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com
Review
VA Eastern Colorado
Healthcare System and Division
of Cardiology, University of
Colorado, Denver, Colorado,
USA
Correspondence to
Dr Stephen W Waldo, VA
Eastern Colorado Healthcare
System, 1055 Clermont Street,
Denver, CO 80220, USA;
stephen.waldo@ucdenver.edu
Received 24 February 2016
Revised 2 May 2016
Accepted 3 May 2016
Published Online First
1 June 2016
To cite: Foley TR,
Armstrong EJ, Waldo SW.
Heart 2016;102:1436–
1441.
1436
Contemporary evaluation and management of lower
extremity peripheral artery disease
T Raymond Foley, Ehrin J Armstrong, Stephen W Waldo
ABSTRACT
Peripheral artery disease (PAD) includes atherosclerosis
of the aorta and lower extremities. Affecting a large
segment of the population, PAD is associated with
impaired functional capacity and reduced quality of life
as well as an increased risk of stroke, myocardial
infarction and cardiovascular death. The evaluation of
PAD begins with the physical examination, incorporating
non-invasive testing such as ankle-brachial indices to
confirm the diagnosis. Therapeutic interventions are
aimed at alleviating symptoms while preserving limb
integrity and reducing overall cardiovascular risk. With
this in mind, risk factor modification with exercise and
medical therapy are the mainstays of treatment for many
patients with PAD. Persistent symptoms or non-healing
wounds should prompt more aggressive therapies with
endovascular or surgical revascularisation. The following
manuscript provides a comprehensive review on the
contemporary evaluation and management of PAD.
INTRODUCTION
Peripheral artery disease (PAD) affects a large
segment of the population with a prevalence that
increases with age.1 The global prevalence of PAD
continues to rise, with the burden increasing from
an estimated 164 million cases in 2000 to 202
million cases in 2010.2 Atherosclerosis is a systemic
process, and the majority of individuals with PAD
also have concomitant disease in the cerebral or
coronary vasculature. Accordingly, patients with
PAD are three times as likely to experience cardio-
vascular death compared with those without PAD.3
Despite the prevalence and systemic cardiovascu-
lar risk associated with PAD, this condition remains
underdiagnosed and undertreated in contemporary
practice.4 A minority of patients suffering from per-
ipheral atherosclerosis are aware of their diagnosis
and the disease goes undetected by physicians in
over 70% of cases.5 Patients with PAD are also sig-
nificantly less likely to receive guideline-directed
medical therapy, increasing the risk of major
adverse cardiovascular events.6 With this in mind,
the present review discusses the clinical manifesta-
tions, diagnostic testing and therapeutic interven-
tions appropriate for this vulnerable population.
CLINICAL MANIFESTATIONS
The clinical manifestations of PAD range in severity
from asymptomatic disease to intermittent claudica-
tion (IC) and critical limb ischaemia (CLI). Many
patients with PAD remain asymptomatic or have
atypical leg discomfort.7 Classic IC, defined as mus-
cular discomfort provoked by exertion and relieved
with rest, occurs in a minority (<30%) of patients
with this disease. CLI represents the most severe
Foley TR, et al. Heart 2016;102:1436–1441. doi:10.1136/heartjnl-2015-309076
manifestation of PAD, and manifests as ischaemic
rest pain or non-healing wounds resulting in tissue
loss. Although CLI is relatively rare, it carries a
very grim prognosis with high rates of amputation
(30%) and mortality (25%) 1 year after the index
presentation.8 A variety of classification schemes
have been devised to characterise the severity of
symptoms among patients with PAD, with the
Fontaine and Rutherford classifications most com-
monly used in clinical practice (table 1).
Acute limb ischaemia (ALI) refers to the abrupt
interruption of blood flow to an extremity. Patients
with PAD are at risk of developing ALI due to
acute thrombosis of a ruptured atherosclerotic
plaque, bypass graft or previously placed stent. Less
commonly, embolic occlusion from a central source
(cardiac) or from a diseased artery may occur. Signs
and symptoms of ALI may include pain, pallor,
diminished or absent pulses and neurological defi-
cits including motor weakness and sensory impair-
ment. In contrast to CLI, in which gradual
ischaemic conditioning promotes the development
of collateral vessels that maintain limb perfusion,
ALI leads to an abrupt disruption of blood flow
that threatens limb integrity unless prompt revascu-
larisation is achieved.
