VASCULAR DISEASE

Vascular Disease
Arteries
Veins
Microcirculation
Lymphatic
Lanser P, Integrated Approach of
cardiovaskular medicine, Diagnsotic of
vaskular disease,principle and technology,
Springer-Verlag Berlin heiderberg 1997,pp
345-346
PAD - ATHEROSCLEROTIC
 What is Peripheral Arterial
Disease?

Arteries to lower
extremities become
stenosed or
occluded usually by
atherosclerosis

Mainly in large and

medium calibre arteries

Most commonly at
bifurcations
ATHEROSCLEROSIS
 Locations of PAD Lesions

The primary sites 20% of cases

are proximal
for atheromatous aortoiliac
lesions

lesions in PAOD
60% of cases
are superficial
femoral lesions

20% of cases
are distal
lesions of the
arteries of the
leg or foot,
rarely isolated
(frequently
upstream
iliofemoral
lesions)
 Who is at Risk from PAD?
Pathological conditions
Hypertension +++
Major risk factor at cerebral level

Dyslipidemia +++
Major risk factor at coronary level

Diabetes mellitus ++
Major risk factor for arteries of the
legs

Obesity +

Blood hyperviscosity,
 Who is at Risk from PAD?
Lifestyle
Smoking +++
Major risk factor for atherosclerosis
of the leg and coronary arteries

Unbalanced diet (fats)

Sedentary lifestyle

Stress?
 Who is at Risk from PAD?
Non-modifiable factors

Age +++

Male sex ++

Genetic factors
 Peripheral Arterial
Disease
Fontaine Classification:

Stage I Asymptomatic:
atherosclerosis developing

Stage II Stable claudicants, pain on exercise, skin

discolouration.

Stage III Rest pain.

Stage IV Trophic changes: ulcers, necrosis

and gangrene.
Stage II: Intermittent Claudication
Stage III: Rest Pain
Stage IV: Serious Trophic
Disorders
CAROTID STENOSIS
EMBOLIC STROKE?
 HOW TO TREAT CAROTID
ARTERY STENOSIS?
MEDICAL THERAPYnon significant
stenosis
CAROTID ENDARTERECTOMY
(SURGICAL/CEA)gold standard
CAROTID ARTERY STENTING
(ENDOVASCULAR/PTA)equal to
CEA
AORTIC ANEURYSM
AORTIC ANEURYSM
OPERATION
AORTIC STENT GRAFT
AORTIC STENT GRAFT in NCVC HARAPAN KITA
AORTIC STENT GRAFT in NCVC HARAPAN KITA
Abdominal Aortic Aneurysm (AAA)
Post Stent Graft
RENAL ARTERY STENOSIS
Under recognized
RAS
Under diagnosed
Under treated
 RENAL ARTERY STENOSIS

10% Fibro Muscular Dysplasia (FMD)

90% Atherosclerotic RAS (ARAS)

Why so important?

Progreessive disorder

Uncontrolled Hypertension
 FIBROMUSCULAR DYSPLASIA
10% of RAS
Tends to affect women
15-50 years
Involves 2/3 distal of
renal artery
Beaded & aneurysmal
appearance
Unknown cause
 ATHEROSCLEROTIC RAS
Age,
Diabetes
CAD
PAD
Hypertension
Renal Failure
Involves :ostial &2/3
proximal of renal
artery
RAS-HYPERTENSION-RENAL FAILURE

Safian, NEJM 2001, 344:6;431-442

NATURAL HISTORY:
THE PROGRESSION
 ACUTE LIMB ISCHEMIA
Sudden decrease limbs blood flow
Threaten the limbs viability life !!
Atherosclerotic/non-atherosclerotic

any sudden decrease or worsening in limb

perfusion causing a threat to extremity
viability TASC Working Group 2000
 ALI RISK
Therapy
Limb loss
Mortality

Early Diagnosis
Prompt Therapy
Prognosis
 ETIOLOGY
Atherosclerotic Non-Atherosclerotic

