© 1999 American Heart Association, Inc.
Original Contributions |
Ankle-Arm Index as a Predictor of Cardiovascular Disease and Mortality in the Cardiovascular Health Study
From the University of Pittsburgh, Pittsburgh, Pa (A.B.N.); University of Washington, Seattle (L.S., D.S.); National Heart, Lung, and Blood Institute, Bethesda, Md (T.A.M.); University of Vermont, Colchester (M.C.); University of Bergen, Bergen, Norway (M.M.); Harvard University, Boston, Mass (J.F.P.); and Johns Hopkins University, Baltimore, Md (N.R.P.).
Correspondence to Anne B. Newman, MD, MPH, University of Pittsburgh School of Medicine, Department of Medicine, Division of Geriatric Medicine, 3520 Fifth Ave, Suite 300, Pittsburgh, PA 15213. E-mail anewman+{at}pitt.edu
 |
Abstract |
|---|
 Top Abstract IntroductionMethodsResultsDiscussionReferences |
|---|
Abstract—Peripheral arterial disease (PAD) in the legs, measured noninvasively by the ankle-arm index (AAI) is associated with clinically manifest cardiovascular disease (CVD) and its risk factors. To determine risk of total mortality, coronary heart disease, or stroke mortality and incident versus recurrent CVD associated with a low AAI, we examined the relationship of the AAI to subsequent CVD events in 5888 older adults with and without CVD. The AAI was measured in 5888 participants
65 years old at the baseline examination of the
Cardiovascular Health Study. All participants had a
detailed assessment of prevalent CVD and were contacted every 6 months
for total mortality and CVD events (including CVD mortality, fatal and
nonfatal myocardial infarction, congestive heart failure, angina,
stroke, and hospitalized PAD). The crude mortality rate at 6 years was
highest (32.3%) in those participants with prevalent CVD and a low AAI
(P<0.9), and it was lowest in those with neither of
these findings (8.7%, P<0.01). Similar patterns
emerged from analysis of recurrent CVD and incident CVD. The
risk for incident congestive heart failure (relative risk
[RR]=1.61) and for total mortality (RR=1.62) in those without CVD at
baseline but with a low AAI remained significantly elevated after
adjustment for cardiovascular risk factors.
Hospitalized PAD events occurred months to years after the AAI was
measured, with an adjusted RR of 5.55 (95% CI, 3.08 to 9.98) in those
at risk for incident events. A statistically significant decline in
survival was seen at each 0.1 decrement in the AAI. An AAI of <0.9 is
an independent risk factor for incident CVD, recurrent CVD, and
mortality in this group of older adults in the
Cardiovascular Health Study.
Key Words: peripheral vascular diseases • ankle-arm index • ankle-brachial pressure index • cardiovascular diseases, epidemiology
|
Introduction |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Epidemiological studies have demonstrated that subclinical cardiovascular disease in one vascular bed is associated with the presence of clinical disease in another bed,1 2 3 4 5 as well as with subsequent cardiovascular and total mortality.6 7 8 9 10 11 12 Degrees of peripheral arterial disease (PAD) in the legs, as measured noninvasively, are common in older adults without overt signs and symptoms of PAD.5 13 Among the elderly, an index of subclinical atherosclerosis with the use of several noninvasive measures that include carotid stenosis and wall thickness by duplex scanning, ECG and echocardiographic abnormalities, a positive Rose questionnaire14 for angina, and an ankle-arm index (AAI) of <0.9 has been shown to be a strong predictor of total and cardiovascular morbidity and mortality in those without prior history of clinical cardiovascular disease at the baseline examination.15 PAD in the legs, as measured by progressive decrements in the AAI, was associated with a stepwise increase in cardiovascular risk factor levels as well as in the prevalence of myocardial infarction (MI), stroke, and congestive heart failure (CHF).5 Past prospective studies of the cardiovascular disease (CVD) risk associated with the presence of PAD have not distinguished between recurrent and incident CVD; thus, the increased risk of mortality may be partly because of the correlation of PAD with prevalent clinical CVD.
The goal of the present study was to evaluate the risk of cardiovascular morbidity and mortality associated with a marker of PAD, the presence of a low AAI (AAI <0.9). Follow-up data of 5888 older adults enrolled in the Cardiovascular Health Study (CHS) were examined for risk of subsequent cardiovascular events and mortality. We hypothesized that the presence of a low AAI in participants without clinical CVD would be associated with a degree of risk for cardiovascular events similar to that found in those with a low AAI and known clinical CVD.
|
Methods |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
The CHS is an ongoing observational study of 5888 adults
65
years old, including 2495 men and 3393 women. The initial cohort of CHS
participants was recruited from a defined sample of Medicare-eligible
persons between April 1989 and May 1990. Participants were recruited
from 4 US communities: Forsyth County, NC; Sacramento County, Calif;
Washington County, Md; and Pittsburgh, Pa. Detailed descriptions of the
CHS have been published.16 17 The original sample of 5201
participants was primarily white: 148 (3%) were black women and 96
(1.8%) were black men. A second cohort of 687 black participants (431
women and 256 men) was enrolled between June 1992 and June 1993, 3
years after the enrollment of the original CHS cohort, to allow sample
sizes sufficient for subgroup analysis. All of the CHS participants underwent a baseline medical history and examination that included ECG, AAI, and pulmonary function testing. During this examination, participants were classified in accordance with the presence or absence of 6 preexisting CVDs: MI, angina, CHF, stroke, transient ischemic attack (TIA), and intermittent claudication. Participants with any of these 6 conditions were classified as having prevalent CVD.
The methods of ascertainment of these conditions have been described elsewhere.18 19 20 21 Briefly, baseline disease status was ascertained from the medical history and confirmed by either the ECG, appropriate prescription medication, hospital record review, or physician questionnaire. Participants with a history of coronary angioplasty, carotid endarterectomy, or bypass surgery were also considered to have prevalent CVD. Prevalent PAD was defined as a positive Rose questionnaire14 for intermittent claudication or a history of lower-extremity bypass surgery, angioplasty, or amputation.
Descriptive variables from the baseline examination were chosen for this analysis on the basis of associations with AAI as reported in a prior cross-sectional analysis.5 These variables were age, sex, race, cigarette use (current or past versus never), history of treated hypertension or history of diabetes, systolic and diastolic blood pressure (mm Hg), total cholesterol (mg/dL), HDL cholesterol (mg/dL), triglycerides (mg/dL), fasting glucose (mg/dL), fasting insulin (µU/mL), serum creatinine (mg/dL), and fibrinogen (mg/dL). All blood was collected and analyzed at the time of baseline examination according to laboratory methods previously reported.5 Major ECG abnormalities were determined by the CHS ECG Reading Center according to a standard protocol and included ventricular conduction defects, major Q or QS abnormalities, minor Q or QS with ST-T–wave abnormalities, left ventricular hypertrophy, isolated major ST-T–wave changes, atrial fibrillation, or first-degree atrioventricular block.
All participants underwent duplicate resting measurements of the blood
pressures used to create the AAI. The AAI is the ratio of the ankle
systolic blood pressure to the arm systolic blood
pressure and is >1.0 in normal adults.22 The AAI was
measured by trained technicians according to a standard protocol,
previously described.5 Briefly, the participant was asked
to lie flat on an examination table, and after 5 minutes of rest,
standard arm blood pressure cuffs were applied to the right arm and to
each ankle (with the lower end of the bladder within 3 cm of the
malleoli). After palpation of the brachial and posterior tibial
arteries, ultrasound gel was applied, and a Doppler stethoscope (8
MHz, Huntleigh Technology, Inc) and a standard mercury manometer were
used to assess systolic blood pressure in the right brachial
artery and in each posterior tibial artery in rapid succession.
Measurements have been shown to be reliable between observers, stable
over time, and highly correlated between left and right
legs.11 We excluded 31 participants (0.5%) with AAI 1.5
in both legs at baseline because previous
analyses5 indicated that this is a falsely high
level caused by noncompressible vessels in the legs. One hundred and
forty-three participants did not have AAI data. Thus, 5714 participants
of the total 5888 are included in this analysis.