DIAGNOSIS
Physical examination
The physical examination is an important tool in
establishing the presence, location and severity of
PAD. Stenotic or occluded arteries will produce
diminished distal pulses, and auscultation over a
diseased vessel may reveal a bruit due to turbulent
flow. Skin discolouration often occurs as a conse-
quence of chronic vasodilation in the setting of
haemodynamically significant disease. Arterial
ulcerations are characterised by a well-demarcated,
‘punched-out’ appearance as demonstrated in
figure 1. Dependent rubor and elevation pallor may
be present in the extremities of individuals with
advanced disease as a consequence of impaired
autoregulation in the dermal arterioles and
capillaries.
Physiological testing
The ankle-brachial index (ABI) is an inexpensive
and reproducible physiological assessment of lower
extremity haemodynamics. The ABI represents the
ratio of the highest ankle pressure in each leg,
obtained at the dorsalis pedis and posterior tibial
arteries with a Doppler probe, to the highest bra-
chial artery pressure. The sensitivity of ABI in
detecting angiographically significant stenoses has
been reported to be as high as 94%–97%, and
several studies have demonstrated an inverse
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Table 1 Disease severity can be stratified according to the
Fontaine and Rutherford classification systems8
Fontaine Rutherford
Stage Symptoms Stage Symptoms
I Asymptomatic 0 Asymptomatic
IIa Mild claudication* 1 Mild claudication
IIb Moderate–severe claudication† 2 Moderate claudication
3 Severe claudication
III Ischaemic rest pain 4 Ischaemic rest pain
IV Ulceration or gangrene 5 Minor tissue loss
6 Major tissue loss
*Mild claudication is defined as symptoms after ambulating >200 m.
†Moderate claudication is defined as symptoms after ambulating <200 m.
relationship between ABI value and the risk of subsequent major
adverse cardiovascular events including mortality.9 The sensitiv-
ity of ABI is diminished in patients with small vessel disease or
medial calcinosis due to hypertension, diabetes or chronic
kidney disease. In patients with non-compressible ABIs (>1.3),
the toe-brachial index (TBI) can be used. The diagnostic criteria
for ABI and TBI are listed in table 2. Some patients with exer-
tional claudication will have normal resting ABIs and thus exer-
cise ABI testing can be instrumental in revealing the presence or
absence of PAD. During exercise, poststenotic arterial vasodila-
tion coupled with an inability of flow to increase beyond a fixed
stenosis leads to a drop in systolic pressure in an affected limb
that will manifest as an abnormal ABI. In a study of symptom-
atic patients referred for physiological testing, 31% of those
with normal resting studies were found to have an ABI <0.9
Figure 1 Lower extremity ulceration induced by arterial insufficiency.
The wound is located in an area of repetitive trauma and is
characterised by a ‘punched-out’ appearance.
Foley TR, et al. Heart 2016;102:1436–1441. doi:10.1136/heartjnl-2015-309076
Review
Table 2 Diagnostic criteria for ankle-brachial and toe-brachial
testing8
Ankle–brachial indices Toe–brachial indices
1.0–1.3 Normal > 0.7 Normal
0.9–1.0 Borderline
0.7–0.9 Mild <0.7 Abnormal
0.4–0.7 Moderate
<0.4 Severe <0.4 Severe
Exercise drop >20 mm Hg or 0.2 is significant.
*Used when ankle-brachial index is non-compressible (>1.3).
after exercise.10 Current guidelines recommend exercise ABI
testing for patients at risk of PAD with normal resting values;
exercise studies may also be useful to distinguish claudication
from pseudoclaudication.11 Pulse volume recordings (PVR) and
segmental pressures can further refine a physiological assessment
and are useful for determining the presence, severity and loca-
tion of obstructive PAD. Figure 2 demonstrates changes in PVR,
based on the severity of disease.12
Anatomical testing
Duplex ultrasound provides another tool for establishing the
location and severity of arterial stenoses. The ratio of the peak
systolic velocity (PSV) at an area of stenosis to the PSV of the
vessel just proximal to the narrowing allows for the quantifica-
tion of the area of stenosis. A velocity ratio of >2.0 corresponds
with a >50% stenosis, while a ratio of >4.0 corresponds with a
75%–99% stenosis in lower extremity vasculature. Angiography
yields a detailed visual assessment of the vasculature that is
important when planning for revascularisation. Catheter-based
angiography allows for a simultaneous diagnostic assessment
and therapeutic option should endovascular intervention be
warranted. CT angiography and magnetic resonance angiog-
raphy provide non-invasive modalities that may be preferred in
patients expected to undergo surgical revascularisation or with
contraindications to invasive arteriography. Positron emission
tomography is rarely used in clinical practice, but may serve as a
research tool moving forward.
