Peripheral Arterial Disease
Mounir J. Haurani MD
Division of Vascular Diseases and Surgery
Department of Surgery
The Ohio State University Medical Center
Disclosures
 Research Agreements with Bolton Medical and Grifols
Pharmaceuticals, payments made to OSU
Objectives
Relate the
pathophysiology of
atherosclerosis
Peripheral Vascular
Disease
Aortic
Carotid Artery
Surgical management
associated with the
sequelae
Atherosclerosis
 Most common cause of peripheral arterial occlusive
disease
 Preferentially involves the internal carotid, infrarenal
aorta, and superficial femoral arteries
 Typically occurs at bifurcations
Pathology
 Lipid Hypothesis
 Response-to-Injury Hypothesis
 Monoclonal Hypothesis
Lipid Hypothesis
 Cholesterol first isolated from gallstones in 1784
 Nikolai Anitschkow produced vascular lesions in
rabbits by feeding them purified cholesterol
Lipid Hypothesis
 Earliest lesions consisted of foam cells that were Sudan
positive and contained birefringent crystals
 Distinctive pattern consisting of location of the lesions
near arterial branch points
Lipid Hypothesis
 Epidemiologic evidence (Framingham Heart Study)

association between cholesterol and incident CHD.
 Trials demonstrated that reducing cholesterol reduces
cardiovascular events
Response To Injury
 Basis lies in the similarities between atherosclerosis and
the response of arteries to experimental injury.
 Injury to the endothelium is a seminal event
 Stimulating the cascade of events leading to lesion
formation.
Response To Injury
 Adhesion of platelets and an influx of LDL
 Platelets stimulate migration of SMCs into the intima
 Neointima responsible for narrowing of the arterial
lumen.
Experimental Model of Response to Injury Hypothesis
Copyright © American Heart Association, Inc. All rights reserved.
Jacobson G M et al. Circulation Research. 2003;92:637-643
Monoclonal Hypothesis
 Each lesion of atherosclerosis is derived from a single
SMC
 Atherosclerotic plaque from four females and compared
them with adjacent normal areas of arterial wall.
 SMCs from the plaque contained only one G6PD isoform
whereas adjacent control areas contained a mixture of
isoforms.
Progression of Atherosclerosis
Rutherford’s Vascular Surgery 7th Edition, Chapter 4 Atherosclerosis
Plaque Complications
 Necrotic core of lipid, macrophages, and smooth
muscle cells
 Calcification
 Endothelial disruption
 Ulceration
 Hemorrhage
 Embolism
Pathophysiology
 Atherosclerosis may cause symptoms via:


stenosis or occlusion
thromboembolism



cardiogenic
arterioarterial
thrombosis of complicated plaque
 Inadequate tissue perfusion
Infrainguinal Arterial Occlusive Disease
 Affects 17% of people over 70
Asymptomatic
Claudication
Rest Pain /
Tissue Loss
Rutherford’s Vascular Surgery 7th Edition, Chapter 4 Atherosclerosis
Claudication
 Pain in the large muscle groups distal to an
arterial lesion after exercise
 Cramping, heaviness, fatigue
 Occurs consistently after a certain distance of
walking
 Reliably abates when patient stops
 The patient is asymptomatic at rest because
there are adequate collaterals for perfusion
without increased metabolic demand
Claudication
CAD
5 Yr
Mortality
• 90%
• 5%
amputation
• 23% MI
• 13%
Stroke
• 5 yr = 20%
• 10 yr
=50%
• 15yr =
70%
Treatment of Claudication
 Risk factor modification




smoking cessation
hypertension
hyperlipidemia
diabetes
 Cilostazol



rheologic agent
increases walking distance
contraindicated in CHF
 Supervised exercise program


30 minutes of cardiovascular exercise daily
5 days per week
Treatment of Claudication
 Procedural intervention for claudication is reserved for
patients with lifestyle-limiting claudication and failure of
medical therapy
 Often, this is related to single level, proximal disease



aortoiliac
femoral
ABI 0.6
Critical Limb Ischemia
 Ischemic rest pain

intense pain across distal foot and arch

burning, stabbing, constant

worsened with elevation

dependent rubor
 Ulceration
 Gangrene

dry

wet
Outcomes of CLI
Treatment of Rest Pain or Tissue Loss




Risk factor modification
Restoration of in-line vascular flow
Management of the wound
Often, this is related to multi level or distal disease



popliteal
tibial
ABI 0.3
Ankle Brachial Index
• Claudication
• Rest pain
• Tissue loss
0.6
0.3
0.2
Aboyans V et al. Circulation. 2012;126:2890-2909
Copyright © American Heart Association, Inc. All rights reserved.
Percutaneous Treatment Results Are
Better…