CHS methods for surveillance and ascertainment of CVD events are described in detail in previous articles15 23 and are summarized as follows. Participants were contacted by the CHS clinical centers every 6 months in regard to subsequent hospitalizations and outpatient visits for specific cardiovascular diagnoses including MI, angina, CHF, stroke, TIA, and PAD. Total mortality included all deaths and was documented by death certificates, inpatient records, nursing home or hospice records, physician questionnaires, and autopsy reports.
CVD mortality was defined to include death from CHD, MI, sudden death, or stroke. Nonfatal events (whether a new or a repeat event for a participant) were evaluated by review of all hospital records (all ICD-9-CM codes), history and physical exams, discharge summaries, and diagnostic and therapeutic procedures. Outpatient records and physician questionnaires were evaluated for outpatient MI, CHF, and stroke. Incident PAD events were defined by a review of all inpatient hospitalizations on the face sheet for diagnosis. All records with an ICD-9 code of 440.2 or 443.9 or a mention of peripheral vascular disease or claudication on the face sheet or in the discharge summary were reviewed. A hospitalized PAD event required the presence of ischemic leg pain and a consistent invasive or noninvasive diagnostic test. Outpatient reports of PAD were confirmed with the use of the AAI and thus were not independent of the predictor variable. Therefore, only hospitalized PAD was used in these analyses, because these diagnoses were made independently of the CHS AAI measurement. Adjudication of each event was reached by consensus.
For this analysis, the following categories of events were evaluated: total mortality, CVD mortality (CHD and stroke), MI, angina, CHF, stroke, and hospitalized PAD. Data through 6 years of follow-up (mean, 5.1 years) for the original CHS cohort and 2 years of follow-up for the black cohort (mean, 22 months) are reported here.
Statistical Analysis
Participants were classified according to the presence or
absence of prevalent clinical CVD at baseline. Participants were also
classified as having a low AAI if the AAI was <0.9 in either leg. We
chose this cut point based on previous analyses in this
population5 and in other published
articles.10 11 12 Associations of follow-up events with
baseline disease and of AAI groups were assessed by crude event rates,
Kaplan-Meier life tables, and Cox proportional hazards models with an
adjustment for age, gender, and other CVD risk factors. The factors
were those associated with a low AAI in previous cross-sectional
analyses5 and included race, past smoking,
pack-years of smoking, diabetes, total cholesterol, HDL
cholesterol, triglyceride level, fasting
glucose, insulin, fibrinogen level, factor VII, and body mass index.
Cox proportional hazards models were used to assess independent
associations between an AAI <0.9 and various end points. Cox models
also were used to assess whether any interaction between a low AAI and
covariates was significant after all main effects for the risk factors
in the Cox models were included. Associations were considered to be
significant at P<0.01. All analyses were performed
with Statistical Analysis System
software.24
|
Results |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
At the baseline examination, 768 of 5714 participants (13.4%) had an AAI of <0.9. This includes the added cohort of 687 blacks whose baseline examination was 3 years after the original cohort. Participants with a low AAI were older and more likely to be male or black. In addition, those with a low AAI were approximately twice as likely to have a history of CVD at the baseline examination (46.7% versus 22%, Table 1
).
|
At 6 years of follow-up, crude and age- and gender-adjusted event rates
were calculated for total mortality as well as for recurrent and
incident CVD events. Rates were calculated separately for those with
and without CVD at baseline. The total mortality rate was highest in
participants with prevalent disease and a low AAI (32.3%) and lowest
in those with neither of these findings (8.7%, P<0.01,
Table 2). Of note, for those without
prevalent CVD but with a low AAI, the mortality rate was quite high
(25.4%).
|
The 1446 participants with CVD at baseline were at a higher risk for
subsequent events than those without such history. However, within this
high-risk group, a low AAI showed age- and gender-adjusted risk ratios
of 1.50 for mortality, 2.04 for CVD mortality, and 1.61 for MI (Table 2
). Thus, within this higher-risk subgroup of CHS participants
with CVD at baseline, the 3 factors of AAI, age, and male gender
distinguished risk of total mortality, CVD mortality, total MI, CHF,
and PAD. After adjustment for other CVD risk factors, risk ratios for
total mortality, MI, and CHF were attenuated and CIs widened to include
1. The majority (74.7%) of the CHS cohort had no history of CVD at the
baseline examination (Table 1). The relative risk (RR)
and absolute risk for CVD events and mortality were significantly
higher in those participants with a low AAI and no prevalent CVD for
all events except stroke (Table 2). The RR of a low AAI for CVD
mortality was higher than for total mortality (RR of 2.86 and 2.44,
respectively, for CVD and total mortality), although CIs
overlapped.
Compared with the use of history of CVD as a predictor of cardiovascular events, in those with no history of CVD the AAI is less sensitive but more specific. For total mortality, the sensitivity and specificity of an AAI <0.9 are 24% and 92%, respectively, compared with 44% sensitivity and 77% specificity for a history of CVD. A similar pattern is found when CVD mortality is used as the outcome event: a low AAI has 30% sensitivity and 91% specificity compared with 64% sensitivity and 77% specificity for history of CVD.
The rate of new clinical PAD events in the legs was significantly
associated with the presence of a low AAI at the baseline examination
in both groups (Table 2). Although the rate of PAD events was 6-
to 11-fold higher in participants with low AAI, the absolute risk of
the development of symptomatic PAD (11.7% in those with
prevalent CVD versus 6.6% in those with no CVD) was less than or
similar to that of other CVD events (including angina and stroke) and
was much less than the risk for total mortality (32.3% of those with
prevalent CVD, 25.4% for those without CVD).
To further evaluate the relationship of a low AAI to mortality, we
focused on the 4268 participants with no CVD at baseline and looked at
the mortality rates by AAI in those with and without several important
risk factors (Table 3). For each risk
factor, the mortality rates were significantly higher in those with a
low AAI than in those with a normal AAI. Whether the risk factor was
present or absent, the RR of mortality was >2-fold higher in those
with a low AAI. For example, those with diabetes and a low AAI had a
31% mortality rate, whereas those with diabetes but a normal AAI had
only a 12% mortality rate. Thus, within diabetics, the RR of mortality
for those with a low AAI was only slightly higher than the RR of
mortality in nondiabetics with a low AAI.
|
The proportion of blacks with a low AAI and no history of CVD was
16.5% (105 of 636) compared with 8.2% (298 of 3600) in the white
participants. Although the majority of the black participants were from
the new cohort, which was followed for only 2 years from the baseline
examination, the presence of a low AAI was strongly related to
subsequent mortality in those 636 black participants free of CVD at
baseline (Table 3). Compared with white participants, the RR of
mortality even with shorter follow-up time appears higher, although the
CIs are wide. These stratified analyses gave similar results
when CVD mortality and MI were evaluated.
Participants with an elevated serum cholesterol (>240 mg/dL) and a low AAI had a death rate similar to those with a cholesterol <240 and a low AAI (27.1% versus 24.7%). The relative risk of mortality in those with a low AAI was higher in the high-cholesterol subgroup (4.04 versus 2.03) and may be related to the lower mortality rate (7.1%) in those with a higher cholesterol but a normal AAI.
To further evaluate the independence of association between a low AAI
and subsequent cardiovascular events in those without
prevalent CVD, models were constructed that included the AAI and all
variables associated univariately with a low AAI at
baseline (Table 4). There were no
significant interactions between a low AAI and covariates for any of
the outcomes evaluated. For total mortality, the RR of a low AAI was
attenuated somewhat at 1.62. Older age, male gender, higher serum
creatinine, major ECG abnormality, and lower forced vital
capacity were all associated with mortality independent of its
association with a low AAI. Results were similar for CVD mortality. For
incident CVD morbidity, we had sufficient numbers of events to evaluate
only CHF and PAD. A low AAI was associated with a 1.61-fold increase in
the risk of incident CHF. Age, male gender, hypertension, higher serum
creatinine, major ECG abnormality, and lower forced vital
capacity were also associated with incident CHF.
|
The risk for PAD remained quite high after adjustment, 5.55 (CI, 3.08 to 9.98), which suggested that the majority of those with an incident PAD event had a low AAI by screening for months to years before significant clinical manifestations. Current smoking and male gender were also strongly associated with incident PAD.
For all analyses, specification of the AAI as a continuous versus categorical variable in the model yielded consistent results.