TREATMENT
The primary objectives in the treatment of PAD include the
management of systemic cardiovascular risk factors as well as
the improvement of functional capacity and quality of life.
These objectives are best achieved through a multifaceted
approach that incorporates appropriate lifestyle modifications,
secondary prevention medications and potentially endovascular
or surgical revascularisation (table 3).
Exercise
Patients with PAD experience a decline in functional capacity
that is associated with reduced health-related quality of life
(HRQOL) and high rates of depression.13 Multiple studies have
demonstrated improved pain-free walking distance and HRQOL
in patients with IC who participate in a supervised exercise pro-
gramme.14 A Cochrane review demonstrated an average increase
in maximum walking distance of 180 m in patients undergoing
supervised exercise therapy (SET) for IC.15 Further, a large ran-
domised control trial (claudication: exercise versus endoluminal
revascularization (CLEVER) confirmed the benefits of a struc-
tured and supervised walking programme to increase functional
capacity in patients with PAD when added to optimal medical
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Figure 2 Pulse volume recordings (PVR). A normal PVR waveform is
characterised by a sharp systolic upstroke (1) followed by a rapid
downstroke (2) with a prominent dicrotic notch (3), as shown in (A).
(B) depicts a mildly abnormal PVR waveform characterised by a sharp
systolic upstroke with a rounded systolic peak and absence of a dicrotic
notch. A moderately abnormal PVR waveform is characterised by a
prolonged systolic upstroke, rounded systolic peak, absence of a dicrotic
notch and prolonged downstroke (C). Finally, a severely abnormal PVR
waveform is represented by a low amplitude tracing with prolonged
upstroke and downstroke, rounded systolic peak and loss of dicrotic
notch (D).
therapy.16 Based on these findings, current professional society
guidelines endorse SET as a first-line treatment for all patients
with PAD.11 17
Smoking cessation
Tobacco use is a potent risk factor for the development of
PAD.18 Individuals with PAD who continue to smoke are more
likely to develop lifestyle-limiting claudication and CLI, and
have a twofold increased risk of limb amputation compared
with those who successfully terminate the habit.19 In contrast,
abstention from smoking is associated with lower mortality rates
and improved amputation-free survival in patients with PAD.20
Based on this, consensus guidelines recommend smoking
1438
Table 3 Professional society recommendations (class I) for the
management of peripheral artery disease (PAD)11
Intermittent Critical limb
Asymptomatic claudication ischemia
Lifestyle Exercise Supervised exercise –
interventions Tobacco cessation
Medications
Anti-platelet Aspirin 81 mg PO daily
therapy Clopidogrel 75 mg PO daily (alternative)
Target blood pressure <140/90 (non-diabetics)
Anti-hypertensives Target pressure <130/80 (diabetics)
Anti-lipid Atorvastatin 40–80 mg PO daily
Rosuvastatin 20–40 mg PO daily
Revascularisation
Endovascular/ – Consider for Consider for rest
surgical lifestyle-limiting pain/non-healing
symptoms wounds
Ancillary services
Wound care – – Consider for
non-healing
wounds
PO, per os.
cessation in all patients with this condition.11 17 The efficacy of
a provider-delivered smoking cessation intervention that
includes counselling and nicotine replacement therapy is cur-
rently being investigated among patients with vascular disease in
the Vascular Physician Offer and Report trial.21
Pharmacological treatment
Antithrombotics
The majority of patients with PAD have evidence of atheroscler-
osis in the coronary or cerebral vasculature, and the presence of
PAD is associated with increased platelet reactivity and aggrega-
tion in response to plaque rupture.22 As a result, patients with
PAD are at increased risk of stroke and myocardial infarction
(MI), as well as three times more likely to die from a cardiovas-
cular event within 10 years than those without this disease.3
Antiplatelet monotherapy with aspirin has been shown to
reduce the risk of atherothrombosis in patients with PAD, and
consensus guidelines recommend that all symptomatic patients
be treated with an antiplatelet drug.11 17 23 Clopidogrel is also
an effective antiplatelet agent in patients with symptomatic
PAD, as was demonstrated in the clopidogrel versus aspirin in
patients at risk of ischemic events trial.24 After a mean follow-up
of 1.91 years, patients with symptomatic PAD treated with clo-
pidogrel had a 23.8% relative risk reduction in the primary
composite endpoint of ischaemic stroke, MI or vascular death
compared with those treated with aspirin.