Thrombosis of Arterial Trauma/Iatrogenic

atherosclerotic plaque Aortic/Arterial Dissection
Thrombosis of indwelling Arteritis With Thrombosis
bypass graft Spontaneus Thrombosis
Vascular procedures Assoc. Hypercoagulable
Cardiac embolism States
Proxymal plaque or Vasospasm with
aneurysm thrombosis
Thrombosed aneurysm Popliteal Cysts causing
thrombosis
 Classification of PAOD
Fontaine Rutherford

Stage Clinical Grade Category Clinical

I Asymptomatic 0 0 Asymptomatic
IIa Mild claudication 0 1 Mild
claudication
IIb Moderate I 2 Mod. claud.
- severe I 3 Severe claud.
claudication
III Ischaemic rest II 4 Rest Pain
pain III 5 Minor Tissue
Loss
IV Ulceration / III 6 Major Tissue
Gangrene Loss
CLINICAL MANIFESTATION

Pain
Pulselessness
5 Ps
Pallor
Paresthesia
Paralysis
 CLINICAL CATEGORIES OF ACUTE
LIMB ISCHEMIA
Category Description/ Findings Doppler Signals
Prognosis
Sensory Muscle Arterial Venous
Loss Weakness

I. VIABLE Non immediately None None Audible Audible

threaten

II. a. Salvageable if Minimal (toes) or None None Audible

T MARGINALLY promptly treated none (often)
H inaudible
R b. Salvageable with More than toes, Mild- (ussualy) Audible
E immediate assoc. rest pain moderate inaudible
IMMEDIATELY
A revascularization
T
E
N

III.IRREVERSIBLE Major tissue loss Profound, Profound, Inaudible Inaudible

or permanent anesthetic paralysis
nerve damage

TASC Working Group 2000

ANATOMIC DISTRIBUTION OF
EMBOLIC OCCLUSION
Brachial 3%
Visceral 2%
Aortic 16%
Iliac 20%
Femoral 47%
Popliteal 12%
VASCULAR DOPPLER
 MRA

LCIA
TOTALLY
OCCLUDED
 DEEP VEIN THROMBOSIS

DVT terjadi bila terbentuk trombus dalam vena

yang berjalan di kompartemen subfascia1
Tromboflebitis sebagai respon inflamasi
trombosis, pada vena superfisial1
Dewasa (80%) di ekstremitas bawah, v. femoralis
komunis, v. iliaka, atau IVC

1. Cheatle TR, Pathology of DVT. In: Strandness DE, Vascular Disease, 1994
2. AHA Medical/Scientific Statement, Management of DVT and PE, 1996
 Patogenesis

Trombus vena terdiri dari deposit intravaskuler

dari fibrin, eritrosit, platelet, dan komponen
leukosit1
Triad Virchow aktivasi faktor koagulasi, stasis
vena, dan abnormalitas dinding pembuluh
darah1,2

1. AHA Medical/Scientific Statement, Management of DVT and PE, 1996

2. Andrew M, Epidemiology of Venous Thromboembolic Events, 1999
Thrombosis:
Patogenesis
Significant Venous Anatomy of the Leg

Deep Veins
Posterior Tibial Veins
Anterior Tibial Veins
Peroneal Veins
Popliteal Veins
DVT and Pulmonary Embolism
 Risk Factor
Usia > 60 tahun
Extensive surgery
Riwayat VTE sebelumnya
Immobilisasi
Bedah ortopedi (panggul dan lutut)
Fraktur pelvis, femur, atau tibia
Bedah kanker
Sepsis postoperatif
Penyakit gagal jantung, inflammatory bowel disease,
sepsis, infark miokard

AHA Medical/Scientific Statement, Management of DVT and PE, 1996

 Treatment
Heparin (Unfractioned, LMWH)
Antiplatelet
Intervention :
 Chronic venous insufficiency

Frequency: CVI is a significant public health problem in

the United States. Of all Americans, estimates indicate
that 2-5% have some changes associated with CVI.
Approximately 24 million Americans have varicose veins.
Approximately 6 million Americans have skin changes
associated with CVI. Venous stasis ulcers affect
approximately 500,000 people.
Epidemiology: Peak incidence occurs in women aged
40-49 years and in men aged 70-79 years.