In a previous study, we showed cross-sectionally that CVD and its risk
factors were associated with a stepwise decrease in the AAI below
1.0.5 In the present study, we were able to evaluate
the relationship of a decrease in AAI to total mortality in those with
and without prevalent CVD at baseline (Figures 1 and 2). A
striking increase in mortality was seen early in follow-up in the
prevalent disease group at an AAI of <0.9. For participants with no
prevalent disease at baseline, mortality rates were similar for those
with an AAI <0.8 to those with an AAI of 0.8 to <0.9 after
several years of follow-up. In addition, for those with no prevalent
disease at baseline and a normal AAI, almost 80% of these older adults
survived without cardiovascular morbidity (Figure 3). For each 0.1 decrement in the AAI
below 1.0, event rates increased, which indicated a lack of a threshold
for predicting mortality.
|
|
|
|
Discussion |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
The majority of total and cardiovascular deaths in older adults occur in those with either clinical or subclinical CVD. Although easily documented by the presence of a low AAI, PAD is quite often asymptomatic in older adults. Even in participants without a history of CVD and without symptoms of claudication,
10% of men and women >65 years old had an AAI
<0.9.5 Thus, the AAI, as a marker of PAD, can provide
important information about subclinical
atherosclerosis. Clearly, participants with a history of prevalent, clinically manifested CVD would be at highest risk for mortality and recurrent events. Even within this group, a low AAI was associated with increased age- and gender-adjusted risk of total and CVD mortality and remained independently associated with CVD mortality but not with total mortality or MI with multivariate adjustment. Regardless of clinical manifestation, participants with a reduction of the AAI of <0.9 are likely to have diffuse, advanced atherosclerosis.
The magnitude of the risk related to a low AAI is similar to that found with the classification of participants with a more extensive battery of noninvasive tests, including echocardiography and carotid ultrasound.15 Cross-sectional analysis in the Atherosclerosis Risk in Communities Study (ARIC) cohort shows that the prevalence of an AAI <0.9 (low AAI) is uncommon in middle-aged and younger people.26 The associations with clinical and subclinical disease and the comparisons with angiography indicate that those with a low AAI have advanced significant atherosclerosis.6 7 8 9 10 11 12 The strong associations (2- to 3-fold hazard ratio) of a low AAI with total and CVD mortality, even in those without a history of CVD, confirm this.
Thus, the AAI is not a useful screening test for early disease; rather, it is a very specific test for advanced disease. Its sensitivity and specificity for CVD mortality are 30% and 91%, respectively. This compares with a sensitivity and specificity of 43% and 70%, respectively, for left ventricular hypertrophy by echocardiogram as a predictor of CVD events.28 When calcium scores by electron-beam CT scan of the coronary arteries were reviewed to measure their ability to predict coronary events, a score threshold of 160 resulted in a sensitivity of 89% and specificity of 77%.29 In CHS, participants with a low AAI had a >2-fold risk of total and CVD mortality, even after the exclusion of those with clinical CVD. The risk was attenuated somewhat but still statistically significant with adjustment for traditional risk factors. A low AAI is not highly sensitive for outcomes, but its predictive value is roughly comparable to having a history of prior CVD.
It has been suggested that the AAI might be used to screen and target
older adults for more aggressive risk factor intervention. Clearly, it
cannot be considered in isolation because an AAI >0.9 does not rule
out the presence of atherosclerosis. One potential role
for the AAI is its use in the elimination of 10% of those
>65 years old with no history of CVD from undergoing more expensive
and sensitive test procedures. Alternatively, it may be useful to
combine it with information from the ECG and electron-beam CT scan; the
combination of information about several vascular beds may be the most
sensitive and specific method to describe the anatomic extent of
disease. The AAI is essentially a screening-level assessment for
anatomic PAD in the legs, and when <0.9, it is quite sensitive and
specific for obstruction compared with a full vascular laboratory
evaluation.30 As a continuous variable, it must be
remembered that AAI is a ratio of blood pressures and may also capture
physiological information about systolic
blood pressure and vascular stiffness. Nevertheless, when the AAI is
used in older adults as a screening test with a cut point of 0.9, it
also identifies a subgroup at higher risk for total and CVD mortality
and is much less expensive and easier to interpret than methods that
rely on vascular imaging, such as carotid duplex scanning.
The presence of a low AAI was associated with an increase in risk for all incident CVD morbidity and mortality except for stroke. In those at risk for incident CVD, the risk remained significantly elevated for total and CVD mortality, as well as CHF and PAD, but not for MI, angina, or stroke after multivariate adjustment. It may be that with longer follow-up, events would increase and CIs would narrow for other morbid events. It is also possible that the risk is highest in the short term and would attenuate with additional follow-up. These issues will be explored with further follow-up.
The association with CHF is interesting and may suggest that much of the CHF is related to atherosclerosis and perhaps myocardial ischemia. However, because the AAI is a ratio of systolic blood pressures, it may also be related to CHF as a measure of vascular stiffness. The diagnosis of CHF in the CHS cohort has been problematic in that it is often found in participants hospitalized for other reasons, such as chronic lung disease, pneumonia, arrhythmia, or postoperatively. Nevertheless, a preliminary report of CHF in this cohort shows that CHF is associated with myocardial ischemia, as well as left ventricular hypertrophy.31
The ability of a low AAI to predict hospitalization for
symptomatic PAD is not surprising, because it is a
screening test for atherosclerotic obstruction in the legs. Of note,
the majority of these events occurred in those with a low AAI, yet some
occurred in those with an AAI 0.9 at baseline. It is possible that
obstruction developed over the years of follow-up or that occlusion
occurred more suddenly. In addition, the cut point of 0.9 is arbitrary
and will misclassify some participants with more mild
atherosclerosis. Further analysis of the change
over time and the types of procedures and symptoms in these individuals
is ongoing. Caution must be used in the interpretation of these data,
because only severe PAD identified by hospital records is included.
Outpatient diagnoses of PAD in CHS included use of the AAI; thus, we
could not make an unbiased assessment of its predictive value for
outpatient events. Sensitivity and specificity of the AAI for PAD may
be reduced if milder degrees of PAD had been included in the
analyses.
The risk ratio for mortality in those with a low AAI was higher in
blacks than whites, although the follow-up time was only 2 years for
the majority of blacks in the CHS cohort. The black participants in CHS
have been found to have more extensive clinical and subclinical
atherosclerosis by multiple measures.32
The relative merits of different risk classification strategies in this
group will require longer follow-up.
Previous studies have demonstrated the relationship between PAD by various measures and mortality in populations including subjects with hyperlipidemia or systolic hypertension.6 7 8 9 10 11 12 The RRs are similar in all of these studies. Previous studies, however, have not distinguished the risk of a low AAI for incident as opposed to recurrent CVD. Although the presence of a low AAI is strongly related to the presence of other clinical manifestations of CVD, a substantial proportion of older adults have no other clinical manifestations of CVD. The data demonstrate that the increased risk of CVD in those with low AAI is not solely related to the association of the AAI with clinically manifest CVD in these individuals. In addition, although a low AAI is associated with other cardiovascular risk factors,5 its association with CVD events is strong regardless of the presence or absence of these other risk factors.
Although symptoms of claudication do not occur until the AAI is
0.8,22 mortality risk appears to increase substantially
at an AAI <0.9. The majority of the participants in this study had
moderate reductions in the AAI (0.8 to 0.9) that would not be
identified by medical history or other components of a routine physical
examination, such as pulse palpation. Of note, those with an AAI 1.0
were at low risk of death or cardiovascular morbidity.
Nevertheless, CVD cannot be excluded by the presence of a normal AAI.
The AAI is reduced when there is obstruction to blood flow in the legs;
thus, it is essentially a marker of fairly advanced
atherosclerosis. As an initial screen, it is quite
specific for subsequent CVD or mortality in older adults. Sensitivity
may be improved by a combination of risk factors and measures of
subclinical atherosclerosis.25 Follow-up
of the CHS cohort for additional cardiovascular events
will explore strategies that optimize the identification of older
adults at high risk of CVD morbidity and mortality.
Acknowledgments
This study was supported by contracts N01-HL-85079,
N01-HC-85080, N01-HC-85083, N01-HC-85084, N01-HC-85085, and
N01-HC-85086 from the National Heart, Lung, and Blood
Institute.