Limited data exist on the use of dual antiplatelet therapy
(DAPT) in patients with PAD. A subgroup analysis of 3096
patients with PAD in the Clopidogrel for High
Atherothrombotic Risk and Ischemic Stabilization, Management
and Avoidance (CHARISMA) trial demonstrated a reduction in
the rate of MI among patients treated with DAPT compared
with aspirin alone.25 Recent observational data suggest that
patients with PAD undergoing endovascular therapy may also
benefit from prolonged DAPT. In a study of 629 patients with
claudication or CLI undergoing diagnostic or interventional
lower extremity angiography, DAPT was associated with a reduc-
tion in major adverse cardiovascular events (MACE) and overall
mortality.26
Foley TR, et al. Heart 2016;102:1436–1441. doi:10.1136/heartjnl-2015-309076
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Vorapaxar is a novel antiplatelet agent that inhibits thrombin-
mediated platelet aggregation by blocking the protease activated
receptor 1. The use of the vorapaxar in addition to aspirin
among patients with PAD has been shown to reduce rates of
ALI and peripheral artery revascularisation in this population,
with an attendant risk of bleeding.27 Recent work suggests that
these findings are equally valid for those undergoing endovascu-
lar or surgical revascularisation.28 It is important to note that
this drug is contraindicated in patients with prior stroke or tran-
sient ischaemic attack, due to an increased risk of intracranial
haemorrhage.29
The optimal antithrombotic strategy in patients with PAD is
an area of active investigation. The Examining Use of Ticagrelor
in PAD (EUCLID) trial is an ongoing study comparing ticagrelor
with clopidogrel in 13 500 patients with symptomatic PAD,
with results expected in 2017.30 The use of rivaroxaban in this
population is also being investigated in the Efficacy and Safety
of Rivaroxaban in Reducing the Risk of Major Thrombotic
Vascular Events in Subjects with Peripheral Artery Disease
Undergoing Peripheral Revascularization Procedures of the
Lower Extremities (VOYAGER-PAD) study, with an anticipated
completion date of 2019.31
Statins
3-Hydroxy-3-methyl-glutaryl-coenzyme A reductase inhibitors,
or statins, improve endothelial function and reduce cardiovascu-
lar morbidity and mortality in patients with PAD.32 Lipid lower-
ing therapy in this population has been associated with
improved walking distance and retardation or regression of ath-
erosclerosis.33 The Heart Protection Study demonstrated a sig-
nificant reduction in the rate of major vascular events (MI, CVA,
revascularisation) in patients with symptomatic PAD treated
with simvastatin compared with placebo.32 Similarly, a recent
observational study demonstrated lower rates of limb amputa-
tion, mortality and major adverse cardiovascular and cerebrovas-
cular events in patients with CLI receiving statin therapy.34
These findings were concordant with a previous study evaluat-
ing patients with CLI undergoing lower extremity bypass graft-
ing, again demonstrating improved 1 year survival among
patients taking statins.35 This evidence provides the background
for current consensus guidelines, which support the use of high-
intensity statin therapy, such as atorvastatin 40–80 mg or rosu-
vastation 20–40 mg, in all patients with PAD.11 17
ACE inhibitors
Hypertension is an established risk factor for PAD and current
guidelines recommend antihypertensive therapy to achieve a
goal blood pressure of <140/90 in non-diabetic and <130/80
in diabetic patients with PAD.11 Recent randomised trials have
suggested that even more aggressive targets (<120/80) may be
appropriate in patients with increased risk of heart disease,
including those with PAD.36 In addition to lowering blood pres-
sure, inhibition of the renin-angiotensin system has been asso-
ciated with lower rates of MI, stroke and death in patients at
high risk for these atherothrombotic complications.37 In particu-
lar, ramipril has been shown to retard atherosclerotic progres-
sion in the carotid arteries and to reduce a composite endpoint
of MI, stroke or cardiovascular death in patients with vascular
disease.38 Further, the use of an ACE inhibitor or angiotensin
receptor blocker in patients with CLI has been associated with
significant reductions in MACE and mortality.39 Based on this,
current consensus guidelines include a IIa recommendation sup-
porting the use of ACE inhibitors in patients with symptomatic
PAD regardless of blood pressure.11
Foley TR, et al. Heart 2016;102:1436–1441. doi:10.1136/heartjnl-2015-309076
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Cilostazol
Cilostazol is a phosphodiesterase 3A inhibitor that promotes
vasodilation and inhibits platelet aggregation through the gener-
ation of cyclic adenosine monophosphate. In prospective, ran-
domised trials and meta-analyses of patients with IC, cilostazol
has been shown to improve maximum walking distance and
pain-free walking distance by as much as 50% and 67%,
respectively.40 Furthermore, limited data suggest that cilostazol
may be effective in reducing restenosis and target lesion revascu-
larisation in patients undergoing endovascular therapy for
PAD.41 Because of the deleterious effect of other phospho-
diesterase inhibitors (eg, vesnarinone and milrinone) on long-
term mortality in patients with heart failure and reduced ejec-
tion fraction, cilostazol is contraindicated in this population.