Proximal vessels (aorta > iliacs > SFA > tibials)
Short lesions
Focal lesions
Stenoses > occlusions
Percutaneous Treatments Are
Worse…





Distal or smaller vessels
Long lesions
Diffuse lesions
Occlusions
At joints or bifurcations



common femoral
profunda
popliteal
Surgical Options
 Endarterectomy
 Bypass


normal inflow
normal outflow
Levels of Disease
 Aortoiliac



aortoiliac endarterectomy
aortofemoral bypass
axillary femoral bypass
 Femoropopliteal


femoral endarterectomy
femoropopliteal bypass
 Tibial


femorotibial bypass
popliteal tibial or pedal bypass
Aortobifemoral
Bypass
In-situ Thrombosis
 Thrombosis of a chronically diseased vessel
Rutherford’s Vascular Surgery 7th Edition, Chapter 4 Atherosclerosis
Acute Limb Ischemia
Pain
Pallor
Paresthesia
Paralysis
Pulseless
Poikilothermia
Aneurysm
AAA Demographics
 200,000 patients diagnosed with non-ruptured AAA each
year
 1.5 to 2 million are estimated to have an undiagnosed
AAA
 50% of patients with untreated aneurysms > 5.5 cm will
die of rupture within five years
 15,000 deaths each year
Risk of Rupture
 Mortality = 35 - 75%


unchanged over past
4 decades
higher with COPD,
multiple comorbidities
J Vasc Surg 2003; 37: 1106-17
Diameter
Annual Risk
of Rupture
< 4 cm
0%
4 - 5 cm
0.5 - 5 %
5 - 6 cm
3 - 15 %
6 - 7 cm
10 - 20 %
7 - 8 cm
20 - 40 %
> 8 cm
30 - 50 %
Rupture
 Approximately 40% of patients with ruptured AAAs die
prior to presentation to the emergency department
 Only 10% to 25% of individuals with ruptured AAA
survive until hospital discharge
 Prevent rupture!
Treatment Options
 Watch and wait



AAA < 5cm, asymptomatic
surgical risks > risk of rupture
lifestyle changes cannot reduce the size of the AAA
 Open surgical repair
 Endovascular repair
Open Versus Endovascular Repair
 No difference in overall mortality
 Advantage in aneurysm related mortality for EVAR
 Increased complication and reintervention rate for EVAR
Stroke
 600,000 strokes per year in U.S.
 150,000 death from stroke per year
 3rd leading cause of death
Stroke
 Thromboembolic (85%)



cardiac embolization
extracranial carotid embolization
intracranial atherosclerosis
 Hemorrhagic (15%)
Symptoms
 Amaurosis

Hollenhorst plaques (cholesterol emboli)
 TIA



abrupt onset
usually lasts 15 minutes or less but up to 24 hours is included in
definition
up to 15% risk of stroke within 3 days
 Stroke

> 24 hours
Symptoms
 Motor or sensory deficit contralateral to affected carotid
artery
 Amaurosis ipsilateral to affected carotid artery
Treatment
 Warfarin – stroke from cardiac embolization
 Aspirin – indicated for all patients with atherosclerotic
disease
 There is no evidence supporting the use of Plavix or
heparin / warfarin to prevent or treat stroke related to
extracranial carotid disease
Carotid Revascularization
 Symptomatic (NASCET)


> 50% stenosis
reduces two year stroke risk from 26% to 9%
 Asymptomatic (ACAS)


>60% stenosis
reduces five year stroke risk from 11% to 6%
Endarterectomy
 Appropriate for most patients
 Lower periprocedural stroke risk
 Higher risk for cardiac complications
What do you
see?
Stenting
 Higher periprocedural stroke risk
 Lower cardiac morbidity
 Consider in:













NYHA III or IV CHF
EF < 30%
unstable angina
recent MI
contralateral occlusion
recurrent stenosis
radiation
COPD
anatomically inaccesible lesion
cervical immobility
prior neck dissection
tracheostomy
contralateral cranial nerve injury
What do you see
Summary
 Atherosclerosis involves many vascular beds
concurrently
 It can present with a spectrum of symptoms
 Treatment is reduction of risk factors with procedural
intervention reserved for failure of medical management
 Several acute manifestations can arise that require
emergent treatment
Thank you
Thank you for completing this module.
If you have any questions or feedback, please contact me:
Mounir.Haurani@osumc.edu
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