Participating Institutions and Principal Staff
Bowman Gray School of Medicine of Wake Forest University,
Forsyth County, NC: Gregory L. Burke, Sharon Jackson, Alan Elster,
Walter H. Ettinger, Curt D. Furberg, Gerardo Heiss, Dalane Kitzman,
Margie Lamb, David S. Lefkowitz, Mary F. Lyles, Cathy Nunn, Ward Riley,
John Chen, and Beverly Tucker; Bowman Gray School of Medicine, ECG
Reading Center, Forsyth County, NC: Farida Rautaharju and Pentti
Rautaharju; University of California – Davis, Sacramento County,
Calif: William Bommer, Charles Bernick, Andrew Duxbury, Mary Hann,
Calvin Hirsch, Lawrence Laslett, Marshall Lee, John Robbins, and
Richard White; Johns Hopkins University, Washington County, Md: M. Jan
Busby-Whitehead, Joyce Chabot, George W. Comstock, Adrian Dobs,
Linda P. Fried, Joel G. Hill, Steven J. Kittner, Shiriki Kumanyika,
David Levine, Joao A. Lima, Neil R. Powe, Thomas R. Price, Jeff
Williamson, Moyses Szklo, and Melvyn Tockman; MRI Reading Center –
Johns Hopkins University, Washington County, Md: R. Nick Bryan, Norman
Beauchamp, Carolyn C. Meltzer, Naiyer Iman, Douglas Fellows, Melanie
Hawkins, Patrice Holtz, Michael Kraut, Grace Lee, Larry Schertz,
Cynthia Quinn, Earl P. Steinberg, Scott Wells, Linda Wilkins, and Nancy
C. Yue; University of Pittsburgh, Allegheny County, Pa: Diane G. Ives,
Charles A. Jungreis, Laurie Knepper, Lewis H. Kuller, Elaine Meilahn,
Peg Meyer, Roberta Moyer, Anne Newman, Richard Schulz, Vivienne E.
Smith, and Sidney K. Wolfson; Echocardiography
Reading Center (Baseline) – University of California, Irvine: Hoda
Anton-Culver, Julius M. Gardin, Margaret Knoll, Tom Kurosaki, and
Nathan Wong; Echocardiography Reading Center
(Follow-Up) – Georgetown Medical Center, Washington DC: John
Gottdiener, Eva Hausner, Stephen Kraus, Judy Gay, Sue Livengood, Mary
Ann Yohe, and Retha Webb; Ultrasound Reading Center – Geisinger
Medical Center, Danville, Pa: Daniel H. O'Leary, Joseph F.
Polak, and Laurie Funk; Central Blood Analysis Laboratory –
University of Vermont, Colchester, VT: Edwin Bovill, Elaine
Cornell, Mary Cushman, and Russell P. Tracy; Respiratory Sciences
University of Arizona, Tucson: Paul Enright; Coordinating Center –
University of Washington, Seattle: Alice Arnold, Annette L.
Fitzpatrick, Bonnie K. Lind, Richard A. Kronmal, Bruce M. Psaty, David
S. Siscovick, Lynn Shemanski, Lloyd Fisher, Will Longstreth, Patricia
W. Wahl, David Yanez, Paula Diehr, and Maryann McBurnie; NHLBI
Project Office, Bethesda, Md: Diane E. Bild, Robin Boineau,
Teri A. Manolio, Peter J. Savage, and Patricia Smith.
Received October 28, 1997; accepted August 4, 1998.
|
References |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
1. Ruckley CV. Symptomatic and asymptomatic disease. In: Fowkes FGR, ed. Epidemiology of Peripheral Vascular Disease. London, UK: Springer-Verlag; 1991:97–108.
2. Shaper AG, Wannamethee SG, Walker MK. Risk factors and cardiovascular outcome: calf pain on walking, risk factors and cardiovascular outcome in middle-aged British men. In: Fowkes FGR, ed. Epidemiology of Peripheral Vascular Disease. London, UK: Springer-Verlag; 1991:127–140.
3.
Salonen JT, Salonen R. Ultrasonographically assessed
carotid morphology and the risk of coronary heart disease.
Arterioscler Thromb. 1991;11:1245–1249.
4. Mautner GC, Mautner SL, Roberts WC. Amounts of coronary arterial narrowing by atherosclerotic plaque at necropsy in patients with lower extremity amputation. Am J Cardiol. 1992;70:1147–1151.[Medline] [Order article via Infotrieve]
5.
Newman AB, Siscovick DS, Manolio TA, Polak J, Fried
LP, Borhani NO, Wolfson SK. Ankle-arm index as a marker of
atherosclerosis in the Cardiovascular
Health Study. Circulation. 1993;88:837–845.
6. Criqui MH, Langer RD, Fronek A, Feigelson HS, Klauber MR, McCann TJ, Browner D. Mortality over a period of 10 years in patients with peripheral arterial disease. N Engl J Med. 1992;326:381–386.[Abstract]
7. Autret A, Saudeau D, Bertand PH, Pourcelot L, Marchal C, DeBoisvilliers S. Stroke risk in patients with carotid stenosis. Lancet. 1987;1:888–890.[Medline] [Order article via Infotrieve]
8. Nadelmann J, Frishman WH, Ooi WL, Tepper D, Greenberg S, Guzick H, Lazar EJ, Heiman M, Aronson M. Prevalence, incidence and prognosis of recognized and unrecognized myocardial infarction in persons aged 75 years or older: the Bronx Aging Study. Am J Cardiol. 1990;66:533–537.[Medline] [Order article via Infotrieve]
9. Kannel WB, Abbott RD. Incidence and prognosis of unrecognized myocardial infarction: an update on the Framingham Study. N Engl J Med. 1984;311:1144–1147.[Abstract]
10.
Vogt MT, Cauley JA, Newman AB, Kuller LH, Hulley SB.
Decreased ankle/arm blood pressure index and mortality in elderly
women. JAMA. 1993;270:465–469.
11.
Newman AB, Sutton-Tyrrell K, Vogt MT, Kuller LH.
Morbidity and mortality in hypertensive adults with a low ankle/arm
blood pressure index. JAMA. 1993;270:487–489.
12.
Leng GC, Fowkes FG, Lee AJ, Dunbar J, Housley E,
Ruckley CV. Use of ankle brachial pressure index to predict
cardiovascular events and death: a cohort study.
BMJ. 1996;313:1440–1444.
13.
Criqui MH, Fronek A, Barrett-Connor E, Klauber MR,
Gabriel S, Goodman D. The prevalence of peripheral
arterial disease in a defined population.
Circulation. 1985;71:510–515.
14. Rose G, McCartney P, Reid DD. Self-administration of a questionnaire on chest pain and intermittent claudication. Br J Prev Soc Med. 1977;31:42–48.[Medline] [Order article via Infotrieve]
15.
Kuller LH, Shemanski L, Psaty BM, Borhani NO, Gardin J,
Haan MN, O'Leary DH, Savage PJ, Tell GS, Tracy R. Subclinical disease
as an independent risk factor for cardiovascular
disease. Circulation. 1995;92:720–726.
16. Fried LP, Borhani NO, Enright P, Furberg CD, Gardin JM, Kronmal RA, Kuller LH, Manolio TA, Mittlemark MB, Newman AB. The Cardiovascular Health Study: design and rationale. Ann Epidemiol. 1991;1:263–276.[Medline] [Order article via Infotrieve]
17. Tell GS, Fried LP, Lind B, Manolio TA, Newman AB, Borhani NO. Recruitment of adults over 65 years and older as participants in the Cardiovascular Health Study. Ann Epidemiol. 1993;3:358–366.[Medline] [Order article via Infotrieve]
18.
Mittelmark MB, Psaty BM, Rautaharju PM, Fried LP,
Borhani NO, Tracy R, Gardin JM, O'Leary DH. Prevalence of
cardiovascular diseases among older adults: the
Cardiovascular Health Study. Am J
Epidemiol. 1993;137:311–317.
19.
O'Leary DH, Polak JF, Wolfson SK Jr, Bond MG, Bommer
W, Sheth S, Psaty BM, Sharrett AR, Manolio TA. Use of sonography to
evaluate carotid atherosclerosis in the elderly: the
Cardiovascular Health Study. Stroke. 1991;22:1155–1163.
20. Gardin JM, Wong ND, Bommer W, Kloptenstein HS, Smith VE, Tabatznik B, Siscovick D, Lobodzinski S, Anton-Culver H, Manolio TA. Echocardiographic design of a multicenter investigation of free-living elderly subjects: the Cardiovascular Health Study. J Am Soc Echocardiogr. 1992;5:63–72.
