Download - Peripheral Arterial Disease (PAD)
Peripheral Arterial Disease(PAD)
Peripheral Arterial Disease(PAD)
M. Saifur Rohman, dr SpJP. PhD. FICADept of Cardiology and Vascular Medicine
Faculty of Medicine, Brawijaya University
M. Saifur Rohman, dr SpJP. PhD. FICADept of Cardiology and Vascular Medicine
Faculty of Medicine, Brawijaya University
OverviewOverview
PAD (peripheral arterial disease) – a marker for MI and ISEpidemiological data on PAD
Risk factors Prevalence Atherothrombosis – coexistence of PAD, coronary and
cerebrovascular disease Natural history Low ABPI as an independent predictor of ischaemic risk
Symptomatology of PAD Diagnosis and management of PADClopidogrel – a new standard of treatment for atherothrombosis
PAD – a marker for MI and IS
Cerebrovascular disease(ischaemic stroke, transient ischaemic attack)
Coronary artery disease(stable/unstable angina, myocardial infarction)
PAD (intermittent claudication, critical leg ischaemia, amputation, gangrene, necrosis)
Atherothrombosis = thrombus formation on top of existing atherosclerosis
Occurs in multiple arterial beds
Risk factors for PADRisk factors for PAD
Murabito JM et al. Circulation 1997;96:44–49; Laurila A et al. Arterioscler Throm Vasc Biol 1997;17:2910–2913;Malinow MR et al. Circulation 1989;79:1180–1188; Brigden ML. Postgrad Med 1997;101:249–262.
Gender (male) Age Smoking Hypertension Diabetes Hyperlipidaemia Fibrinogen Homocysteinaemia
PAD
Ischaemicstroke
Myocardialinfarction
Atherosclerosis Atherothrombosis
PAD
Atherogenesis
Progression of Plaque toward ruptureProgression of Plaque toward rupture
Prevalence of PAD – variation according to diagnostic criterionPrevalence of PAD – variation according to diagnostic criterion
6.3 million individuals with symptomatic, established PAD are diagnosed in the USA and EU1
Epidemiological studies imply that real* prevalence may be approx. 20 million (= 9.5% of the population > 50 years old)
In 613 men and women (mean age 66 years), real prevalencewas found to be underestimated by two- to seven-fold2
ABPI (ankle:brachial pressure index) correlates with angiographically determined disease3
ABPI < 0.9 is a marker of diffuse atherothrombosis4
1 17 Western European countries. Statistical Supplement; WHO Yearbooks, Annual Statistics, 1997;2 Criqui MH et al. Vasc Med 1997;2:221–226; 3Shinozaki T et al. J Clin Epidemiol 1998;15:1263–1269; 4Kornitzer M et al. Angiology 1995;46:211–219.*ABPI < 0.9, symptomatic or not, diagnosed or not.
Epidemiology of PAD – effect of age and genderEpidemiology of PAD – effect of age and gender
Epidemiological data on PAD vary according to:Population studiedMethod of diagnosing PAD
Incidence and prevalence of intermittent claudication* increase with age
Prevalence in men aged 45–50 years is 1% Prevalence is 3–3.5% in men aged > 50 yearsSimilar trend in women, increase with age
More common in men than in womenTwice as many men as women aged > 50 years have intermittent
claudication (3.5% and 2%, respectively)
Predominance in males disappears after age of 70Weitz JI et al. Circulation 1996;94:3026–3049. * Rose questionnaire criteria Bull. Wld Hlth Org. 1962;27:645-658
Atherothrombosis – coexistence of symptomatic PAD and coronary or cerebrovascular diseaseAtherothrombosis – coexistence of symptomatic PAD and coronary or cerebrovascular disease
Per
cen
tag
e o
f g
rou
p
Concurrentcardiovascular disease(MI, CABG, stroke orstroke surgery)
PADNo
0
10
20
30
40
50
Men Women
Yes YesNo
Criqui MH et al. Vasc Med 1997;2:221–226.
Atherothrombosis – symptomatic atherosclerosisin CAPRIE (overlap between PAD, CAD and CVD)Atherothrombosis – symptomatic atherosclerosisin CAPRIE (overlap between PAD, CAD and CVD)
1CAPRIE Steering Committee. Lancet 1996;348:1329–1339.
CAPRIE1 (n = 19 185)
Cerebrovascular disease (CVD)
Peripheral Arterial Disease (PAD)
Coronary artery disease (CAD)
24.6% 29.9%
19.2%
3.3%3.8%
7.3%
11.9%
5-year natural history of PAD5-year natural history of PAD
100 patients with asymptomatic PAD
100 patientswith claudication who do notseek medical advice
Local Events 100 patients diagnosed
with claudicationSystemic Events
• CHD 15• Other cardiovascular
and cerebrovascular 5• Non-cardiovascular 10
PLUS
Major amputation 2 patients
10 to 20 non-fatal MIs or strokes
Dormandy JA. Hosp Update 1991;April:314–318.