Yale D Podnos, MD, MPH et al, Chronic Venous Insufficiency, E medicine,

University of California Medical Center at Irvine, oktober 2003
Venous Anatomy

Superficial Veins
Lesser Saphenous

Greater Saphenous
Distribution of valves in veins
of the lower limb
Perforator Veins - connect
superficial & deep systems
Anterior Perforators
Lateral Perforators
Medial Perforators
account for 80-90%
of cases with incompetent
perforator veins (Linton)
 Klipper - Trenaunay
syndrome and other
Valvular factors
Insufficiency

Heredity
Venous
Wall Chronic venous
Alterati insufficiency
ons = multifactor disease

Overweigh
t
Hormonal
Leg and foot Lifestyl
factors
(pregnancy, oral problems e
hormone (i.e. platypodia,
therapy) malformations, decreased
muscular pump efficacy,
I. Lovrievi Prof. dr. sc. D.joint
DeSyo alterations)
Dr. Sc, CRONICAL VENOUS INSUFICIENCY: HYPOSTATIC ULCER ,
Departement for Vascular and Endovascular surgery Clinical Hospital Sisters of Charity, ZAGREB
Pathophysiology of Chronic Venous
Insufficiency & Venous Ulceration

Fibrin Cuff Theory

pericapillary fibrin deposits

White Cell Trapping Theory

damage due to WBC adhesion to capillaries

Hollaway GA, Ooi SK, Weingarten MS. Management of venous insufficiency and
ulceration. Number 3 in a monograph series. Curative Health Services, 2001
Pathophysiology of Chronic Venous
Insufficiency & Venous Ulceration

Lipodermatosclerosis
 Pathophysiology of Chronic
Venous Insufficiency & Venous
Ulceration

Atrophie Blanche
 PATHOLOGICAL FEATURES OF THE ULCER AND THE
PERIPHERAL TISSUE

ULCER BASE Surrounding

Highly skin
inflamed
Hyperproliferat
May ion
contain
necrotic Abnormal
tissue tissue-
degrading
Tissue- enzymes
degrading
enzymes Cellular
processes
Degradatio abnormal
n of tissue
matrix Susceptible to
damage
Degradatio
n of Require
biologicaly protection from
useful wound exudate
moleculec
e.g.growth ULCER EDGE
factors
Epidermis ready to heal
Cellular
Degradation of tissue matrix
processes
 Investigation
Random BSL
Doppler US may
assist
Plethysmography and
Venography obsolete
Duplex US gold
standard
 Compression
Bandaging (short stretch, elasticated, 4-
layered)
Graduated stocking
Sequential device
Proven benefit
Cullum et al. (2002)
Nelson et al. (2002)
Topical or systemic agents inconclusive
 Ligation and stripping

GOLDEN RULES Problems

Haematoma
Junctional incompetence on
Saphenous neuralgia
DUPLEX Recurrence
Phlebectomy when > 6mm dia. ?close fascia
Strip LSV when > 1cm dia.
Holme et al (1990)
Comparable results
neuralgia in
partial strip
 Sclerotherapy
Residual, recurrent,
incompetent perforating
veins < 6mm
Polidocanol/STS
Equal efficacy
(Goldman, 2002)
Trans-catheter US-
guided therapy for LSV
reflux (Min et al, 2000)
ANGIOGENESIS THERAPY
Angiogenesis Gene Therapy
Hepatocyte Growth Factor(HGF)
Naked Plasmid DNA HGF
IM injection at ischemic region
Naked Plasmid DNA HFD
Injection IM
Conservative Treatment of
Arterial Occlusive Disease
Sjukri Karim
Vascular Division
 Background
Peripheral Arterial Occlusive Disease (PAOD) is
caused by variety of obstructive vascular
process
80%atherosclerosis clinical manifestation
on limbs, brain and heart
Pathogenesis of PAOD : embolic occlusions,
inflamatory and immunologic angiopathies and
vasculitides
Appropriate causal treatment should be provided
as an adjunct or alternative to symptomatic
therapy
 Treatment options
Management based on : etiology, stages and
status of individual patient
2nd prevention : stage 1 and 2
Exercise trainingstage 2
Vasoactive drugs
Restoring patency : fibrinolytic, PTA, surgical
Stage 3-4 :revascularization without delay
 Overview of the management of AOD by
stages