21. Enright PL, Kronmal RA, Higgis M, Schenker M, Haponik EF. Spirometry reference values for women and men aged 65 to 85 years of age: Cardiovascular Health Study. Am Rev Respir Dis. 1993;147:125–133.[Medline] [Order article via Infotrieve]
22. Carter SA. Role of pressure measurements in vascular disease. In: Bernstein EF, ed. Noninvasive Diagnostic Techniques in Vascular Disease. St Louis, Mo: CV Mosby Co; 1985:514–544.
23. Ives DG, Fitzpatrick AL, Bild DE, Psaty BM, Kuller LH, Crowley PM, Cruise RG, Theroux S. Surveillance and ascertainment of cardiovascular events: the Cardiovascular Health Study. Ann Epidemiol. 1995;5:278–285.[Medline] [Order article via Infotrieve]
24. SAS Institute Inc. SAS User's Guide: Basics. Version 6 edition. Cary, NC: SAS Institute Ind; 1990.
25. Devereux RB, Alderman MH. Role of preclinical cardiovascular disease in the evolution from risk factor exposure to development of morbid events. Circulation. 1993;88:1544–1555.
26. Zheng ZJ, Sharrett AR, Chambless LE, Rosamond WD, Nieto FJ, Sheps DS, Dobs A, Evans GW, Heiss G. Associations of ankle-brachial index with clinical coronary heart disease, stroke and preclinical carotid and popliteal atherosclerosis: the ARIC Study. Atherosclerosis. 1997;131:115–125.[Medline] [Order article via Infotrieve]
27.
Folsom AR, Wu KK, Rosamond WD, Sharrett AR, Chambless
LE. Prospective study of hemostatic factors and incidence of
coronary artery disease: the ARIC study.
Circulation. 1997;96:1102–1108.
28. Levy D, Garrison MS, Savage DD, Kannel WB, Castelli WP. Left ventricular mass and incidence of coronary heart disease in an elderly cohort. Ann Intern Med. 1989;110:101–107.
29. Arad Y, Spadaro LA, Goodman K, Lledo-Perez A, Sherman S, Lerner G, Guerci AD. Predictive value of electron beam CT of the coronary arteries: 19-month follow-up of 1173 asymptomatic subjects. Circulation. 1996;3:1951–1953.
30. Stoffers HE, Kester AD, Kaiser V, Rinkens PE, Kistlaar PJ, Knottnerus JA. The diagnostic value of the measurement of the ankle-brachial systolic pressure index in primary health care. J Clin Epidemiol. 1996;49:1401–1405.[Medline] [Order article via Infotrieve]
31. Kitzman DW, Gardin JM, Arnold A, Gottdiener JS, Lyles M, Smith VE, Enright P, Lima J, Soloman R, Polak J, Cushman M, Bryan N, for the CHS Research Group. Heart failure with preserved systolic LV function in the elderly: clinical and echocardiographic correlates from the Cardiovascular Health Study. Circulation. 1996;94(suppl I):I-433.
32. Manolio TA, Burke GL, Psaty BM, Newman AB, Haan M, Powe N, Tracy RP, O'Leary DH. Black-white differences in subclinical cardiovascular disease among older adults: the Cardiovascular Health Study. J Clin Epidemiol. 1995;48:1141–1152.[Medline] [Order article via Infotrieve]
This article has been cited by other articles:
 |
|
 |
|
  C. Diehm, J. R. Allenberg, D. Pittrow, M. Mahn, G. Tepohl, R. L. Haberl, H. Darius, I. Burghaus, H. J. Trampisch, and for the German Epidemiological Trial on Ankle Brac Mortality and Vascular Morbidity in Older Adults With Asymptomatic Versus Symptomatic Peripheral Artery Disease Circulation, November 24, 2009; 120(21): 2053 - 2061. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. Helfand, D. I. Buckley, M. Freeman, R. Fu, K. Rogers, C. Fleming, and L. L. Humphrey Emerging Risk Factors for Coronary Heart Disease: A Summary of Systematic Reviews Conducted for the U.S. Preventive Services Task Force Ann Intern Med, October 6, 2009; 151(7): 496 - 507. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. H. Ix, R. Katz, I. H. De Boer, B. R. Kestenbaum, M. A. Allison, D. S. Siscovick, A. B. Newman, M. J. Sarnak, M. G. Shlipak, and M. H. Criqui Association of chronic kidney disease with the spectrum of ankle brachial index the CHS (Cardiovascular Health Study). J. Am. Coll. Cardiol., September 22, 2009; 54(13): 1176 - 1184. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Hong Zhang, X.-Y. Li, Yajun Si, Xilie Lu, Liping Chen, and Zhaoyang Liu Manifestation of lower extremity atherosclerosis in patients with high ankle-brachial index The British Journal of Diabetes & Vascular Disease, July 1, 2009; 9(4): 160 - 164. [Abstract] [PDF]
|
|
|
|
 |
|
 A. El-Menyar, H. Amin, I. Rashdan, K. Souliman, D. Deleu, K. Saadat, W. Al Mahmeed, S. Bakir, A. Wasif, A. Ben Brek, et al. Ankle-Brachial Index and Extent of Atherosclerosis in Patients From the Middle East (the AGATHA-ME Study): A Cross-Sectional Multicenter Study Angiology, June 1, 2009; 60(3): 329 - 334. [Abstract] [PDF]
|
|
|
|
 |
|
 J. Bleys, A. Navas-Acien, M. Laclaustra, R. Pastor-Barriuso, A. Menke, J. Ordovas, S. Stranges, and E. Guallar Serum Selenium and Peripheral Arterial Disease: Results From the National Health and Nutrition Examination Survey, 2003-2004 Am. J. Epidemiol., April 15, 2009; 169(8): 996 - 1003. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 G. Carmo, A Mandil, B. Nascimento, B. Arantes, J. Bittencourt, E. Falqueto, and A. Ribeiro Can we measure the ankle-brachial index using only a stethoscope? A pilot study Fam. Pract., February 1, 2009; 26(1): 22 - 26. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S.-C. Chen, J.-M. Chang, S.-J. Hwang, J.-C. Tsai, C.-S. Wang, H.-C. Mai, F.-H. Lin, H.-M. Su, and H.-C. Chen Significant Correlation between Ankle-Brachial Index and Vascular Access Failure in Hemodialysis Patients Clin. J. Am. Soc. Nephrol., January 1, 2009; 4(1): 128 - 134. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. Rosano, H. Aizenstein, J. Brach, A. Longenberger, S. Studenski, and A. B. Newman Special Article: Gait Measures Indicate Underlying Focal Gray Matter Atrophy in the Brain of Older Adults J. Gerontol. A Biol. Sci. Med. Sci., December 1, 2008; 63(12): 1380 - 1388. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. H. Criqui, J. K. Ninomiya, D. L. Wingard, M. Ji, and A. Fronek Progression of Peripheral Arterial Disease Predicts Cardiovascular Disease Morbidity and Mortality J. Am. Coll. Cardiol., November 18, 2008; 52(21): 1736 - 1742. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. Khaleghi, Z. Ali, T. H. Mosley Jr., S. T. Turner, and I. J. Kullo Association of Soluble Cell Adhesion Molecules with Ankle-Brachial Index in a Biethnic Cohort of Predominantly Hypertensive Individuals Clin. Chem., November 1, 2008; 54(11): 1788 - 1795. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
Y. He, T. H. Lam, B. Jiang, J. Wang, X. Sai, L. Fan, X. Li, Y. Qin, and F. B. Hu Passive Smoking and Risk of Peripheral Arterial Disease and Ischemic Stroke in Chinese Women Who Never Smoked Circulation, October 7, 2008; 118(15): 1535 - 1540. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K. He, K. Liu, M. L Daviglus, E. Mayer-Davis, N. S. Jenny, R. Jiang, P. Ouyang, L. M Steffen, D. Siscovick, C. Wu, et al. Intakes of long-chain n-3 polyunsaturated fatty acids and fish in relation to measurements of subclinical atherosclerosis Am. J. Clinical Nutrition, October 1, 2008; 88(4): 1111 - 1118. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 T. Hayashi, Y. Obi, T. Kimura, K.-i. Iio, S. Sumitsuji, Y. Takeda, Y. Nagai, and E. Imai Cardiac troponin T predicts occult coronary artery stenosis in patients with chronic kidney disease at the start of renal replacement therapy Nephrol. Dial. Transplant., September 1, 2008; 23(9): 2936 - 2942. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. Espinola-Klein, H. J. Rupprecht, C. Bickel, K. Lackner, S. Savvidis, C. M. Messow, T. Munzel, S. Blankenberg, and for the AtheroGene Investigators Different Calculations of Ankle-Brachial Index and Their Impact on Cardiovascular Risk Prediction Circulation, August 26, 2008; 118(9): 961 - 967. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. T Hirsch, L. Hartman, R. J Town, and B. A Virnig National health care costs of peripheral arterial disease in the Medicare population Vascular Medicine, August 1, 2008; 13(3): 209 - 215. [Abstract] [PDF]