Current consensus guidelines support the use of cilostazol in
patients with IC who do not have heart failure.11 17
Revascularisation
Revascularisation should be considered in patients with lifestyle-
limiting claudication despite exercise therapy and optimal
medical therapy (OMT) as well as in those with CLI. Current
professional society guidelines recommend an endovascular-first
strategy in most clinical situations.11 Surgical revascularisation
may be preferable in patients with arterial anatomy that is not
well suited to a percutaneous approach.
Aortoiliac disease
Patients with PAD affecting the distal aorta and iliac arteries
often present with buttock or thigh claudication. Diminished
femoral pulses and a pressure decrement between the brachial
artery and high thigh on physiological testing supports the pres-
ence of aortoiliac disease. The Physician Initiated Multicentre
Belgian-Italian trial investigating Abbott Vascular iliac stents in
the treatment of TASC A, B, C and D iliac lesions
(BRAVISSIMO) study demonstrated excellent 24 month patency
rates in patients with aortoiliac disease treated with endovascu-
lar therapy regardless of anatomical complexity, as represented
by Trans-Atlantic Inter-Society Consensus Document on
Management of Peripheral Arterial Disease (TASC) designa-
tion.42 Furthermore, the combination of stent revascularisation
and optimal medical care (OMC) has been shown to increase
peak walking time and patient reported physical functioning sig-
nificantly more than OMC alone in patients with aortoiliac
disease.16 In light of such evidence, current European Society of
Cardiology (ESC) and American College of Cardiology (ACC)/
American Heart Association (AHA) guidelines for PAD recom-
mend an endovascular-first strategy for aortoiliac revascularisa-
tion in most cases.11 17 For patients with low operative risk and
complex aortoiliac disease characterised by multiple unilateral
stenosis, bilateral external iliac artery occlusions or unilateral
occlusions involving the common and external iliac arteries (eg,
TASC D), surgical revascularisation with aortoiliac, aortofe-
moral or femoral–femoral bypass should be considered.
Common femoral artery disease
Surgical endarterectomy is considered the gold standard for
common femoral artery (CFA) disease, with a reported technical
success rate approaching 100% and a 1-year primary patency
rate of 93% that persists for up to 5 years.43 However, a recent
study of patients undergoing CFA endarterectomy demonstrated
30-day mortality and wound complication rates of 3.4% and
8%, respectively.44 Endovascular approaches to CFA revasculari-
sation offer a minimally invasive alternative in patients who are
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not candidates for surgical endarterectomy. A retrospective ana-
lysis of 321 patients with CFA lesions (≥70%) who underwent
primary balloon angioplasty with bailout stenting demonstrated
a 92.8% primary success rate with relatively low target lesion
revascularisation rates at 1 year.45 These data suggest that endo-
vascular therapy of CFA disease may be technically feasible.
However, large multicentre studies comparing endovascular and
surgical approaches for this condition are not yet available.
With this in mind, the 2007 TASC II guidelines support CFA
endarterectomy in CFA disease requiring revascularisation.8 In
patients who are not surgical candidates, an endovascular
approach could be considered.
