Usefulness of Postexercise Ankle-Brachial Index to Predict

All-Cause Mortality
Mobeen A. Sheikh, MDa,*, Deepak L. Bhatt, MDb, Jianbo Li, PhDc, Songhua Lin, MSc, and
John R. Bartholomew, MDd
Peripheral arterial disease predicts future cardiovascular events and all-cause mortality. Con-
ventional methods of assessment might underestimate its true prevalence. We sought to
determine whether a postexercise ankle-brachial index (ABI), not only improved peripheral
arterial disease detection, but also independently predicted death. This was an observational
study of consecutive patients referred for ABI measurement before and after the fixed-grade
treadmill or symptom-limited exercise component to a noninvasive vascular laboratory from
January 1990 to December 2000. The subjects were classified into 2 groups. Group 1 included
patients with an ABI of >0.85 before and after exercise, and group 2 included patients with a
normal ABI at rest but <0.85 after exercise. A total of 6,292 patients underwent ABI mea-
surements with exercise during the study period. Propensity score matching of the groups was
performed to minimize observational bias. Overall mortality, as determined using the United
States Social Security death index, was the end point. The 10-year mortality rate of groups 1
and 2 was 32.7% and 41.2%, respectively. An abnormal postexercise ABI result independently
predicted mortality (hazard ratio 1.3, 95% confidence interval 1.07 to 1.58, p 0.008).
Additional independent predictors of mortality were age, male gender, diabetes, and hyper-
tension. After the exclusion of patients with a history of cardiovascular events, the predictive
value of an abnormal postexercise ABI remained statistically significant (hazard ratio 1.67, 95%
confidence interval 1.29 to 2.17, p <0.0001). In conclusion, our results have shown that the
postexercise ABI is a powerful independent predictor of all-cause mortality and provides
additional risk stratification beyond the ABI at rest. 2011 Elsevier Inc. All rights reserved.
(Am J Cardiol 2011;107:778 782)

A diagnosis of peripheral arterial disease (PAD) serves
as a marker for systemic atherosclerosis. The National Cho-
lesterol Education Panel guidelines1 have recognized PAD
as a disease equivalent to the presence of coronary artery
disease (CAD). This serves to highlight the newfound ap-
preciation for a PAD diagnosis in the cardiovascular risk
assessment and determining the vigor of preventive strate-
gies. The ankle-brachial index (ABI) is a useful tool to
screen for PAD; however, conventional ABI measurements
have been obtained in the at rest state and might underes-
timate the true prevalence of PAD. Although it has been
recognized in clinical practice that obtaining a measurement
of the ABI after exercise might improve the sensitivity of
PAD detection,2 the postexercise ABI has not thus far been
validated as a screening test nor has the association with
all-cause mortality been determined in a United States-
based population. In the present study, we assessed the
a
Interventional Cardiac and Vascular Service, The Medical Group,
Beverly, Massachusetts; bDepartment of Cardiology, Veterans Affairs Bos-
ton Healthcare System, Integrated Interventional Cardiovascular Program,
Brigham and Womens Hospital, and Thrombolysis In Myocardial Infarc-
tion Study Group, Harvard Medical School, Boston, Massachusetts; and
Departments of cBiostatistics and Epidemiology and dCardiovascular Med-
icine, Cleveland Clinic, Cleveland, Ohio. Manuscript received August 15,
2010; manuscript received and accepted October 19, 2010.
*Corresponding author: Tel: (617) 860-3536; fax: (978) 232-7027.
E-mail address: msheikhmd@gmail.com (M.A. Sheikh).
prognostic value of the postexercise ABI among patients
referred for testing with exercise for clinical reasons. We
also sought to determine whether an abnormal postexercise
ABI results was an independent predictor of death and could
potentially identify a population at greater mortality risk
that would otherwise have been missed using the conven-
tional at rest ABI measurements.
Methods
Consecutive patients referred to the Cleveland Clinic
noninvasive vascular laboratory from January 1990 to De-
cember 2000 for either complete pulse volume recordings of
the lower extremities or standard ABI measurement before
and after a fixed-grade treadmill protocol or symptom-lim-
ited exercise test were considered for analysis. The patients
had to be 40 years old and residents of the United States
with a valid Social Security number. The indication for
testing was at the sole discretion of the referring physician.
