd.
102 Current Cardiology Reviews, 2008, Vol. 4, No. 2
Khan et al.
Fig. (1). High ankle pressure ABI (HAP) and Low ankle pressure ABI (LAP) calculations shown in a hypothetical case.
tients with ABI less or equal to 0.5 are likely to have lower
extremity pain while resting [20]. Criqui et al. reported that
the incidence of claudication (applying Rose criteria) was 49
% in patients with ABI < 0.6 compared to 34 % in patients
with ABI between 0.6 and < 0.9 [21].
Several specific ABI values indicate evidence of correlation with the leg function in multiple studies. In a study of
865 women aged 65 and older, McDermott et al. discovered
that subjects with ABI < 0.6 were at higher risk of having
impaired walking abilities [13]. In an earlier study McDermott et al. [22] reported that among patients with PAD, decreases in ABI values are associated with decreases in six
minute walk distance, maximum walking speed, and walking
endurance. Each increase of 0.4 in the ABI was associated
with an increase in the six minute walk distance and usual
and maximal walking speed.
An ABI <0.4 increases the risk of limb loss, gangrene,
ulceration and delayed wound healing [6,23]. However, an
absolute ankle systolic pressure less than 60 mmHg, rather
than the ABI value, has been found to correlate better in
terms of viability of the lower extremities in PAD [2,24].
SENSITIVITY AND SPECIFICITY OF THE ABI IN
THE DIAGNOSIS OF PAD
Numerous studies have reported that the ABI, when
compared to angiography, has a sensitivity of more than 90%
and a specificity of more than 95% in diagnosing 50% stenosis of the lower extremity arteries [6,11,12,16,17,25,26].
However, Schroder et al. recently reported that the HAP ABI
had a sensitivity of 68% and a specificity of 99% [27]. The
authors reported the LAP ABI sensitivity and specificity to
be 89 and 93% respectively. Niazi et al. reported that the
HAP ABI had a sensitivity of 69% with a specificity of 83%.
The sensitivity and specificity of the LAP ABI was 84% and
64% respectively [28].
Feigelson et al. [29] evaluated the sensitivity of an ABI <
0.8 to be 39 % within the entire cohort and 70% in patients
with PAD (This study is reported by ACC/AHA guidelines
that ABI has a sensitivity of 89% in diagnosing PAD). Lijmer et al. has reported that an ABI value of 0.91 had a sensitivity of 79% and a specificity of 96% to detect 50% or
more stenosis of lower extremity arteries defined on angi-
Critical Review of the Ankle Brachial Index
ography [30]. Angiograms of the lower extremities were
available for only 53 patients (12% of the total patients in
study). Stoffers et al. applied ROC analysis and reported the
sensitivity and specificity for ABI < 0.97 to be 79% and 82%
respectively [31]. When two vascular technicians using ultrasound technology interpreted the ankle arterial pulse wave
forms as “pathologic”, the diagnosis of PAD was determined. No angiographic confirmation for the diagnosis of
PAD was provided.
Based on the evaluated studies, we find that the lower
ankle pressure ABI has better sensitivity in diagnosing PAD.
Additionally, the context in which few studies [24,32-34] are
reported (that ABI has been shown to be > 90% sensitive and
> 95% specific to diagnose 50% stenosis of lower arteries) is
inaccurate. Carter and Yao [32,33] only concluded that ABI
was low in patients with PAD without providing any ABI
sensitivities. Ouriel did report in his two studies [23,34] that
ABI < 0.97 has a sensitivity of more than 97% and specificity of more than 100% respectively in diagnosing PAD.
Nevertheless, the lack of the authors definition of PAD in
terms of diameter stenosis of the arteries weakens the validation of their findings.
ROLE OF THE ABI IN THE FOLLOW UP OF PAD
PATIENTS AFTER LOWER EXTREMITY INTERVENTION
Mclafferty et al. reported the sensitivity and specificity of
ABI to detect the progression of lower extremity arterial
disease after surgical intervention [35]. One hundred fourteen patients (193 Limbs) were followed for a mean of 3.3
years. A baseline ABI was established for each patient, followed by another ABI within a week of the revascularization
procedure. Progression of the PAD was documented with
arterial duplex scanning or arteriography of the lower extremities if clinically indicated. Disease progression was
only monitored in native arteries and not in the bypass grafts.
The authors reported that a drop of the ABI more than 0.15
carried a sensitivity of 41% and a specificity of 84% to detect the progression of lower extremity arterial disease.
Decrinis et al. tested the sensitivity and specificity of
ABI in patients who had undergone angioplasty of the superficial femoral artery stenosis [36]. ABI were performed postoperative day one, three, six and twelve months after the
procedure. Follow up angiograms of the lower extremities
were performed one year after angioplasty. A total of 116
patients were enrolled in the study. (Angiographic definition
of re-stenosis was progression of post PTA 50% stenosis to
more than 70% at follow up angiogram or an increase in the
stenosis severity to 10 % or more of predilation obstruction.)
