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78
CHAPTER 5 Atrial Fibrillation
51. Saravanan P, Bridgewater B, West AL, et al . Omega-3 fatty acid supplementa-
tion does not reduce risk of atrial fi brillation after coronary artery bypass sur-
gery: a randomized, double-blind, placebo-controlled clinical trial. Circ Arrhythm
Electrophysiol 2010; 3 (1): 46–53.
52. Santangeli P, Ferrante G, Pelargonio G, et al . Usefulness of statins in preventing
atrial fi brillation in patients with permanent pacemaker: a systematic review.
Europace 2010; 12: 649–654 .
53. Liakopoulos OJ, Choi YH, Kuhn EW, et al . Statins for prevention of atrial fi bril-
lation after cardiac surgery: a systematic literature review. J Thorac Cardiovasc
Surg 2009; 138: 678–686 e1 .
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7979
Chapter 6
Peripheral Artery Disease
Amjad AlMahameed
Introduction
The three major atherothrombotic syndromes encountered in clinical practice
are coronary artery disease (CAD), cerebrovascular disease, and peripheral
artery disease (PAD). The updated American College of Cardiology/American
Heart Association Clinical guidelines defi ned PAD by the presence of an abnor-
mal ankle–brachial index (ABI) of 0.9 or less, regardless of symptoms.
1,2
The ABI
refl ects the atherothrombotic burden in the body and serves as a marker for
vascular disease elsewhere and for future cardiovascular events. Intermittent
claudication, as originally defi ned by the World Health Organization (WHO)/
Rose questionnaire, is present in less than one third of symptomatic patients.
Other symptoms, also referred to as atypical claudication or exertional leg
dysfunction, ought to be sought in all patients. Noninvasive vascular labora-
tory testing offers a safe and reliable means for accurate diagnosis and disease
localization. Other noninvasive imaging studies (computed tomographic angiog-
raphy [CTA] and magnetic resonance angiography [MRA]) offer supplemen-
tal information and are often obtained prior to revascularization procedures.
Treatment goals of PAD include improving overall functional status and qual-
ity of life, preventing progression of systemic atherosclerosis in the peripheral
arteries and elsewhere, reducing future cardiovascular and cerebrovascular
events, and, in advanced cases, limb salvage. This chapter will review asymp-
tomatic and symptomatic PAD and offer contemporary approaches to diagno-
sis and management.
Epidemiology of PAD
Several epidemiologic studies evaluated the prevalence of PAD across defi ned
populations (Table 6.1). These studies used the ABI, and most considered an ABI
of 0.9 or less the cutoff value for diagnosis. Signifi cant interstudy variations in PAD
prevalence are noted and can be explained by differences in the populations eval-
uated and the method of ABI measurement employed. For example, the lower
PAD prevalence in the MESA study is likely a result of excluding subjects with
clinically evident cardiovascular and cerebrovascular disease, while the higher
prevalence noted in the PARTNERS study is likely related to including older indi-
viduals, while younger subjects enrolled in this study had to have major PAD risk
factors, specifi cally diabetes or smoking.
3,4
Furthermore, the methodology used
for obtaining the ABI was not standardized in some of these studies. This may in
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CHAPTER 6 Peripheral Artery Disease
Table 6.1 Prevalence of Asymptomatic PAD and IC in Select Epidemiologic, Population-Based Studies
Study (year) Population
Characteristics
PAD
Prevalence
IC
Prevalence
Comments
Cardiovascular Health
Study
21
(1993)
• 5,714 community dwellers
• > 65 yrs of age
13.4% 2% of the “entire”
population
• ABI < 0.9
• IC: Rose questionnaire
Atherosclerosis Risk in Communities
Study (ARIC)
45
(1997)
• 15,106 middle-aged adults
• 45–64 yrs of age
3.1% NA
• PAD was defi ned by ABI ≤ 0.9.