For the purposes of the present study, the patients were
divided into 2 groups according to their ABI result: group 1,
a normal ABI of 0.85 both at rest and after exercise; and
group 2, a normal ABI at rest that was abnormal (0.85) in
either limb after exercise. The exclusion criteria were a
history of lower limb revascularization, either surgical or
percutaneous, the lack of pressure values secondary to com-
pletely or partially calcified arteries or an inaudible Doppler
signal, unilateral studies, and nonatherosclerotic etiologies
for lower extremity occlusive vascular disease.

0002-9149/11/$ see front matter 2011 Elsevier Inc. All rights reserved. www.ajconline.org
doi:10.1016/j.amjcard.2010.10.060
 Miscellaneous/Postexercise ABI 779

At testing, the patient information, including demo- Table 1

graphic data, pulse pressure measurements, and risk factor Demographic and risk factor profile of patients in groups 1 and 2 after
profile, were stored in an institutional review board-ap- propensity score matching
proved vascular laboratory database. Additional data were Variable Group 1 Group 2 p
collected, if required, by reviewing the electronic and paper (n 713) (n 713) Value
medical records and adding to the database in a manner that Men 484 (67.9%) 467 (65.5%) 0.3395
protected patient confidentiality. The criteria for the various Race
risk factors were as follows. CAD was defined as present if White 659 (92.4%) 664 (93.1%) 0.6090
the patient had a history of angina, congestive heart failure, Black 47 (6.6%) 44 (6.2%) 0.7452
or myocardial infarction or had undergone percutaneous Age (years) 64.5 (9.2) 64.7 (9.5) 0.6745
coronary intervention or coronary artery bypass grafting. 4049 58 (8.1%) 59 (8.3%)
Similarly, a history of a cerebrovascular accident or abdom- 5059 149 (20.9%) 159 (22.3%)
inal aortic aneurysm was defined as a history of stroke, 6069 302 (42.4%) 259 (36.3%)
transient ischemic attack, or previous carotid endarterec- 70 204 (28.5%) 236 (33.1%)
Smoker 21 (3.0%) 25 (3.5%) 0.5488
tomy and previous identification on suitable imaging studies
Hypertension 230 (32.3%) 234 (32.8%) 0.8211
or previous surgical repair, respectively. The assessment for Diabetes mellitus 87 (12.2%) 91 (12.8%) 0.7486
hypertension, diabetes, and hyperlipidemia was determined Coronary artery disease 236 (33.1%) 243 (34.1%) 0.6947
by a combination of questioning at testing, chart review, and Cerebrovascular accident 69 (9.7%) 798 (10.9%) 0.4332
medication use. Smoking history was determined by self- Abdominal aortic aneurysm 39 (5.5%) 41 (5.8%) 0.8180
reported current use at testing. Hyperlipidemia 126 (17.7%) 129 (18.1%) 0.8358
Doppler-derived systolic pressures at the level of the
Group 1, patients with normal ankle-brachial index at rest and after
brachial artery and posterior tibial and dorsalis pedis arteries exercise, group 2: patients with normal ankle-brachial index at rest but
were obtained by recording the level at which the first abnormal after exercise.
Doppler sound was heard after deflation of the cuff placed
over the upper arm and ankle, respectively. The index was
calculated using the greater of the 2 ankle pressures (pos- Table 2
terior tibial or dorsalis pedis) obtained on each leg, with the Demographic and risk factor profile of patients in groups 1 and 2
greater of the brachial pressures. The patients exercised on Variable Group 1 Group 2 p Value
a treadmill for either 5 minutes or until the onset of leg pain (n 1,700) (n 716)
that limited them from continuing. The exercise was also
Men 960 (56.5%) 470 (65.36%) 0.0001
terminated by the onset of any cardiopulmonary symptoms,
Race
especially if these were the principal restriction to exercise. White 1,453 (85.5%) 667 (93.3%) 0.0001
Once the exercise had been completed, the patient returned Black 216 (12.7%) 44 (6.2%) 0.0001
to the bed in the supine position and both ankle pressures Age (years) 63.9 (10.6) 64.7 (9.5) 0.0729
were obtained (first in the symptomatic extremity or the 4049 213 (12.5%) 59 (8.2%)
extremity with the lower pressure at rest) followed by the 5059 362 (21.3%) 159 (22.2%)
brachial pressure in the arm with the greater pressure at rest. 6069 601 (35.4%) 262 (36.6%)
The ABI thus obtained was referred to as the postexercise 70 524 (30.8%) 236 (33.0%)
ABI in the present study. When the patients had undergone Smoker 27 (1.6%) 28 (3.9%) 0.0005
more than one test during the study period, only the first was Hypertension 451 (26.5%) 237 (33.1%) 0.0011
Diabetes mellitus 161 (9.5%) 92 (12.9%) 0.0133
taken. The United States Social Security death index was
Coronary artery disease 392 (23.1%) 246 (34.4%) 0.0001
used to match all subjects to their records according to name Cerebrovascular accident 101 (5.9%) 79 (11.0%) 0.0001
and Social Security number. The vital status was deter- Abdominal aortic aneurysm 64 (3.8%) 43 (6.0%) 0.0145
mined as of May 2007. Hyperlipidemia 194 (11.4%) 131 (18.3%) 0.0001
The continuous data are displayed as the mean SD.