For an ABI drop of 0.10 the sensitivity and specificity were
72% and 82% respectively in predicting restenosis using
their criteria. An ABI drop of 0.15 had a sensitivity and
specificity of 66% and 100% respectively for restenosis. In
predicting the patency of the post PTA vessel, an improvement of ABI of 0.10 post PTA had sensitivity and specificity
of 79 % and 92%. ABI improvement of 0.15 post PTA had
sensitivity and specificity of 67% and 100% respectively for
patency of post PTA artery.
Current Cardiology Reviews, 2008, Vol. 4, No. 2
103
ABNORMAL ABI AS MARKER OF ATHEROSCLEROSIS AND PREDICTOR OF FUTURE CARDIOVASCULAR MORBIDITY AND MORTALITY
The unique role that ABI plays as a marker of atherosclerosis is clear by its correlation with cardiovascular disease
(CVD) in multiple population based studies [9-18]. The
measurement of ABI has been recommended as part of risk
assessment and primary prevention of CVD in asymptomatic
individuals who have intermediate risk factors for CVD
[37,38]. There is consensus that an abnormal ABI in an otherwise asymptomatic individual would categorize him in the
high risk category for future CVD. The American Diabetes
Association recommends routinely screening all patients
with diabetes above age 50 and in all diabetics with risk factors (e.g. smoking, hyperlipidemia etc) for PAD under age
50 [39].
1) Cardiovascular Disease (CVD) and Mortality
Numerous epidemiologic studies have reported up to four
fold increased rates of cardiovascular disease and mortality
with abnormal ABI [9-18,40-49]. Findings of some of these
are summarized in Table 1.
Vogt et al. reported that the mortality rates from atherosclerotic heart disease doubled (RR 2.0 95% CI 1.4-2.9) with
each 0.5 units drop in the ABI [16]. The ten year mortality
rates of CVD in patients with an ABI < 0.5 was 37%, compared to a 27 % in patients with ABI values ranging between
0.5- 0.7, 22 % in patients with ABI 0.7- 0.9 and 17 % in patients with ABI values >0.9(P=0.0039). Relative risk for all
cause mortality was higher (1.95, 95% CI 1.42-2.68) in subjects with ABI < 0.5 compared to subjects with ABI values
ranging between 0.51-0.7 (RR 1.59, 95% CI 1.18-2.15).
O’Hare et al. investigated the rates of cardiovascular disease and mortality across different levels of ABI [40]. The
cohort included 5748 subjects, their mean age was 73 years,
and the mean follow-up was 11 years. The study found that
subjects with an ABI < 0.6 was consistently associated with
increased CV mortality (hazard ratio [HR] 2.13 95%,CI
1.49-30.5), all cause mortality (HR 1.82,95%CI 1.42-2.32)
and cardiovascular events(HR 1.60,95% CI 1.09-2.34) compared to participants with ABI 1.10-1.20. In the Framingham
Offspring study the prevalence of CAD was 30% in patients
with an ABI < 0.9 compared to 10% in subjects with ABI
>1.0 (P 0.001) [41]. Among the participants of the HOPE
trial, the percent rates of CV disease, CV death and all cause
mortality in subjects with an ABI >0.9 were 10.1,5.3 and 8.8
respectively, compared to 13.7, 8.6,12.8 in the ABI group
0.6-0.9, and 13.4, 9.4 and 14.7 in the ABI group < 0.6 respectively [42].
2) Risk for Stroke / Transient Ischemic Attack (TIA)
Zheng et al. reported that the risk of Stroke /TIA for men
with ABI < 0.9 was four times (Odds Ratio 4.2 -4.9, 95% CI
1.8-9.5) than in those with an ABI >0.9 [43]. In the
Framingham study, the risk of stroke/ TIA was two fold
(Hazards ratio 2.0, 95% CI 1.1-3.7) among participants with
an ABI< 0.9 [15]. In the Framingham offspring study the
prevalence of stoke was 9% in men with ABI< 0.9 compared
104 Current Cardiology Reviews, 2008, Vol. 4, No. 2
Table 1.
Khan et al.
Cardiovascular, Stroke / TIA and All Cause Mortality Across Range of ABI in Published Studies
Study
No Study Subjects
ABI
Effect Measure
CVD
CVD Mortality
All Cause Mortality
Stroke/ TIA
Diehm et al. 12
6880
< 0.9
Odds Ratio
1.53
N/A
N/A
1.77
Vogt et al.
1930
>0.9
Relative
N/A
<0.9-0.71
Risk
No Significant
association
16
<0.7-0.51
RR 2.0 each
1.0
< 0.5 Drop in
1.15-0.95
ABI.
1.59-1.70
<0.50
O’Hare et al.