|
|
|
|
|
|
E. T Fung, A. M Wilson, F. Zhang, N. Harris, K. A Edwards, J. W Olin, and J. P Cooke A biomarker panel for peripheral arterial disease Vascular Medicine, August 1, 2008; 13(3): 217 - 224. [Abstract] [PDF]
|
|
|
|
|
|
R. Migliacci, R. Nasorri, P. Ricciarini, and P. Gresele Ankle-brachial index measured by palpation for the diagnosis of peripheral arterial disease Fam. Pract., August 1, 2008; 25(4): 228 - 232. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. C.A. Stene, R. Frikke-Schmidt, B. G. Nordestgaard, P. Grande, P. Schnohr, and A. Tybjaerg-Hansen Functional Promoter Variant in Zinc Finger Protein 202 Predicts Severe Atherosclerosis and Ischemic Heart Disease J. Am. Coll. Cardiol., July 29, 2008; 52(5): 369 - 377. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Ankle Brachial Index Collaboration Ankle Brachial Index Combined With Framingham Risk Score to Predict Cardiovascular Events and Mortality: A Meta-analysis JAMA, July 9, 2008; 300(2): 197 - 208. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 G. Brevetti, G. Giugliano, G. Oliva, S. Lanero, J.I. De Maio, and M. Chiariello The impact of comorbidity burden on the cardiovascular risk in the Peripheral Arteriopathy and Cardiovascular Events study QJM, July 1, 2008; 101(7): 575 - 582. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
Y. P. Liew, J. R. Bartholomew, S. Demirjian, J. Michaels, and M. J. Schreiber Jr. Combined Effect of Chronic Kidney Disease and Peripheral Arterial Disease on All-Cause Mortality in a High-Risk Population Clin. J. Am. Soc. Nephrol., July 1, 2008; 3(4): 1084 - 1089. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R Schutte, T Nawrot, T Richart, L Thijs, H A Roels, L M Van Bortel, H Struijker-Boudier, and J A Staessen Arterial structure and function and environmental exposure to cadmium Occup. Environ. Med., June 1, 2008; 65(6): 412 - 419. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K. Sutton-Tyrrell, L. Venkitachalam, A. M. Kanaya, R. Boudreau, T. Harris, T. Thompson, R. H. Mackey, M. Visser, G. D. Vaidean, A. B. Newman, et al. Relationship of Ankle Blood Pressures to Cardiovascular Events in Older Adults Stroke, March 1, 2008; 39(3): 863 - 869. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. K. Willmann, K. Chen, H. Wang, R. Paulmurugan, M. Rollins, W. Cai, D. S. Wang, I. Y. Chen, O. Gheysens, M. Rodriguez-Porcel, et al. Monitoring of the Biological Response to Murine Hindlimb Ischemia With 64Cu-Labeled Vascular Endothelial Growth Factor-121 Positron Emission Tomography Circulation, February 19, 2008; 117(7): 915 - 922. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. S. Conte Buflomedil in Peripheral Arterial Disease: Trials and Tribulations Circulation, February 12, 2008; 117(6): 717 - 719. [Full Text] [PDF]
|
|
|
|
 |
|
 G. Brevetti, V. Schiano, E. Laurenzano, G. Giugliano, M. Petretta, F. Scopacasa, and M. Chiariello Myeloperoxidase, but not C-reactive protein, predicts cardiovascular risk in peripheral arterial disease Eur. Heart J., January 2, 2008; 29(2): 224 - 230. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. Simon, G. Chironi, and J. Levenson Comparative performance of subclinical atherosclerosis tests in predicting coronary heart disease in asymptomatic individuals Eur. Heart J., December 2, 2007; 28(24): 2967 - 2971. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. Laurin, K. H. Masaki, L. R. White, and L. J. Launer Ankle-to-Brachial Index and Dementia: The Honolulu-Asia Aging Study Circulation, November 13, 2007; 116(20): 2269 - 2274. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. Sritara, C. Sritara, M. Woodward, S. Wangsuphachart, F. Barzi, B. Hengprasith, and T. Yipintsoi Prevalence and Risk Factors of Peripheral Arterial Disease in a Selected Thai Population Angiology, November 1, 2007; 58(5): 572 - 578. [Abstract] [PDF]
|
|
|
|
|
|
L. M. Reich, G. Heiss, L. L. Boland, A. T. Hirsch, K. Wu, and A. R. Folsom Ankle brachial index and hemostatic markers in the Atherosclerosis Risk in Communities (ARIC) study cohort Vascular Medicine, November 1, 2007; 12(4): 267 - 273. [Abstract] [PDF]
|
|
|
|
 |
|
 J. W. Knowles, T. L. Assimes, J. Li, T. Quertermous, and J. P. Cooke Genetic Susceptibility to Peripheral Arterial Disease: A Dark Corner in Vascular Biology Arterioscler Thromb Vasc Biol, October 1, 2007; 27(10): 2068 - 2078. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. M. Wilson, E. Kimura, R. K. Harada, N. Nair, B. Narasimhan, X.-Y. Meng, F. Zhang, K. R. Beck, J. W. Olin, E. T. Fung, et al. {beta}2-Microglobulin as a Biomarker in Peripheral Arterial Disease: Proteomic Profiling and Clinical Studies Circulation, September 18, 2007; 116(12): 1396 - 1403. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. Zeller Current state of endovascular treatment of femoro-popliteal artery disease Vascular Medicine, August 1, 2007; 12(3): 223 - 234. [Abstract] [PDF]
|
|
|
|
 |
|
 A. E. Aquarius, J. Denollet, J. F. Hamming, D. P. Van Berge Henegouwen, and J. De Vries Type-D Personality and Ankle Brachial Index as Predictors of Impaired Quality of Life and Depressive Symptoms in Peripheral Arterial Disease Arch Surg, July 1, 2007; 142(7): 662 - 667. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 G. E. Kikano and M. T. Brown Antiplatelet Therapy for Atherothrombotic Disease: An Update for the Primary Care Physician Mayo Clin. Proc., May 1, 2007; 82(5): 583 - 593. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. C. Kaplan, A. P. McGinn, M. N. Pollak, L. H. Kuller, H. D. Strickler, T. E. Rohan, A. R. Cappola, X. Xue, and B. M. Psaty Association of Total Insulin-Like Growth Factor-I, Insulin-Like Growth Factor Binding Protein-1 (IGFBP-1), and IGFBP-3 Levels with Incident Coronary Events and Ischemic Stroke J. Clin. Endocrinol. Metab., April 1, 2007; 92(4): 1319 - 1325. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. M. McDermott The International Pandemic of Chronic Cardiovascular Disease JAMA, March 21, 2007; 297(11): 1253 - 1255. [Full Text] [PDF]
|
|
|
|
|
|
B. L.W. Bendermacher, J. A.W. Teijink, E. M. Willigendael, M.-L. Bartelink, R. J.G. Peters, R. A. de Bie, H. R. Buller, J. Boiten, M. Langenberg, and M. H. Prins A clinical prediction model for the presence of peripheral arterial disease -- the benefit of screening individuals before initiation of measurement of the ankle--brachial index: an observational study Vascular Medicine, February 1, 2007; 12(1): 5 - 11. [Abstract] [PDF]
|
|
|
|
|
|