• IC: Rose questionnaire
Strong Heart Study
46
(1999)
• 4,549 American Indians
• 45–74 yrs of age
5.3% 0.3–0.8%
• 60% were women
• ABI < 0.9
• IC: Rose questionnaire
PARTNERS Study
4
(2001)
• 6,979 primary care patients:
• Age either > 70 yrs or 50–69 with
DM or smoking history
29% 11% of the PAD
population
• IC: San Diego Claudication
Questionnaire (modifi ed from Rose
questionnaire)
Framingham Offspring
Study
47
(2002)
• 3,313 attendees of the
Framingham Offspring Study
3.6% M: 1.9%
F: 0.8%
• PAD was defi ned by ABI < 0.9
• IC: Physician-Administered Intermittent
Claudication Questionnaire
National Health and Nutrition
Examination Survey (NHANES)
5
(2004)
• 2,174 men and women
• > 40 yrs of age
4.3% NA
• ABI < 0.90
• Brachial systolic blood pressure
assessed in one arm
• Ankle systolic blood pressure assessed
only in posterior tibial artery
Multi-Ethnic Study of
Atherosclerosis
3
(MESA) (2005)
• 6,570 adults without clinical
cardiovascular disease or
cerebrovascular disease
• 45–84 yrs of age, mean 63 yrs
3.7% NA
• ABI < 0.9
PAD was diagnosed by screening ABI and intermittent claudication (IC) by administering a prespecifi ed patient questionnaire.
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CHAPTER 6 Peripheral Artery Disease
fact offer a reasonable explanation for the unexpectedly low PAD prevalence
noted in the NHANES survey, where the blood pressure was measured in only
one arm and the ankle pressure in only one tibial artery (the posterior tibial).
5
Therefore, cases of subclavian artery stenosis or dorsalis pedis occlusion may
have been missed. Nonetheless, these and other studies consistently showed a
higher prevalence with advanced age, and in subjects with established CAD and
cerebrovascular disease, as well as those with traditional risk factors, particularly
tobacco consumption and diabetes mellitus (DM). Smoking and DM are the most
potent risk factors for PAD, and the odds ratios for associations of DM and smok-
ing with symptomatic PAD are 3.0 to 4.0 respectively.
6
Intermittent claudication (IC) was originally defi ned by the WHO/Rose
questionnaire as “exertional calf pain that causes the patient to stop walking,
resolves within 10 minutes of rest, does not resolve while the patient is walk-
ing, and does not begin at rest.”
7
The major liabilities of the Rose questionnaire
are its susceptibility to false-negative fi ndings, as it overlooks leg symptoms
other than pain and discards symptoms affecting the buttocks and the thighs.
Moreover, the Rose questionnaire lacks validated data on laterality (side
affected). Therefore, contemporary studies used other tools, such as the San
Diego Claudication Questionnaire, which is a modifi cation of the Rose ques-
tionnaire that allows for lateralization of leg symptoms (right, left, or both)
and categorizes leg symptoms as classic claudication (meeting all Rose crite-
ria), atypical leg pain (exertional but did not meet all Rose criteria), or no leg
pain. Interestingly, in the validation study of this modifi ed questionnaire, which
included 508 patients aged 39 to 95 years who were referred for PAD noninva-
sive testing, 40 percent of subjects were classifi ed as having atypical claudication
(not Rose).
8
The Framingham offspring study used yet another physician-admin-
istered IC questionnaire that asked about exertional leg discomfort that was
related to steepness or rapidity of walking and was relieved with rest.
9
These
examples clearly indicate that the method of IC assessment can infl uence the
rate of detection and prevalence.
Overall, PAD affects at least 8 million Americans, compared to 2.2 million
affected by atrial fi brillation, and it disproportionately affects black and older
Americans (12 to 20 percent of Americans older than 65 years have the
disease).
10
This high prevalence and the signifi cant functional impairment and
quality-of-life defi cit seen in both symptomatic and asymptomatic patients (see
below) merit considering PAD a public health issue in the United States. We
strongly advocate early detection of affected patients and increased awareness
of the disease for both health care providers and patients.