The categorical data are displayed as frequencies and per- Group 1, patients with normal ankle-brachial index at rest and after
exercise, group 2: patients with normal ankle-brachial index at rest but
centages within the population. The continuous data were
abnormal after exercise.
analyzed using the nonparametric Wilcoxon test and cate-
gorical data using the chi-square test. Survival analysis was
done using Cox proportional hazard modeling, adjusted for observational nature of the present study. The propensity
confounding factors. The proportionality assumption was score matching was done in all aspects, except for their
tested with all time-dependent covariates simultaneously. postexercise ABI results, using a greedy algorithm.3 This
The relative risks (hazard ratio) were estimated and 95% was accomplished using a nonparsimonious logistic regres-
confidence intervals given. Patient age at testing, gender, sion model, with all available covariates included to derive
race, and history of CAD, cerebrovascular accident, smok- a propensity score for patients with an abnormal postexer-
ing, diabetes, hypertension, hyperlipidemia, abdominal aor- cise ABI result, and then using the propensity scores to
tic aneurysm, and appropriate transformations were in- match those from group 2 to the patients in group 1. Patients
cluded in the modeling. with missing values were excluded from matching and ad-
The patients from group 2 were matched one-to-one to ditional analysis. The resulting matched groups were com-
the patients from group 1 using propensity scores before pared for each covariate to confirm the similarity between
survival analysis to minimize any bias introduced by the the 2 groups (Table 1). The propensity score was also
780 The American Journal of Cardiology (www.ajconline.org)

Figure 1. Kaplan-Meier curves of mortality rates for matched groups 1 and 2 from testing. Patients in both groups had normal ABI values at rest. Patients
in group 2 had an ABI of 0.85 after exercise, and patients in group 1 had maintained a normal ABI value even after exercise and served as the control group.

Table 3 After matching, 1,426 patients (713 each in group 1 and 2),
Statistically significant independent predictors among propensity score as defined in the Methods section, were included in the
matched patients
present study.
Predictor HR (95% CI) p Value The baseline demographic and risk factor profiles of the
Postexercise ankle-brachial index 1.67 (1.292.17) 0.0001
matched and unmatched patient groups are listed in Tables
in patients with no history of 1 and 2. The mean patient age was 64.1 10.3 years, and
cardiovascular events 40.8% were women. Notable differences were present be-
Hypertension 1.55 (1.231.96) 0.0002 tween the 2 groups before matching. The subjects in group
Age per decade 1.54 (1.381.71) 0.0001 2 had a greater percentage of white men and were more
Male gender 1.37 (1.061.75) 0.014 likely to be older, have a history of CAD, cerebrovascular
Postexercise ABI 1.34 (1.071.58) 0.008 accident, or abdominal aortic aneurysm, take medications
Diabetes mellitus 1.34 (1.011.77) 0.044
for hyperlipidemia, hypertension, or diabetes, and be cur-
Group 1, patients with normal ankle-brachial index at rest and after rent smokers at testing. This bias was minimized by match-
exercise, group 2: patients with normal ankle-brachial index at rest but ing the patients from group 2 with those from group 1 using
abnormal after exercise. propensity scores (Table 1).