30 deaths:Surgical revascularization
10 patients
Worsening claudication25 patients
PAD mortality – 10-year survival rates of subjects in the San Diego Artery StudyPAD mortality – 10-year survival rates of subjects in the San Diego Artery Study
Criqui MH et al. N Engl J Med 1992;326:381–386.
Time (years)0 2 4 6 8 10 12
0.00
0.25
0.50
0.75
1.00
Surv
ival
Severe symptomatic
Symptomatic
Asymptomatic
Normal
Intermittent claudication – an independent risk factor for increased mortality ratesIntermittent claudication – an independent risk factor for increased mortality rates
Smith GD et al. Circulation 1990;82:1925–1931.
In the Whitehall study (n = 18 388), mortality rates in individuals with intermittent claudication were twiceas high as those in healthy controls (17 years’ follow-up study)
Increased mortality even after adjustment for coronary risk factors
Cardiac ischaemia at baseline Systolic blood pressure Plasma cholesterol concentration Smoking behaviour Employment grade Degree of glucose intolerance
Low ABPI is a strong predictor ofcardiovascular mortalityLow ABPI is a strong predictor ofcardiovascular mortality
Reduced ABPI is a significant independent predictor of cardiovascular and coronary mortality
Age-adjusted relative risks for 10-year cardiovascular and coronary mortality are higher in those with ABPI < 0.9
The risk of cardiovascular death increases with decreasing ABPI
ABPI measurement is underutilized and can be usefully incorporated in risk assessment and screening programmes
ABPI measurements are inexpensive, simple and non-invasive
Kornitzer M et al. Angiology 1995;46:211–219. McKenna M et al. Atherosclerosis 1991;87:119–128.
Dormandy JA et al. J Cardiovasc Surg 1989;30:50–57.
ABPI – inverse relationship with 5-year risk of cardiovascular events and deathABPI – inverse relationship with 5-year risk of cardiovascular events and death
Dormandy JA, Creager MA. Cerebrovasc Dis 1999;9(Suppl 1):1–128 (Abstr 4).
10.2% relative risk increaseper 0.1 decrease in ABPI
(p = 0.041)
1.00.80.60.40.20.0
1.0
1.5
2.0
2.5
ABPI
Ris
k re
lativ
e to
AB
PI
Symptomatology of PAD Symptomatology of PAD
Intermittent claudication Exercise-induced ischaemic calf-muscle pain while walking
and/or weakness, relieved by rest
Mortality rate from stroke and MI two to three times greaterthan in age-matched controls1
Prognosis varies with multiple risk factors and/or severityof disease
Critical limb ischaemia Pain at rest, eventually resulting in gangrene and amputation2
1Dormandy JA et al. J Cardiovasc Surg 1989;30:50–57.2European Working Group on Critical Leg Ischemia. Circulation 1991;84(Suppl IV):IV1–IV26.
Diagnosis of PAD Diagnosis of PAD
Evaluation of pulses and auscultation of bruits
Ankle:arm blood pressure index (ABPI) Ratio of ankle:brachial systolic blood pressure Simple, non-invasive, suitable for routine screening
Exercise testing Pain-free and maximal walking distance Size and duration of drop in ankle systolic BP upon
claudication
Weitz JI et al. Circulation 1996;94:3026–3049.
Progression of Plaque toward rupture
Thrombus forms and extends into the lumen
Adventitia
Lipid core
Thrombus
Weissberg, 1999
Thrombus formation Acute Limb IschemiaThrombus formation Acute Limb Ischemia
Definition of Acute Limb IschemiaDefinition of Acute Limb Ischemia
SuddenSudden decrease of arterial limb perfusion causing threat to limb
viability
Etiology of acute limb ischemiaEtiology of acute limb ischemia
Acute arterial embolism:
Acute traumatic ischemia:
Of a relatively Of a relatively health arterial health arterial treetree
Acute arterial thrombosis: Of a previously Of a previously diseased arterial diseased arterial treetree
PathophysiologyPathophysiologyAcute Embolic Ischemia
Acute Thrombotic
Ischemia
An embolus suddenly
occludes a relatively healthy
arterial tree
AtherosclerosiAtherosclerosiss causes
progressive narrowing of the arterial
treeStimulates
development of collaterals
Sluggish flow & rough
surface will favor acute thrombosis
It usually arrest at arterial
bifurcation
Aortic bifurcation
Iliac bifurcation
Femoral bifurcation
Popliteal trifurcation
An embolus can originate from the heart (MS with atrial fibrillation, MI with mural
thrombus) or dilated diseased arteries (aortic aneurism)
It is important to differentiate between embolic & thrombotic ischemia: It is important to differentiate between embolic & thrombotic ischemia:
Because the Because the management is management is
differentdifferent
Clinical Features Suggestive of acute EmbolismEmbolism::
Sudden onset of symptomsSudden onset of symptoms
Known embolic sourceKnown embolic source
Absence of previous claudicationAbsence of previous claudication
Normal pulse in the other limbNormal pulse in the other limb