ABI as a measure of the systemic atherothrombotic
burden regardless of symptoms
The association between PAD and cardiovascular disease and adverse events has
been established in both symptomatic and asymptomatic patients. In one report,
pooled data from 11 studies from six different countries, comprising 44,590 subjects
(including the US CHS, ARIC study, Framingham Heart Study, and Strong Heart
Study) demonstrated that abnormal ABI (less than 0.9), regardless of symptoms,
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CHAPTER 6 Peripheral Artery Disease
corresponded to a substantive increase in the risk of all-cause mortality, cardio-
vascular mortality, coronary heart disease, and stroke (pooled RR 1.60, 1.96, 1.45,
1.35 consecutively).
11
Importantly, this association was independent of age, sex,
and conventional cardiovascular risk factors such as smoking, dyslipidemia, and
hypertension, as well as the presence of established cardiovascular disease.
Similarly, a recent meta-analysis of 16 cohort population studies with 480,325
person-years (total of 48,294 subjects) found a reverse-J-shaped distribution for
the risk of death by ABI, with a normal (low risk) ABI of 1.11 to 1.40 (Fig. 6.1).
In this analysis, the overall estimated 10-year cardiovascular mortality in the low
ABI group (0.90 or less) was remarkably higher compared to the normal ABI
group (HR 3.5 for women and 4.2 for men). After adjusting for the Framingham
Risk Score (FRS), which is used to predict risk of total CHD, including coronary
death, myocardial infarction (MI), and angina, the association between low ABI
(0.90 or less) and 10-year cardiovascular mortality remained signifi cant (HR
2.92 in men versus 2.97 in women), and so was the association between low
ABI and 10-year major coronary events (HR 2.16 in men versus 2.49 in women).
This remained true for every category of the FRS and indicated that low ABI
functioned as an independent and useful risk stratifi cation tool over that pro-
vided by the FRS alone. In fact, this study determined that regardless of PAD
symptoms, inclusion of the ABI in cardiovascular risk stratifi cation using the FRS
resulted in reclassifi cation of the risk category and modifi cation of treatment
recommendations in 4,106 of the 21,433 (19 percent) men and in 8,154 of the
22,486 (36 percent) women.
12
Although most population-based epidemiologic studies that highlighted
the association between low ABI and adverse cardiovascular events excluded
patients with clinically evident cardiovascular disease at entry, a similar asso-
ciation was evident when cohorts of patients with established cardiovascular
disease, including MI and angina, were evaluated.
13–15
Several studies suggest a reverse relationship between the ABI value and
adverse cardiovascular outcomes. This is not surprising given that lower ABI signi-
fi es more severe PAD and a larger overall systemic atherothrombotic burden. In
8.0
4.0
2.0
1.0
0.5
≤0.60 0.61-0.70 0.71-0.80 0.81-0.90 0.91-1.00 1.01-1.10 1.11-1.20
(Reference)
Ankle Brachial Index
Men
Women
1.21-1.30 1.31-1.40 > 1.40
Hazard Ratio (95% Confidence Interval)
Figure 6.1 Hazard ratios are not adjusted for age or cardiovascular risk factors. (From
reference 12.)
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CHAPTER 6 Peripheral Artery Disease
one retrospective review of 422 patients with abnormal ABI, the relative hazard
of death at 4.3 years of follow-up was 1.8 for patients with ABIs of 0.3 or less
compared with those who had ABIs of 0.5 to 0.91.
16
The implication of a declining ABI over time was addressed in an interesting
prospective evaluation of 508 patients who underwent two ABI measurements
within a 10-year period. A decline in the ABI by more than 0.15 was associated
with an increased risk of all-cause mortality (RR 2.4) and cardiovascular mortal-
ity (RR of 2.8) at 3-year follow-up and with cardiovascular morbidity and mor-
tality (RR 1.9) at 6-year follow-up. This association was independent of the
most recent ABI value and of other atherosclerotic risk factors. Interestingly,
one in six (16.7 percent) patients in this cohort had a deteriorating ABI, sug-
gesting that this is a relatively common event in a vascular laboratory popula-
tion. Therefore, attention to a deteriorating ABI is necessary as it may signify
impending cardiovascular events regardless of the severity of the baseline PAD
and clustering of traditional risk factors.