Stage of Secondar Physical Vasoactive PGE1 PTA surgery

AOD y Therapy drugs Lysis
prevention
I + 0 0 0 0 0

IIa + + (+) ((+)) ((+)) 0

IIb (+) + + (+) (+) (+)

III ((+))-0 0 0-((+)) + + +

IV ((+))-0 0-+ 0-((+)) + + +

Acute 0 0 0 + + +
ischemia
Nonsurgical Treatment Methode
Goal : restore adequate mobility improving blood flow
and eliminating rest pain, relieving claudication, healing
trophic changes
Steps :
-risk factor control
-smoking cessation
-exercise training
-adjunctive medical therapy
-PTA if possible (might be combined w/ intra-arterial
thrombolysis)
 Specific Form therapy
Prevention atherosclerosis
Hemorrheologic therapy
 Prevention of atherosclerosis
Risk factor control :
life style modifications
lipid lowering agents
antihypertension
Antidiabetics
smoking cessation
 Local Prevention
Walking distance log : step counter,
constant walking speed
Autonomic monitoring : weight, urine color,
hemodynamic (BP, HR), blood sugar
Local self examination
 Local self examination
Where; nailfolds, tip of toes, interdigital
spaces, heel, sole of foot
When : new shoes are purchased
When : the eet are cold and wet
After prolonged walking
After pedicure
How : using a hand mirror or helper as
needed
 Exercise training and physical
therapy
Basic conservative treatment : muscular
training /exercise training
Exercise training stopped before onset of
pain/claudication
 Exercise Training
Training in groupsmore effective
Contraindicated :fontaine class 3-4, acute
ischemia, exercise induced arrythmia
Coronary involvement (40-90%)heart
failureworsening claudication
 Level of patient motivation on exercise training
Unfavourable condition Favourable condition
History >1 yr <1 yr
Initial walking distance <100-200m >100-200m
Occlusion Bilateral pelvic or Short, unilateral
multilevel occlusion
Hemodynamics
Post-stenotic doppler <60mmHg >80mmHg
pressure
VOP reactive hyperemia <8ml/100ml/min >8ml/100ml/min
Cardiopulmonary function Insufficiency normal
Hematocrit >50% <45%
Coexisting Disease Low-back syndrome, None
osteoarthritis
 Hemorrheology Therapy
Vascular contentsincrease severity of
blood flow disturbance
Increase hematocritrheologic
propertiesshorten claudication distance
Blood removal/hemodilutionincrease
exercise capacity
 Hemorrheologic Therapy
Possible ways to increase volume flow of
blood (Hagen-Poiseuille law)
p.r4
Vt =---------
8.l.
Vt : Volume flow of blood per unit time
p: pressure gradient across the vascular segment
r : vessel diameter/radius
l : length of vascular segment
: viscocity
 Augmentation of blood flow volume

Increase diameter and inflow (stroke

volume)
Inflow cannot be increase (heart failure
etc)blood volume
blood viscosity
 Hemorrheologic therapy
Bloodnon-Newtonian fluid
Reduction of flow velocity disproportionate
increase in whole blood viscosity
High hematocrit + low velocity increase
viscosity
Plasma viscosity and RBC flexibilityinfluence
whole blood viscosity
 Hemorrheologic therapy
Improvement of blood fluidity :
1. Lowering hematocrit
2. Reducing fibrinogen
3. Improving erythrocyte fluidity
 hemodilution
Hypervolemic hemodilution with colloidal
agents
Isovolumic hemodilution
 Hypervolumic hemodilution with
colloidal agents
Colloidal solutions (500ml/d) continous
iv
hematocrit (hyper-oncotic effect)
erythrocyte aggregation
. Disadvantages :
1. volume load might be dangerous for
heart failure and hypertensive pt
2. Short action (half life 3-4 hrs)
 Hypervolumic hemodilution with
colloidal agents
Dose : 500ml colloid solution iv for 2
hrs (to maintain volume expanding
effect)
Risk of oncotic injuries to renal tubules :
1. longterm therapy> 3 weeks
2. Dose>1000ml/day
3. Preexisting renal damages
 Isovolemic Dilution
Hematocrit>45%
Advanced stages : IIb, III, IV
Blood withdrawal+volume replacement
(isooncotic HAES/dextran, 4-6% albumin, re-
transfusion autolog plasma)
Avoid volume overload
 Hemodynamic effect

peripheral resistance
cardiac output
blood flow velocity
blood flow
 Isovolemic Dilution
Period 3-4 days :
500ml blood is removed
500ml autolog plasma/collidal sloution/4%-6%
albumin infused
Until Hematocrit 35%-40%
hematocrit 3%-5% for each hemodilution
Hematocrit of CAD patient should not reduced
below 38%-40%
 Fibrinogen Reduction with Low Dose Fibrinolytic
Agents