5748
40
Ostergen
8986
et al. 42
1.95-2.13
0.91-1.0
Hazard
1.37
1.60
1.40
0.81-0.90
Ratio
1.72
2.37
1.73
0.71-0.81
1.63
2.01
1.80
0.61-0.70
1.57
2.31
2.08
<0.61
1.60
2.13
1.82
Included in
CVD.
> 0.9
Four year
10.1
5.3
8.8
3.5
0.9-0.6
Clinical outcomes
13.7
8.6
12.8
4.3
13.4
9.4
14.7
5.9
P 0.0038
P <0.0001
P .0002
P 0.234
4.5
N/A
N/A
4.3
<0.6
(Percent rates).
Zheng et al.
15106
<0.9
Odds Ratio
43
0.91-1.0
Leng et al.
45
1592
1.0-0.9
0.9-0.71
Five Year
Incidence
<0.7
(P<0.05)
(P <.001)
2.4
1.7
5%
6%
11%
3%
7%
8%
16%
3%
9%
21%
34%
3%
P.057
P <.001
P <.001
P .020
N/A: Data not provided; CVD: Cardiovascular Disease; TIA: Transient Ischemic attack.
to 2 % in men with ABI > 1.0 (0.001) [41]. In the Cardiovascular Health Study, patients with ABI <0.8 had twice the
rates of stroke/TIA [44]. Similarly, Leng et al. reported that
subjects with an ABI <0.9 had increased risk of stroke(RR
1.98, 95% CI 1.05-3.77) [45].
range of ABI a value < 0.6 has been found with increased
CV events (Table 1).
3) Abnormal ABI as Predictor of Morbidity and Mortality in Post-Coronary Artery Bypass Graft Patients
Heald et al. performed a systematic review of 11 published studies with a combined number of 44590 subjects
[47]. The authors reported that ABI < 0.9 was associated with
increased all cause mortality (RR 2.35, P< 0.001), cardiovascular and cerebrovascular mortality (RR 2.34, P =0.002),
fatal and non-fatal coronary heart disease (RR 2.13, P=
0.003) and fatal and non-fatal stroke (RR 1.86, P=0.07).
Abnormal ABI has been found as prognostic indicator for
survival and complications among patients undergoing coronary artery bypass surgery. Aboyans V et al. studied the role
of abnormal ABI as a marker for long term prognosis in the
post coronary artery bypass graft patients (CABG) [48]. The
mean age of the patients was 69 years with a follow-up of
4.4 years. Patients with clinical PAD (defined as history of
vascular surgery and/or history of intermittent claudication)
and sub clinical PAD (defined as ABI<0.85) had three fold
excess risk of primary end points (composite of cardiovascular death, non-fatal acute coronary syndrome, non-fatal
stroke, TIA and coronary or peripheral revascularization)
compared to patients without PAD after CABG. Risk of
acute coronary syndrome was more than two times (HR 2.12
to 2.35) in patients with clinical and sub clinical PAD.
An ABI < 0.9 identifies subjects with increased future
cardiovascular morbidity and mortality. However, across the
Burek et al. studied the five year mortality rates in Post
CABG/ Coronary PTCA patients. The five year mortality
In a meta analysis of nine studies Doobay reported the
predictive value of ABI in predicting future cardiovascular
events [46]. The authors reported that an ABI less than 0.9
has a sensitivity and specificity of 16.55 and 92.7% for CAD
(likelihood ratio 2.53), 16.0% and 92.2% for stroke (likelihood ratio 2.45) and 41.0% and 87.9% for cardiovascular
mortality (likelihood ratio 5.61), respectively.
Current Cardiology Reviews, 2008, Vol. 4, No. 2
Critical Review of the Ankle Brachial Index
rate was 14 % in patients with ABI < 0.9 compared to 3% in
patients with ABI > 0.9 (RR 4.9 95% CI 1.8-13.4, P 0.001)
[49]. The investigators reported that abnormal ABI< 0.9 was
a strong predictor of mortality among patients with multivessel CAD.
[11]
[12]
[13]
CONCLUSION
We conclude that ABI is the screening test of choice for
the diagnosis of patients with PAD due its simplicity, reproducibility and cost effectiveness. Recent studies suggest the
use of low ankle pressure ABI as the method for calculating
the ABI due to its better sensitivity. Use of ABI is recommended as part of management of patients who have undergone lower extremity revascularization procedures.
[14]
[15]
[16]
As surrogate marker for atherosclerosis, ABI has been
found to give very important prognostic information regarding future cardiovascular events. We notice different methods and cutoff points for abnormal ABI have been used in
different epidemiologic studies. There is a need for a uniform method of ABI to be used in studies. Current evidence
suggests the use of ABI for identifying high risk patients for
future cardiovascular and cerebrovascular mortality. In doing
so, one can aggressively modify risk factors to prevent both
short and long term events.
ACKNOWLEDGMENTS
[17]
[18]
[19]
[20]
[21]
The authors thank Ms Anum Niazi for helping us review
and edit the presentation of the paper.
[22]
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