CI confidence interval; HR hazard ratio. During a mean duration of 6.9 3.2 years from the date
of testing, a total of 416 deaths occurred in both matched
included in the Cox proportional hazard model in the anal- groups, 189 in group 1 and 227 in group 2. In the propensity
ysis. All the analyses were done using the SAS, version 8.2, score-matched patients, an abnormal postexercise ABI re-
statistical package (SAS, Cary, North Carolina). sult was a strong independent predictor of mortality from all
causes, with a hazard ratio of 1.3 (95% confidence interval
1.07 to 1.58, p 0.008). The 5- and 10-year mortality rate
Results for group 1 and 2 was 15.4% and 17% and 32.7% and
From January 1990 to December 2000, 11,295 patients 41.2%, respectively. The Kaplan-Meier curve graphically
underwent either complete or limited lower extremity pulse demonstrated the increased mortality of patients in group 2
volume recording studies with ABI measurement at the (Figure 1). The independent clinical predictors of death are
Cleveland Clinic noninvasive vascular laboratory. Of these, summarized in Table 3. An abnormal postexercise ABI
6,292 were performed with a fixed-grade treadmill or symp- result was as strong a predictor of mortality as diabetes in
tom-limited exercise component. For the purposes of the the present analysis.
present study, the patients with an abnormal ABI at rest Similar results were obtained when the patients with any
were not considered. A total of 2,416 patients met the history of cardiovascular events (CAD, cerebrovascular ac-
inclusion criteria according to the postexercise ABI results. cident, or abdominal aortic aneurysm) were excluded from
 Miscellaneous/Postexercise ABI
both groups and subjected to the same analysis (hazard ratio
1.67, 95% confidence interval 1.29 to 2.17, p 0.0001).
Thus, for the prediction of mortality, adding the exercise
component to the ABI measurement added incremental in-
formation in both patients with and without a history of
cardiovascular event.
Discussion
The results from the present study have demonstrated
that the postexercise ABI might not simply help in diagnos-
ing PAD in more patients but could independently identify
patients at a greater mortality risk who would have re-
mained unidentified using conventional testing. It must be
re-emphasized that the diagnosis of PAD is important, not
only from a lower extremity standpoint, but also as a marker
of systemic atherosclerosis.
It has been demonstrated that PAD is a marker of future
cardiovascular-related mortality, independent of both con-
ventional risk factors and baseline cardiovascular disease.4,5
The reason for this greater mortality rate is poorly under-
stood. Various hypotheses have been investigated, some of
which included systemic endothelial dysfunction,6,7 ele-
vated levels of C-reactive protein,8 other related inflamma-
tory markers,9 increased levels of white blood cells,10 en-
hanced platelet activation,1113 and hemostatic factors, such
as plasma fibrinogen and von Willebrand factor.14
In an age in which increasing emphasis has been placed
on estimating the risk of future cardiovascular events, it was
surprising that a predictor as potent as PAD has not been
routinely included in risk factor analyses. A part of the
continued underrecognition could have been because only a
fraction of patients with PAD are symptomatic,15 and, in
most cases, their symptoms will not be that of classic in-
termittent claudication.15,16 However, even patients with
symptomatic PAD have been treated less aggressively in
terms of risk factor modification and medical therapy than
those with other manifestations of atherosclerotic disease,
such as CAD.17 Additionally, if we were to wait for the
development of symptoms, it might be already too late. This
fact has been demonstrated in an earlier study at our insti-
tution in which all patients presenting for lower extremity
revascularization surgery also underwent diagnostic coro-
nary angiography. Only 10% of these patients had angio-
graphic evidence of normal coronary arteries.18
The measurement of the ABI does add a fair degree of
objectivity to the diagnosis of PAD; however, it was our
hypothesis that an ABI measured in the at rest state would
be analogous to ruling out CAD using an at rest electrocar-
diogram. Although abnormal findings on an electrocardio-
gram at rest would be suggestive of CAD, normal findings
by no means rule it out. The findings from an exercise
electrocardiogram will be much more sensitive. In light of
the impressive statistics supporting the predictive role of
PAD in terms of cardiovascular morbidity and all-cause
mortality, it was our contention that a more sensitive mea-
sure of PAD detection, such as that afforded by a postex-
ercise ABI, could identify an additional population of pa-
tients worthy of secondary preventive measures that might
otherwise be missed. The clinical effect of the ABI has been
considered limited owing to the low prevalence of abnormal
781
at rest ABI values in patients 60 years old. Very limited
epidemiologic information has been available on what per-
centage of patients with a normal ABI value at rest would
have abnormal findings after exercise, although 2 recent
studies have reported data that ranged from 31%19 to
86.2%.20 However, neither of these studies was population
based. A normal subject should maintain or increase the
ankle systolic pressure even with moderate exercise levels.
The key is early detection, and when an area of narrowing
exceeds 50% in terms of diameter reduction, the systolic
pressure will decrease beyond the site of involvement.
Stress testing has commonly been used for the evaluation of
cardiac performance, because it has been recognized to
provide an enhanced index of myocardial perfusion. The
principles are similar for the legs.