The severity of acute ischemia depends on:The severity of acute ischemia depends on:
a)a) Capability of existing collaterals to carry blood around the acute obstruction (collaterals are more developed in
patients with preexisting chronic ischemia) Accordingly, arterial embolism is more likely to produce sudden symptoms & severe ischemia then arterial thrombosis
b) b) The location of obstruction in relation to the number of axial arteries
Aorta & common iliac One axial a. with limited collateral pathways
Internal & external iliac Two axial aa. With better collateral potentials
Two axial aa. With better collateral potentialsSuperficial & deep femoral
Popliteal artery One axial a. with limited collateral pathways
Three axial aa. with better collateral potentialsTibial arteries
c)c) The extent of obstructionThe larger the obstruction, the more collaterals are lostd)d) The duration
Flow distal to the obstruction is sluggish. If collaterals cannot increase the flow above a critical point, a stagnation clot will develop in the distal arterial tee. This the reason why heparin should be given as early as possible
For Example:
Popliteal a occlusion (a single axial a.) results in severe ischemia, while posterior tibial occlusion may be asymptomatic if other leg arteries are patent
Clinical Evaluation of Acute Ischemia (Clinical Picture)Clinical Evaluation of Acute Ischemia (Clinical Picture)
Symptoms of acute ischemia:Symptoms of acute ischemia:
Pain: Diffuse foot & leg severe aching pain of acute onset (more acute in embolic ischemia)
Pain may diminish in intensity by time if collaterals open improving circulation, or if ischemia progresses causing ischemic sensory loss
Coldness is an early symptom
Numbness followed by sensory loss (late)
Muscle weakness (heavy limb) followed by paralysis (late)
Clinical Evaluation of Acute Ischemia Clinical Evaluation of Acute Ischemia (Clinical Picture)(Clinical Picture)
Signs of acute ischemia
5P5PsPain: symptom
++
Pulseless
Pale
Parathesia
Paralysis
InspectionInspection
COLOR:
EarlyEarly: pale
LaterLater: cyanosed mottling fixed mottling & cyanosis
Pallor
Reversible mottling
An area of fixed
cyanosis surrounded
by reversible mottling
Empty veins: compare the Rt. (ischemic) & Lt. (normal)
Fixed mottling & cyanosis
Clinical Evaluation of Acute Ischemia (Clinical Picture)
Signs of acute ischemia
5P5PsPainPain: : symptomsymptom
++
PulselessPulseless
PalePale
ParathesiaParathesia
ParalysisParalysis
PalpationPalpation
Loss of sensory function
Numbness will progress to anesthesia
Progress of Sensory loss
Light touch
Vibration sense
Proprioreception
Deep pain
Pressure sense
LateLate
Clinical Evaluation of Acute Ischemia (Clinical Picture)
Signs of acute ischemia
5P5PsPainPain: : symptomsymptom
++
PulselessPulseless
PalePale
ParathesiaParathesia
ParalysisParalysis
PalpationPalpation
Loss of motor function:Loss of motor function:
Indicates advancedadvanced limb threatening ischemia
Late irreversible ischemia: Muscle turgidity
Intrinsic foot muscles are affected first, followed by the leg muscles
Detecting early muscle weakness is difficult because toes movements are produced mainly by leg muscles
Classes of Acute IschemiaClasses of Acute Ischemia
Clinical FindingsClinical Findings DopplerDoppler PrognosisPrognosis
ClassClass Sensory Sensory lossloss
Motor Motor weaknessweakness
Arterial Arterial signalssignals
Venous Venous SignalsSignals
I.I. ViableViable -ve-ve -ve-ve audibleaudible audibleaudible Not immediately Not immediately threatenedthreatened
II.aII.a Marginal Marginal threatthreat
Minimal Minimal sensory losssensory loss
No muscle No muscle weaknessweakness
Often not Often not audibleaudible
audibleaudible Salvageable if prompt ttt Salvageable if prompt ttt (there is time for (there is time for
angiography)angiography)
II.bII.b Immediate Immediate threatthreat
Rest pain w Rest pain w sensory loss sensory loss more than toesmore than toes
Mild to Mild to moderatemoderate
Usually Usually not audiblenot audible
audibleaudible Salvageable with Salvageable with immediate ttt immediate ttt (no time for (no time for
angiography)angiography)
III.III.IrreversibleIrreversible Severe Severe anesthesiaanesthesia
Paralysis Paralysis w w muscle rigormuscle rigor
InaudibleInaudible InaudibleInaudible Not salvageable, Not salvageable, permanent N. & muscle damage ,permanent N. & muscle damage ,
needs amputationneeds amputation
Summary Summary
PAD is a marker of atherosclerosis in the coronary and cerebral arteries
PAD is often underestimated and underdiagnosed, and requires proper diagnosis:
Risk factors need to be managed: smoking cessation, regular exercise training
Atherogenesis=CAD
Plaque rupture=Limb Ischemix