17,18
A recent scientifi c statement from the American Heart Association on the
measurement and interpretation of the ABI adopted the fi ndings of this and
other studies and recommended that an ABI decrease of more than 0.15 over
time can be effective to detect signifi cant PAD progression.
19,20
Such a mild
decline over a mean follow-up period of 2.5 years correlated in another study
that followed vascular surgery patients with a revascularization operation rate
2.5 times higher and symptom progression rate 1.8 times higher than patients
without this change in the ABI over the same period.
20
Lower ABI is also a marker of subclinical and clinical cardiac and vascu-
lar disease elsewhere. In the CHS, lower ABI (0.90 or less) was associated
with an increased risk of carotid atherosclerosis, left ventricular (LV) hyper-
trophy, and LV wall motion abnormalities.
21
In the international REduction of
Atherothrombosis for Continued Health (REACH) registry, which enrolled
68,000 patients with symptomatic CAD, cerebrovascular disease, or PAD or
at least three major risk factors, patients with symptomatic PAD represented
12.2 percent of the registry population. In this most globally inclusive registry of
patients at high risk of atherothrombosis, approximately 60 percent of the PAD
population had atherothrombotic disease in other arterial territories.
22
These
data should be taken in context with the clinical status, and clinicians should be
vigilant and ready to investigate the presence and severity of associated disease
when clinically indicated.
23
In summary, an abnormal ABI (0.90 or less) is a reliable tool for assessment
of lower limb arterial perfusion as well as a local and systemic marker of the
atherothrombotic burden and future events in both symptomatic and asymp-
tomatic PAD patients.
Clinical evaluation
Considering the low sensitivity of the Rose questionnaire, relying on reported
history of IC will likely result in missing the vast majority of such patients.
4
It is
now accepted that most patients with PAD are either asymptomatic or pres-
ent with atypical symptoms that are best characterized as activity-induced leg
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CHAPTER 6 Peripheral Artery Disease
discomfort. These may include aching, tightness, cramping, heaviness, or a sense
of fatigue in a muscle group or the whole leg. These symptoms do not consis-
tently resolve with rest, limit exercise at a reproducible distance, or meet all
“Rose questionnaire” criteria.
24
We make sure during the initial evaluation to search for overlapping comor-
bidities that may be contributing to the symptoms. Such comorbidities are
more common in patients with atypical symptoms than those with classic IC,
and they include lumbar spine radiculopathy, degenerative joint disease, and
venous insuffi ciency.
24
We also make sure to assess the patient’s functional
limitations and, for sedentary patients, inquire about self-imposed limitations
on physical activity to avoid the exertional leg discomfort.
A comprehensive vascular examination is key and involves palpating the
peripheral pulses (abdominal aorta, femoral, popliteal, dorsalis pedis, and poste-
rior tibial arteries) in both legs and grading the pulse quality as 0 (not palpable),
+1 (diminished), +2 (normal pulse), or +3 (bounding). Bounding pulses in the
abdominal aorta and popliteal arteries are especially concerning for aneurys-
mal disease. We also auscultate the aortic, renal, iliac, and femoral arteries for
bruits. Diastolic bruits are more likely to correlate with severe stenotic lesions
than systolic bruits. Doppler interrogation of the arteries with decreased or
absent pulses is then carried out and the signal is graded as triphasic, biphasic,
or monophasic.
Using a hand-held Doppler and a stethoscope, we then perform a bedside
ABI by measuring the systolic blood pressure (SBP) in the right brachial artery
followed by the dorsalis pedis and posterior tibial in each leg and fi nally the bra-
chial artery in the left arm. We then calculate the ABI for each leg as the ratio
of the higher pedal SBP divided by the higher brachial SBP. A value of 0.90 or
less establishes the diagnosis of PAD, and global cardiovascular risk reduction
strategies are instituted.