The findings of our study could also have important
public health and economic implications. The National
Cholesterol Education Panel (in establishing the Adult
Treatment Guidelines) has taken the important step to in-
clude the presence of PAD as a CAD equivalent, similar to
diabetes. It is important to note that no conditions in these
guidelines were set forth in terms of the presence or absence
of symptoms. Currently, reimbursement for ABI testing
under Medicare guidelines is only allowed if the patient had
a history of symptoms secondary to lower limb ischemia.
However, symptoms have been poorly predictive, and one
needs to use maximum objective strategies to improve PAD
detection, considering its mortality implications, such as
were demonstrated in our study using the postexercise ABI.
Furthermore, the exercise portion for diagnostic purposes
does not necessarily have to be a treadmill protocol but
could just as easily be performed by having patients walk
down the office hallway or even perform active pedal plan-
tar flexion (the details of the latter testing technique have
been previously published21). Only a handful of studies
have examined the prognostic role of postexercise ABI
measurements in the clinical setting. Two such studies dem-
onstrated it to be of value in identifying failing lower ex-
tremity angioplasty,22,23 and another study showed that a
postexercise ABI did not add prognostic information24 It is
imperative to note the patients in these studies already had
previously diagnosed PAD, determined by either abnormal
ABI values at rest or percutaneous revascularization, both of
which were exclusion criteria in our study. A more contem-
porary publication from Europe, consisting of patients with
both abnormal and normal at rest ABI values, also demon-
strated increased mortality in the abnormal postexercise
ABI cohort.20 Although the patients with abnormal postex-
ercise ABI values in that study were a part of a subgroup
analysis, it was also their contention that adding the exercise
portion to the ABI measurement adds incremental prognos-
tic information in terms of mortality prediction.
We sought to prove that in patients with appropriate risk
factors and a high index of suspicion for PAD (determined
by typical or atypical symptoms), an at rest ABI value alone
would not conclusively exclude PAD. The use of postexer-
cise ABI testing might help identify a subgroup of patients
with a normal ABI value at rest who have a CAD risk
equivalent and subsequent greater mortality, in a noninva-
sive and cost-effective manner. How this approach compares
with other modalities for the early detection of atherosclerotic
782 The American Journal of Cardiology (www.ajconline.org)
vascular disease such as brachial artery reactivity testing, ca-
rotid intima medial thickness, or electron beam computed to-
mography is an area of potential future investigation.
The limitations of our study were the same as those
traditionally associated with any observational study. An
unrecognized selection bias might have been present for
patients referred for ABI testing with exercise. However, it
is unlikely that this bias would have had a substantial effect
on the association between postexercise ABI and mortality.
Other limitations included a lack of information pertaining
to the use of statins and antithrombotic medications at
testing. Also, most of the risk factors noted were determined
by self-reported rates, which perhaps best explains the low
rates of smoking in the patient groups.
1. Third Report of the National Cholesterol Education Program (NCEP).
Expert Panel on detection, evaluation, and treatment of high blood
cholesterol in adults (Adult Treatment Panel III) final report. Circu-
lation 2002;106:31433421.
2. Ouriel K, McDonnell AE, Metz CE, Zarins CK. Critical evaluation of
stress testing in the diagnosis of peripheral vascular disease. Surgery
1982;91:686 693.
3. Joffe MM, Rosenbaum PR. Invited commentary: propensity scores.
Am J Epidemiol 1999;150:327333.
4. Eagle KA, Rihal CS, Foster ED, Mickel MC, Gersh BJ; Coronary
Artery Surgery Study (CASS) Investigators. Long-term survival in
patients with coronary artery disease: importance of peripheral vascu-
lar disease. J Am Coll Cardiol 1994;23:10911095.
5. Newman AB, Shemanski L, Manolio TA, Cushman M, Mittelmark M,
Polak JF, Powe NR, Siscovick D; Cardiovascular Health Study Group.
Ankle-arm index as a predictor of cardiovascular disease and mortality
in the Cardiovascular Health Study. Arterioscler Thromb Vasc Biol
1999;19:538 545.
6. Silvestro A, Scopacasa F, Ruocco A, Olivia G, Schiano V, Zincarelli
C, Brevetti G. Inflammatory status and endothelial function in asymp-
tomatic and symptomatic peripheral arterial disease. Vasc Med 2003;
8:225232.