Femoral-popliteal disease
The ACC/AHA and ESC guidelines currently recommend an
endovascular-first approach to revascularisation of most lesions
in the superficial femoral artery (SFA) and popliteal artery, while
an endovascular strategy can also be considered for more ana-
tomically complex (eg, TASC D) lesions.11 17 Both guidelines
support the use of angioplasty for femoral-popliteal disease, but
are in conflict with regard to primary stent placement. The
results of clinical trials suggest that in intermediate to long
lesions (>70 mm), primary stenting is associated with improved
patency.46 However, ACC/AHA include a class III recommenda-
tion against the use of primary stenting, while the ESC guide-
lines suggest that stenting is reasonable first-line therapy for
intermediate length lesions.11 17
Recently, data have emerged demonstrating improved clinical
outcomes and primary patency in patients with SFA disease
treated with drug eluting stents (DES) compared with bare
metal stents (BMS). The use of DES was associated with
improved clinical outcomes including freedom from claudica-
tion and tissue loss.47 In some cases, however, mechanical forces
within the lower extremity vasculature increase the likelihood of
stent fracture and restenosis. This is particularly prominent in
areas of flexion, including the popliteal artery. With this in
mind, the direct delivery of paclitaxel to the arterial wall with
drug coated balloons (DCB) allows for effective endovascular
therapy without a permanent implant. Recent trials have shown
lower rates of target lesion revascularization (TLR) and resten-
osis in femoral-popliteal lesions treated with DCB angioplasty
compared with percutaneous transluminal angioplasty (PTA)
alone.48
Infrapopliteal disease
Infrapopliteal disease refers to PAD affecting the distal popliteal
artery, encompassing the tibioperoneal trunk, posterior tibial,
peroneal and anterior tibial arteries. The bypass versus angio-
plasty in severe ischemia of the leg trial found no difference in
amputation-free survival between angioplasty and surgical
bypass in patients with CLI and infrainguinal disease.49
Subsequent posthoc analysis suggested, however, that overall
survival among those living 2 years after the index procedure
may be improved with a surgical approach.50 For those that
receive endovascular therapy, recent trials have demonstrated
improved 12-month patency with DES of the infrapopliteal
arteries compared with BMS or PTA alone in patients with
severe claudication or CLI.51 In contrast, the use of DCBs in the
infrapopliteal arteries has not been associated with superior clin-
ical outcomes when compared with PTA, with one trial showing
a trend towards increased major amputation in patients with
CLI treated with DCB angioplasty.52
Endovascular and surgical approaches to revascularisation of
the infrapopliteal arteries in patients with CLI are being
1440
compared in the ongoing the best endovascular versus best sur-
gical therapy in patients with CLI study.53 The primary outcome
is rate of major adverse limb events or death and study comple-
tion is expected in 2018.
Current ACC/AHA and ESC guidelines support an endovas-
cular approach to revascularisation in patients with infrapopli-
teal disease and CLI.11 17 Both guidelines recommend initial
therapy with PTA and bailout stenting with BMS if necessary.
The guidelines may be updated to reflect contemporary data
demonstrating improved outcomes in patients with infrapopli-
teal disease treated with DES in the future.
Novel therapies
Stem cells and angiogenic growth factors are effective in stimu-
lating angiogenesis in animal models and represent a potential
mechanism for restoring perfusion to ischaemic tissue in
patients with PAD. To date, randomised controlled trials have
failed to show consistent clinical benefit in IC and CLI despite
promising findings in preclinical studies.54 The applications of
stem cell therapy and angiogenesis in PAD remain active areas
of clinical investigation.
CONCLUSIONS
PAD affects more than 200 million people worldwide and has
increased in prevalence by 23.5% between 2000 and 2010.2
This trend is expected to continue as life expectancy increases
around the world and exposure to cardiovascular risk factors
persists. In addition to functional impairment and decreased
quality of life, patients with PAD suffer high rates of cardiovas-
cular morbidity and mortality. Raising awareness about the
appropriate diagnosis and management of PAD is a pressing
issue, as many of these patients are undiagnosed or under-
treated. In addition to smoking cessation and regular exercise,
treatment plans should include medical therapy aimed at redu-
cing systemic cardiovascular risk. In patients with lifestyle-
limiting claudication or CLI, endovascular or surgical revascular-
isation is indicated to alleviate symptoms and preserve limb
integrity.
Twitter Follow T Foley at @TRFoley4
Contributors All authors have made substantial contributions to the conception of
the work, drafting or revision of the manuscript for intellectual content and approval
of the final version being submitted.
Competing interests EJA is a consultant/advisory board member to Abbott
Vascular, Medtronic, Merck and Spectranetics.
Provenance and peer review Commissioned; externally peer reviewed.
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 Downloaded from http://heart.bmj.com/ on September 11, 2016 - Published by group.bmj.com

Contemporary evaluation and management of

lower extremity peripheral artery disease
T Raymond Foley, Ehrin J Armstrong and Stephen W Waldo

Heart 2016 102: 1436-1441 originally published online June 1, 2016

doi: 10.1136/heartjnl-2015-309076

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