4
Measuring the ABI before and after exercise may be useful in patients with
symptoms suggestive of claudication but with a normal resting ABI. A drop in
pressure with exercise may indicate that there is signifi cant aortoiliac or com-
mon femoral (infl ow) obstructive disease.
When indicated, further testing is pursued and the rationale is discussed with
the patient. This is particularly important in cases where the ABI is not reliable
(values more than 1.40, which indicate medial arterial calcifi cation typically seen
in elderly patients and those with diabetes and chronic kidney disease) or when
the ABI is diffi cult to obtain (presence of bandages, braces, or open wounds
that cannot be covered by an impermeable dressing or the presence of a distal
bypass graft or, in some cases, a stent).
We then systematically classify the clinical category for patients with a rest
ABI of 0.90 or less based on the Rutherford Classifi cation (Table 6.2). This tool
incorporates clinical fi ndings with objective data from noninvasive functional
testing usually performed in the vascular laboratory. For Rutherford Grade 0
and I (patients with claudication), we document the initial claudication distance
(distance walked to initial leg discomfort) and the absolute claudication dis-
tance (furthest distance patient is able to walk) for future reference.
Based on our initial impression of the patient’s functional status, we fre-
quently choose to perform the 6-minute walk test and document the ability to
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85
CHAPTER 6 Peripheral Artery Disease
complete the test and the distance walked. This is particularly helpful in doc-
umenting disease progression and worsened functional status prospectively.
Patients with an ABI of 0.90 or less who deny leg symptoms (both typical and
atypical) are at increased risk for functional decline compared to persons with
a normal ABI (average mean decline in 6-minute walk test at 2 years –76.8 ver-
sus –8.67 feet per year, p = 0.04, respectively).
25
The 6-minute walk test is also
informative even in patients who report reasonable claudication and absolute
walking distances. In the same prospective cohort evaluated by McDermott
et al., PAD patients with an ABI of less than 0.50 who were able to walk con-
tinuously for 6 minutes at baseline were more than 12 times less likely than
those with a normal baseline ABI (defi ned as ABI 1.10 to 1.5) to complete the
test without stopping at 2 years.
25
In a busy clinical practice, the 6-minute walk
test can be performed at a separate scheduled visit by the physical therapy (PT)
service. Another advantage of such evaluation by PT is to assess balance, walk-
ing speed, and walking endurance, as these are often impaired in PAD patients,
even in those who deny leg symptoms.
24,25
We conclude our initial evaluation (which typically requires two visits,
1 month apart) and present the data to the patient along with a simplifi ed inter-
pretation of the fi ndings and the potential implications of PAD on systemic and
functional outcomes. We fi nd this discussion to be a powerful motivational tool
for patients to incorporate substantive and complex lifestyle changes; particu-
larly regular walking exercise, weight loss, and complete smoking cessation.
Critical limb ischemia (CLI) is suspected when rest pain (or rapidly pro-
gressive short-distance pain for at least 2 weeks), tissue loss (ulcerations or
Table 6.2 Clinical Categories of Chronic Limb Ischemia—
Rutherford Classifi cation
48
Grade Category Clinical Description Objective Criteria (vascular
lab-based)
0 0 Asymptomatic Normal TM
I 1 Mild Claudication Complete TM
Post-exercise AP >50 but
<20 mmHg resting value
2 Moderate Claudication Between 1 and 3
3 Severe Claudication Cannot complete TM
Post-exercise AP <50 mmHg
II 4 Ischemic Rest Pain Resting AP <40 mmHg, fl at PVR
TP <30 mmHg
III 5 Minor Tissue Loss Resting AP <60 mmHg, fl at PVR
TP <40 mmHg
IV 6 Major Tissue Loss
(non-salvageable)
Same as Category 5
TM, treadmill at 2 mph with 12% incline up to 5 minutes; equivalent to 4 to 5 Mets; AP, arterial
pressure; PVR: pulse volume recording, TP, toe pressure
Source: Reprinted from Rutherford RB, Baker JD, Ernst C, et al. Recommended standards for
reports dealing with lower extremity ischemia: Revised version. J Vasc Surg 1997 ; 26:517–523, with
permission from Elsevier.