Systemic administration of fibrinolytic

agentssafer than snake venom for reducing
fibrinogen level >400-500mg%
Urokinase is preferred (no allergic reactions)
Initial dose 100.000 IU/h with concomitant
heparin administration, followed by
individualized dosing schedule
 Systemic treatment of
vasoactive drugs
controversial for many years
3 drugs approved by German Federal Health
Agency
1. Pentoxyfylline
2. Naftidrofuryl
3. Buflomedyl
Improve claudication-free walking distance
significantly (placebo controlled double blind
multicenter study)
 Vasoactive drugs
Response : IV infusion better than oral
Gain in walking distance achieved more
rapidly on IV infusion (3-4 weeks)
compare to oral (2-3 months)
>30% improvement in exercise capacity in
14 days (IV infusion) compare to 4 weeks
(oral)
 Vasoactive drugs
Effects :
1. Microcirculation (pentoxyfylline and
naftidrofuryl improve RBC flexibilityrheologic
properties/ leucocyte adhesiveness)
2. Hemodynamic (cilostazol vasodilatation and
inhibits platelet aggregation)
3. Muscle metabolism (naftidrofuryl and PGE1
reduced aerobic metabolism of muscle in
hypoperfused area)
 Vascular Center
Sjukri Karim
Vascular Division
Dept. of Cardiology and Vascular Medicine
 How important of
Vascular Center?
Peripheral vascular Diseases need a
multidicipline approach, not only on
hospital based, but at a primary care level
Most of patient with cardiac/coronary
problems, suffered from PAD as well (vice
versa) COCALIS concept (coronary-
carotid-limb ischemia)
Vascular center :diagnostic, therapy and
rehabilitation
 How important of
Vascular Center?
Vascular center : multidisipline diagnosis
and care at one visit (one stop service)
Advantages : decrease work load,
reduction of total cost (avoid repeat
examination)patient satisfactory
 Which specialists should be
involved?
Vascular medicine (angiology)
Cardiologist
Vascular surgeon
Cardiothoracic surgeon
Hematologist
Neurologist
Radiologist
Diabetologist (endocrinologist)
Physiotherapist
 Cooperation

One roof system (one place service)

Integration of medical,surgical and radiological
aspects diagnosis and management
Weekly meeting, journal reading, conferences
Teaching of vascular medicine at pre and post
graduate levels, preventive education to the public
at one roof system
A single center would be easier to develop inter-
diciplinary standards and quality assurance
 Advantages
Registry of vascular diseases
Epidemiological knowledge
Risk factors recognition
Markers of predicting deteriorations of vascular
diseases
Patient-oriented medical approach
Evidence-based therapy
Facilitate multidiciplinary integrated and
structured educational approach to vascular
medicine
 Criteria of establishing vascular
center
Objective of vascular center
Patient population
Methodology and sources of information
Level and branch of consultation
Involved departments
Accreditation and quality certification
 Budgeting and financial
Recognition and reimbursement of standardized
diagnostic and therapeutical algorithms of
vascular diseases
Accreditation specific vascular techniques and
therapy
Financial of vascular program and preventive
vascular medicine
Length of stay in hospital, avscular procedures
etc
 Long term advantages of
vascular center
Increased population of elderly increased pt of
vascular disease
Vascular pt : high risk cardiovascular patients
need uniform assessment and improvement of
primary and secondary prevention in vascular
medicine
Optimal diagnostic and therapeutic approach
with interdiciplinary standards and quality
assurance
 Conclusions
Vascular center is necessary in order to
obtain an optimal diagnostic and
therapeutic approach in vascular medicine
Vascular center under one roof would lead
to a more efficient patient-oriented
assessment of vascular disease at lower
cost
THANKYOU