A. Guerrero, R. Montes, J. Munoz-Terol, A. Gil-Peralta, J. Toro, M. Naranjo, P. Gonzalez-Perez, C. Martin-Herrera, and A. Ruiz-Fernandez Peripheral arterial disease in patients with stages IV and V chronic renal failure Nephrol. Dial. Transplant., December 1, 2006; 21(12): 3525 - 3531. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. M. Murabito, C.-Y. Guo, C. S. Fox, and R. B. D'Agostino Heritability of the Ankle-Brachial Index: The Framingham Offspring Study Am. J. Epidemiol., November 15, 2006; 164(10): 963 - 968. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. Lamina, C. Meisinger, I. M. Heid, H. Lowel, B. Rantner, W. Koenig, F. Kronenberg, and for the KORA Study Group Association of ankle-brachial index and plaques in the carotid and femoral arteries with cardiovascular events and total mortality in a population-based study with 13 years of follow-up Eur. Heart J., November 1, 2006; 27(21): 2580 - 2587. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. Simon, G. Chironi, and J. Levenson Performance of Subclinical Arterial Disease Detection as a Screening Test for Coronary Heart Disease Hypertension, September 1, 2006; 48(3): 392 - 396. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. A. Beckman, M. R. Jaff, and M. A. Creager The United States Preventive Services Task Force Recommendation Statement on Screening for Peripheral Arterial Disease: More Harm Than Benefit? Circulation, August 22, 2006; 114(8): 861 - 866. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
B. A. Golomb, T. T. Dang, and M. H. Criqui Peripheral Arterial Disease: Morbidity and Mortality Implications Circulation, August 15, 2006; 114(7): 688 - 699. [Full Text] [PDF]
|
|
|
|
|
|
V. Schiano, G. Brevetti, G. Sirico, A. Silvestro, G. Giugliano, and M. Chiariello Functional status measured by walking impairment questionnaire and cardiovascular risk prediction in peripheral arterial disease: results of the Peripheral Arteriopathy and Cardiovascular Events (PACE) study Vascular Medicine, August 1, 2006; 11(3): 147 - 154. [Abstract] [PDF]
|
|
|
|
 |
|
 T. Yoshimura, E. Suzuki, K. Egawa, Y. Nishio, H. Maegawa, S. Morikawa, T. Inubushi, A. Hisatomi, K. Fujimoto, and A. Kashiwagi Low Blood Flow Estimates in Lower-Leg Arteries Predict Cardiovascular Events in Japanese Patients With Type 2 Diabetes With Normal Ankle-Brachial Indexes Diabetes Care, August 1, 2006; 29(8): 1884 - 1890. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. A.S. Cordeiro and J. A.C. Lima Atherosclerotic plaque characterization by multidetector row computed tomography angiography. J. Am. Coll. Cardiol., April 18, 2006; 47(8 Suppl): C40 - C47. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
L. J. Shaw, P. Raggi, T. Q. Callister, and D. S. Berman Prognostic value of coronary artery calcium screening in asymptomatic smokers and non-smokers Eur. Heart J., April 2, 2006; 27(8): 968 - 975. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
E. Selvin, K. Wattanakit, M. W. Steffes, J. Coresh, and A. R. Sharrett HbA1c and Peripheral Arterial Disease in Diabetes: The Atherosclerosis Risk in Communities study Diabetes Care, April 1, 2006; 29(4): 877 - 882. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. E. Norman, W. A. Davis, D. G. Bruce, and T. M.E. Davis Peripheral arterial disease and risk of cardiac death in type 2 diabetes: the fremantle diabetes study. Diabetes Care, March 1, 2006; 29(3): 575 - 580. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. H. Wild, C. D. Byrne, F. B. Smith, A. J. Lee, and F. G. R. Fowkes Low ankle-brachial pressure index predicts increased risk of cardiovascular disease independent of the metabolic syndrome and conventional cardiovascular risk factors in the edinburgh artery study. Diabetes Care, March 1, 2006; 29(3): 637 - 642. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
I. Kardys, H.-H. S. Oei, I. M. van der Meer, A. Hofman, M. M.B. Breteler, and J. C.M. Witteman Lipoprotein-Associated Phospholipase A2 and Measures of Extracoronary Atherosclerosis: The Rotterdam Study Arterioscler Thromb Vasc Biol, March 1, 2006; 26(3): 631 - 636. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
G. J. Hankey, P. E. Norman, and J. W. Eikelboom Medical Treatment of Peripheral Arterial Disease JAMA, February 1, 2006; 295(5): 547 - 553. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
N. Eldrup, H. Sillesen, E. Prescott, and B. G. Nordestgaard Ankle brachial index, C-reactive protein, and central augmentation index to identify individuals with severe atherosclerosis Eur. Heart J., February 1, 2006; 27(3): 316 - 322. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. E. Aquarius, J. De Vries, D. P. V. B. Henegouwen, and J. F. Hamming Clinical indicators and psychosocial aspects in peripheral arterial disease. Arch Surg, February 1, 2006; 141(2): 161 - 166. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
O. Takahashi, T. Shimbo, M. Rahman, R. Musa, W. Kurokawa, T. Yoshinaka, and T. Fukui Validation of the auscultatory method for diagnosing peripheral arterial disease Fam. Pract., February 1, 2006; 23(1): 10 - 14. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
H. Tomiyama, H. Hashimoto, Y. Hirayama, M. Yambe, J. Yamada, Y. Koji, K. Shiina, Y. Yamamoto, and A. Yamashina Synergistic Acceleration of Arterial Stiffening in the Presence of Raised Blood Pressure and Raised Plasma Glucose Hypertension, February 1, 2006; 47(2): 180 - 188. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. M. O'Hare, R. Katz, M. G. Shlipak, M. Cushman, and A. B. Newman Mortality and Cardiovascular Risk Across the Ankle-Arm Index Spectrum: Results From the Cardiovascular Health Study Circulation, January 24, 2006; 113(3): 388 - 393. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Mochida, H. Sakamoto, Y. Sawada, H. Yokoyama, M. Sato, H. Sato, Y. Oyama, M. Kurabayashi, J.-i. Tamura, and T. Sakamaki Visceral Fat Obesity Contributes to the Tortuosity of the Thoracic Aorta on Chest Radiograph in Poststroke Japanese Patients Angiology, January 1, 2006; 57(1): 85 - 91. [Abstract] [PDF]
|
|
|
|
|
|
B. Fletcher, K. Berra, P. Ades, L. T. Braun, L. E. Burke, J. L. Durstine, J. M. Fair, G. F. Fletcher, D. Goff, L. L. Hayman, et al. Managing Abnormal Blood Lipids: A Collaborative Approach Circulation, November 15, 2005; 112(20): 3184 - 3209. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Bo, M. Zanocchi, L. Poli, and M. Molaschi The Ankle-Brachial Index Is Not Related to Mortality in Elderly Subjects Living in Nursing Homes Angiology, November 1, 2005; 56(6): 693 - 697. [Abstract] [PDF]
|
|
|
|
 |
|
 M. Kennedy, C. Solomon, T. A. Manolio, M. H. Criqui, A. B. Newman, J. F. Polak, G. L. Burke, P. Enright, and M. Cushman Risk Factors for Declining Ankle-Brachial Index in Men and Women 65 Years or Older: The Cardiovascular Health Study Arch Intern Med, September 12, 2005; 165(16): 1896 - 1902. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. Lind, B. Hedblad, L. Stavenow, G. Engstrom, L. Janzon, M. Ogren, and F. Lindgarde Incidence of Myocardial Infarction and Death in Relation to Walking-Induced Calf Pain and Plasma Levels of Inflammation-Sensitive Proteins Angiology, September 1, 2005; 56(5): 507 - 516. [Abstract] [PDF]
|
|
|
|
|
|