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86
CHAPTER 6 Peripheral Artery Disease
wounds), or gangrenous changes are noted in the distal limb. Other supportive
clinical signs include dependent rubor (skin erythema secondary to maintaining
the limb in a dependent position such as dangling from the side of the bed while
sleeping to alleviate rest pain) and elevation pallor (skin pallor that occurs upon
leg elevation for more than 1 minute and persists for more than 30 to 40 sec-
onds before the color returns).
Acute limb ischemia (ALI) is a distinct syndrome that manifests as a sudden
decrease in limb perfusion that threatens the viability of the limb.
6
It is char-
acterized clinically by a sudden or rapid worsening of IC (within 2 weeks of
symptom onset) to foot or leg pain, paresthesias, muscle weakness, or paralysis
occurring at rest. The pulses distal to the occlusion are absent, but Doppler
signal (arterial, venous, or both) may be detectable. The skin turns cool, pale,
and often mottled, and the sensation and strength are usually diminished. Limb
salvage depends on prompt recognition and timely revascularization.
26
In general, we depend on noninvasive vascular laboratory testing to establish
the diagnosis and plan most revascularization procedures. Figure 6.2 outlines
our protocol for referring patients to the Vascular Laboratory for additional
noninvasive vascular studies.
We seek additional imaging studies, such as CTA and MRA, sparingly and
typically prior to aortoiliac reconstruction procedures. Invasive angiography is
restricted to cases where a revascularization strategy has been devised.
Management strategies
Treatment goals in PAD are outlined in Table 6.3. Medical therapy to slow
the progression of systemic atherosclerosis and lower the incidence of
Rest ABI <0.9 Rest ABI 0.91–1.40 Rest ABI >1.40
Perform Exercise ABI
Exercise ABI <0.9 Exercise ABI >0.9
Rest TBI >0.7
No PAD
Rest TBI <0.7
Aorto-iliac disease suspected
Infra-inguinal disease suspected
Arterial Duplex US
(PSV, Spectral br oadening and wave form)
• GFR >50: CTA or MRA
• GFR <50: Duplex US
Segmental BP and PVR
Figure 6.2 Establishing the diagnosis of PAD: the role of the Vascular Laboratory and
noninvasive vascular studies.
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87
CHAPTER 6 Peripheral Artery Disease
Table 6.3 Treatment Goals in PAD
Goal Benefi ts Strategies
(1) Improve
functional status
and quality of life
• Improves symptoms
• Improves quality of life
• Improves exercise
capacity
• Supervised walking
exercise
• Self-administered walking
program
• Maintain optimal weight
• Proper footwear and foot
care
• Address other causes of
limb dysfunction
• Pharmacotherapy:
cilostazol, statins, and ACE
inhibitors
• Revascularization:
percutaneous and surgical
(2) Prevent
progression of
atherothrombosis
• Reduces future
disability
• Reduces future
cardiovascular and
cerebrovascular events
• Reduces the need for
future
• Treat diabetes and
achieve target HgbA1C
• Treat hyper-
homocysteinemia
• Lifestyle changes: optimal
BMI and waist/hip ratio,
healthy diet
• Smoking cessation
program: offer referral to
a formal program. Offer
varenicline, bupropion,
or nicotine replacement
therapy. Address smoking
cessation and maintenance
every visit.
• Pharmacotherapy with
statins (target LDL
<70–100), ACE inhibitors
(target blood pressure
< 140/90 mmHg,
< 130/80 mmHg if diabetes
or chronic kidney disease
present)
• Aspirin 75–325 mg daily
(or clopidogrel 75 mg
daily) for all symptomatic
patients and select
asymptomatic patients
who may have other
indications
• Combination ASA and
clopidogrel may be offered
to those who are not at
increased risk of bleeding
and who are at high
perceived cardiovascular
risk
• Treat diabetes (target
HgbA1C < 7.0%)
(continued)
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