7. Brevetti G, Silvestro A, Di Giacomo S, Bucur R, Di Donato A,
Schiano V, Scopacasa F. Endothelial dysfunction in peripheral arterial
disease is related to increase in plasma markers of inflammation and
severity of peripheral circulatory impairment but not to classic risk
factors and atherosclerotic burden. J Vasc Surg 2003;38:374 379.
8. Ridker PM, Cushman M, Stampfer MJ, Tracy RP, Hennekens CH.
Plasma concentration of C-reactive protein and risk of developing
peripheral vascular disease. Circulation 1998;97:425 428.
9. Brevetti G, Piscione F, Silvestro A, Galasso G, Di Donato A, Oliva G,
Scopacasa F, Chiarello M. Increased inflammatory status and higher
prevalence of three-vessel coronary artery disease in patients with
concomitant coronary and peripheral atherosclerosis. Thromb Haemost
2003;89:1058 1063.
10. Kirk G, Hickman P, McLaren M, Stonebridge PA, Belch JJ. Interleu-
kin-8 (IL-8) may contribute to the activation of neutrophils in patients
with peripheral arterial occlusive disease (PAOD). Eur J Vasc Endo-
vasc Surg 1999;18:434 438.
11. Robless PA, Okonko D, Lintott P, Mansfield AO, Mikhailidis DP,
Stansby GP. Increased platelet aggregation and activation in peripheral
arterial disease. Eur J Vasc Endovasc Surg 2003;25:16 22.
12. Reininger CB, Boeger CA, Steckmeier B, Spannagl M, Scweiberer L.
Mechanisms underlying increased platelet reactivity in patients with
peripheral arterial disease. Preliminary results. Int Angiol 1999;18:
163170.
13. Cassar K, Bachoo P, Brittenden J. The role of platelets in peripheral
vascular disease. Eur J Vasc Endovasc Surg 2003;25:6 15.
14. Smith FB, Lee AJ, Hau CM, Rumley A, Lowe GD, Fowkes FG.
Plasma fibrinogen, haemostatic factors and prediction of peripheral
arterial disease in the Edinburgh Artery Study. Blood Coagul Fibri-
nolysis 2000;11:4350.
15. Criqui MH, Denenberg JO, Bird CE, Fronek A, Klauber MR, Langer
RD. The correlation between symptoms and non-invasive test results
in patients referred for peripheral arterial disease testing. Vasc Med
1996;1:6571.
16. McDermott MM, Mehta S, Greenland P. Exertional leg symptoms
other than intermittent claudication are common in peripheral arterial
disease. Arch Intern Med 1999;159:387392.
17. McDermott MM, Mehta S, Ahn H, Greenland P. Atherosclerotic risk
factors are less intensively treated in patients with peripheral arterial
disease than in patients with coronary artery disease. J Gen Intern Med
1997;12:209 215.
18. Hertzer NR, Beven EG, Young JR, OHara PJ, Ruschhaupt WF, Graor
RA, Dewolfe VG, Maljovec LC. Coronary artery disease in peripheral
vascular patients: a classification of 1000 coronary angiograms and
results of surgical management. Ann Surg 1984;199:223233.
19. Stein R, Hriljac I, Halperin JL, Gustavson SM, Teodorescu V, Olin
JW. Limitation of the resting ankle-brachial index in symptomatic
patients with peripheral arterial disease. Vasc Med 2006;11:29 33.
20. Feringa HH, Bax JJ, van Waning VH, Boersma E, Elhendy A,
Schouten O, Tangelder MJ, van Sambeek MH, van den Meiraceker
AH, Poldermans D. The long-term prognostic value of the resting and
postexercise ankle-brachial index. Arch Intern Med 2006;166:529
535.
21. McPhail IR, Spittell PC, Weston SA, Bailey KR. Intermittent claudi-
cation: an objective office-based assessment. J Am Coll Cardiol 2001;
37:13811385.
22. Hartmann A, Gehring A, Vallbracht C, Landgraf H, Liermann D,
Kollath J, Kaltenbach M. Noninvasive methods in the early detection
of restenosis after percutaneous transluminal angioplasty in peripheral
arteries. Cardiology 1994;84:2532.
23. Tong Y, Somjen G, Teeuwsen W, Royle JP. Percutaneous transluminal
angioplasty: follow-up with treadmill exercise testing. Cardiovasc
Surg 1994;2:503507.
24. Sikkink CJ, van Asten WN, Vant Hof MA, van Langen H, van der
Vliet JA. Decreased ankle/brachial indices in relation to morbidity and
mortality in patients with peripheral arterial disease. Vasc Med 1997;
2:169 173.