K. Nasir, E. Guallar, A. Navas-Acien, M. H. Criqui, and J. A.C. Lima Relationship of Monocyte Count and Peripheral Arterial Disease: Results From the National Health and Nutrition Examination Survey 1999-2002 Arterioscler Thromb Vasc Biol, September 1, 2005; 25(9): 1966 - 1971. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. Koster, B. W. J. H. Penninx, H. Bosma, G. I. J. M. Kempen, T. B. Harris, A. B. Newman, R. N. Rooks, S. M. Rubin, E. M. Simonsick, J. T. M. van Eijk, et al. Is There a Biomedical Explanation for Socioeconomic Differences in Incident Mobility Limitation? J. Gerontol. A Biol. Sci. Med. Sci., August 1, 2005; 60(8): 1022 - 1027. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. Muntner, R. P. Wildman, K. Reynolds, K. B. DeSalvo, J. Chen, and V. Fonseca Relationship Between HbA1c Level and Peripheral Arterial Disease Diabetes Care, August 1, 2005; 28(8): 1981 - 1987. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. M. O'Hare, R. A. Rodriguez, and P. Bacchetti Low Ankle-Brachial Index Associated With Rise in Creatinine Level Over Time: Results From the Atherosclerosis Risk in Communities Study Arch Intern Med, July 11, 2005; 165(13): 1481 - 1485. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. V. Doobay and S. S. Anand Sensitivity and Specificity of the Ankle-Brachial Index to Predict Future Cardiovascular Outcomes: A Systematic Review Arterioscler Thromb Vasc Biol, July 1, 2005; 25(7): 1463 - 1469. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. G. Federman, D. C. Ranani, R. S. Kirsner, and D. M. Bravata Lipid-Lowering Therapy in Patients With Peripheral Arterial Disease: Are Guidelines Being Met? Mayo Clin. Proc., April 1, 2005; 80(4): 494 - 498. [Abstract] [PDF]
|
|
|
|
|
|
G. I. Parameswaran, K. Brand, and J. Dolan Pulse Oximetry as a Potential Screening Tool for Lower Extremity Arterial Disease in Asymptomatic Patients With Diabetes Mellitus Arch Intern Med, February 28, 2005; 165(4): 442 - 446. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. L. Leibson, J. E. Ransom, W. Olson, B. R. Zimmerman, W. M. O'Fallon, and P. J. Palumbo Peripheral Arterial Disease, Diabetes, and Mortality Diabetes Care, December 1, 2004; 27(12): 2843 - 2849. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A.J. Lee, J.F. Price, M.J. Russell, F.B. Smith, M.C.W. van Wijk, and F.G.R. Fowkes Improved Prediction of Fatal Myocardial Infarction Using the Ankle Brachial Index in Addition to Conventional Risk Factors: The Edinburgh Artery Study Circulation, November 9, 2004; 110(19): 3075 - 3080. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
E. R Mohler III, D. Treat-Jacobson, M. P Reilly, K. E Cunningham, M. Miani, M. H Criqui, W. R Hiatt, and A. T Hirsch Utility and barriers to performance of the ankle brachial index in primary care practice Vascular Medicine, November 1, 2004; 9(4): 253 - 260. [Abstract] [PDF]
|
|
|
|
|
|
Y. Aso, K.-i. Okumura, S. Wakabayashi, K. Takebayashi, S. Taki, and T. Inukai Elevated Pregnancy-Associated Plasma Protein-A in Sera from Type 2 Diabetic Patients with Hypercholesterolemia: Associations with Carotid Atherosclerosis and Toe-Brachial Index J. Clin. Endocrinol. Metab., November 1, 2004; 89(11): 5713 - 5717. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. Ebrahimi, J. R. Saleh, E. J. Toggart, B. Hayatdavoudi, C. J. Wolf, N. N. Wadhani, and A. P. Shah Lipid-Lowering Therapy in Patients with Peripheral Arterial Disease Journal of Cardiovascular Pharmacology and Therapeutics, October 1, 2004; 9(4): 271 - 277. [Abstract] [PDF]
|
|
|
|
|
|
E. Selvin and T. P. Erlinger Prevalence of and Risk Factors for Peripheral Arterial Disease in the United States: Results From the National Health and Nutrition Examination Survey, 1999-2000 Circulation, August 10, 2004; 110(6): 738 - 743. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. R. Brady, S. G. Thompson, F. G. R. Fowkes, R. M. Greenhalgh, J. T. Powell, and on behalf of the UK Small Aneurysm Trial Participa Abdominal Aortic Aneurysm Expansion: Risk Factors and Time Intervals for Surveillance Circulation, July 6, 2004; 110(1): 16 - 21. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H. Sillesen What does the future hold for the patient with peripheral arterial disease? Eur. Heart J. Suppl., July 1, 2004; 6(suppl_C): C43 - C48. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
Y. Aso, K.-i. Okumura, T. Inoue, R. Matsutomo, N. Yoshida, S. Wakabayashi, K. Takebayashi, and T. Inukai Results of Blood Inflammatory Markers Are Associated More Strongly With Toe-Brachial Index Than With Ankle-Brachial Index in Patients With Type 2 Diabetes Diabetes Care, June 1, 2004; 27(6): 1381 - 1386. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
I. M. van der Meer, M. L. Bots, A. Hofman, A. Iglesias del Sol, D. A.M. van der Kuip, and J. C.M. Witteman Predictive Value of Noninvasive Measures of Atherosclerosis for Incident Myocardial Infarction: The Rotterdam Study Circulation, March 9, 2004; 109(9): 1089 - 1094. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
H. E. Resnick, R. S. Lindsay, M. M. McDermott, R. B. Devereux, K. L. Jones, R. R. Fabsitz, and B. V. Howard Relationship of High and Low Ankle Brachial Index to All-Cause and Cardiovascular Disease Mortality: The Strong Heart Study Circulation, February 17, 2004; 109(6): 733 - 739. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. Duprez HOPE brings hope for the use of the ankle-brachial index as cardiovascular risk marker Eur. Heart J., January 1, 2004; 25(1): 1 - 2. [Full Text] [PDF]
|
|
|
|
|
|
J. Ostergren, P. Sleight, G. Dagenais, K. Danisa, J. Bosch, Y. Qilong, S. Yusuf, and for the HOPE study investigators Impact of ramipril in patients with evidence of clinical or subclinical peripheral arterial disease Eur. Heart J., January 1, 2004; 25(1): 17 - 24. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
H.-H. S. Oei, R. Vliegenthart, A. Hofman, M. Oudkerk, and J. C.M. Witteman Risk factors for coronary calcification in older subjects: The Rotterdam Coronary Calcification Study Eur. Heart J., January 1, 2004; 25(1): 48 - 55. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
L. V. Buitron-Granados, C. Martinez-Lopez, and J. Escobedo-de la Pena Prevalence of Peripheral Arterial Disease and Related Risk Factors in an Urban Mexican Population Angiology, January 1, 2004; 55(1): 43 - 51. [Abstract] [PDF]
|
|
|
|
|
|
J. Amighi, S. Sabeti, O. Schlager, W. Mlekusch, M. Exner, W. Lalouschek, R. Ahmadi, E. Minar, and M. Schillinger Low Serum Magnesium Predicts Neurological Events in Patients With Advanced Atherosclerosis Stroke, January 1, 2004; 35(1): 22 - 27. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A Theodoridou, L Bento, D P D'Cruz, M A Khamashta, and G R V Hughes Prevalence and associations of an abnormal ankle-brachial index in systemic lupus erythematosus: a pilot study Ann Rheum Dis, December 1, 2003; 62(12): 1199 - 1203. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
E. R. Mohler III Peripheral Arterial Disease: Identification and Implications Arch Intern Med, October 27, 2003; 163(19): 2306 - 2314. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. M. Murabito, J. C. Evans, M. G. Larson, K. Nieto, D. Levy, and P. W. F. Wilson The Ankle-Brachial Index in the Elderly and Risk of Stroke, Coronary Disease, and Death: The Framingham Study Arch Intern Med, September 8, 2003; 163(16): 1939 - 1942. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. Holvoet, T. B. Harris, R. P. Tracy, P. Verhamme, A. B. Newman, S. M. Rubin, E. M. Simonsick, L. H. Colbert, and S. B. Kritchevsky Association of High Coronary Heart Disease Risk Status With Circulating Oxidized LDL in the Well-Functioning Elderly: Findings From the Health, Aging, and Body Composition Study Arterioscler Thromb Vasc Biol, August 1, 2003; 23(8): 1444 - 1448. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
E. Suzuki, K. Egawa, Y. Nishio, H. Maegawa, M. Tsuchiya, M. Haneda, H. Yasuda, S. Morikawa, T. Inubushi, and A. Kashiwagi Prevalence and Major Risk Factors of Reduced Flow Volume in Lower Extremities With Normal Ankle-Brachial Index in Japanese Patients With Type 2 Diabetes Diabetes Care, June 1, 2003; 26(6): 1764 - 1769. [Abstract] [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||