Aterosclerosi il danno d'organo: vasculopatia periferica - di P. Buonamico

ATEROSCLEROSI IL DANNO
D’ORGANO:
VASCULOPARTIA
PERIFERICA

Dott. P. Buonamico

Etiopatogenesi E SM
Insulino Resistenza
•Ridotta produzione insulino-indotta di ossido nitrico (NO)
(antiaterogenica)
Nessuna influenza sulla crescita e migrazione dei
miociti, insulino dipendente, che è invece aterogena.
•Potenziata produzione angiotensina II stimolata da
Plasminogen activator inhibitor-1 (PAI-1) che può contribuire
ad un effetto pro-trombotico.
•Ridotta sensibilità del muscolo scheletrico all’insulina (per cui
ne deriva vasocostrizione ed ipertensione)

Fagan TC Am J Med 1988

ARTERIOSCLEROSI

DISTRETTI INTERESSATI

ARTERIOSCLEROSI
MANIFESTAZIONI CLINICHE

 CORONAROPATIA

 INSUFFICIENZA CEREBRO-VASCOLARE

 IPERTENSIONE RENO-VASCOLARE
 INSUFFICIENZA CELIACO-MESENTERICA

 MALATTIA ANEURISMATICA

ARTERIOPATIA OSTRUTTIVA CRONICA
DEGLI ARTI INFERIORI

Arteriopatia Aterosclerotica
Carotidea
• IMT
• ATEROMASIA CAROTIDEA
• STENOSI CAROTIDEA
• PATOLOGIA ANEURISMATICA
• PATOLGIA VASCOLARE
ENDOCRANICA

Imt e Aterotrombosi
Stabilizzazione delle lesioni
• Ridotta vulnerabilità della placca:
– Riduzione del core lipidico o cambiamento della sua composizione;
– Riduzione della concentrazione di macrofagi o dell'attività di degrado della
matrice;
– Aumento densità SMC e sintesi di matrice.

• Ridotta trombogenicità della placca:
– Riduzione core lipidico;
– Riduzione densità dei macrofagi e contenuto/attività del tissue factor;
• Aumentata funzionalità endoteliale:
– Ripristino funzioni vasodilatatorie normali;
– Ridotto fenotipo protrombotico;

• Eliminazione di fattori estrinseci che favoriscono la rottura della placca

MISURA US

Pignoli P, Tremoli E, Poli A, Oreste P, Paoletti R. Intimal plus medial
thickness of the arterial wall: a direct measurement with ultrasound
imaging. Circulation 1986

Misurazione IMT
Intimal plus medial thickness of the arterial wall: a direct
measurement with ultrasound imaging. Pignoli P, Tremoli E,
Poli A, Oreste P, Paoletti R. Circulation. 1986 Dec;74(6):1399-406.

A study in vitro of specimens of human aortic and common carotid arteries
was carried out to determine the feasibility of direct measurement (i.e., not
from residual lumen) of arterial wall thickness with B mode real-time imaging.
Measurements in vivo by the same technique were also obtained from common
carotid arteries of 10 young normal male subjects. Aortic samples were
classified as class A (relatively normal) or class B (with one or more
atherosclerotic plaques). In all class A and 85% of class B arterial samples a
characteristic B mode image composed of two parallel echogenic lines
separated by a hypoechoic space was found. The distance between the two
lines (B mode image of intimal + medial thickness) was measured and
correlated with the thickness of different combinations of tunicae evaluated by
gross and microscopic examination. On the basis of these findings and the
results of dissection experiments on the intima and adventitia we concluded
that results of B mode imaging of intimal + medial thickness did not differ
significantly from the intimal + medial thickness measured on pathologic
examination.

Among " emergent" risk factor ,
hyperhomocisteinemia , stress, standing at work …
seems to be linked with an increase of intima media
thickness.

• Baseline CCA-IMT is an independant predictor of
carotid plaque occurrence ( EVA Study ) with a
prevalence of plaque threfold higher in the subject
with high IMT at baseline (7) .

IMT e Rischio cardiovascolare
• L’IMT dell’arteria carotide comune e della
carotide interna è associata con il rischio di Stroke
e di infarto miocardico (IMA) in pazienti anziani
asintomatici (> 65 anni). Il rischio relativo per
IMA e Stroke tra la minore e la maggiore IMT è
3.87 (cardiovacular health study), con follow up
mediano di 6.2 anni.
• O'Leary et al.Carotid artery intima and media thickness as a risk factor for
myocardial infarction and stroke in older adults. Cardiovascular Health Study
Collaboration Research Group. N Engl J Med 1999 Jan7;340(1):14-22

Misura IMT
• In pratica va misurata sulla carotide comune
a partire da un centimetro al di sotto della
biforcazione (carotide comune) e al di sopra
di questa (carotide interna).
• Vanno misurate entrambe le pareti
prossimale e distale.

Correlazione dell’IMT con la
coronaropatia

Grobbee DE, Bots ML. Carotid artery intima-media thickness as an
indicator of generalized atherosclerosis. J Intern Med 1994; 236: 567–573

Hodis HN, Mack WJ, LaBree L, Selzer RH, Liu CR, Liu CH, et al. The
role of carotid arterial intima-media thickness in predicting clinical
coronary events. Ann Intern Med 1998; 128: 262–269

• S Coccheri and G Palareti: The cardiovascular risk burden of
intermittent claudication
Eur. Heart J. Suppl., March 1, 2002; 4(suppl_B): B46 - B49.

• P.M. Rothwell: The Interrelation between carotid, femoral and
coronary artery disease
Eur. Heart J., January 1, 2001; 22(1): 11 - 14.

• S. Cuomo, et al :Increased carotid intima-media thickness in children-
adolescents, and young adults with a parental history of premature
myocardial infarction
Eur. Heart J., 2002; 23(17): 1345 - 1350

• J. Luedemann, et al : Association Between Behavior-Dependent
Cardiovascular Risk Factors and Asymptomatic Carotid
Atherosclerosis in a General Population
Stroke, 2002; 33(12): 2929 - 2935.

S. Cuomo, et al :Increased carotid intima-media thickness in children-
adolescents, and young adults with a parental history of premature
myocardial infarctionEur. Heart J., 2002; 23(17): 1345 - 1350

• Conclusions Vascular structural changes associated
with a parental history of premature myocardial
infarction are already detectable in childhood and
adolescence and occur independently of several
traditional cardiovascular risk factors.

• (mean of combined sites: age 5–18 years:
0·45±0·076mm vs 0·40±0·066mm in controls,
P=0·008; age 19–30 years: 0·48±0·077mm vs
0·45±0·078mm in controls,P =0·007)

Association Between Behavior-Dependent Cardiovascular Risk Factors and
Asymptomatic Carotid Atherosclerosis in a General Population (Luederman J,
stroke 2002)

• Conclusions— Physical activity and optimal
diet are associated with reduced risk of early
atherosclerosis in subjects who never smoked,
while no benefit of an otherwise optimal
lifestyle is observed in smokers.
•

Prevalence and Relation to Ambulatory Blood Pressure in a Middle-
aged General Population in Northern Italy: The Vobarno Study M. L.
Muiesan, et al. Hypertension. 1996;27:1046-1052.

• Prevalence of intima-media thickening (intima-media
thickness >1 mm) was 11% in normotensive subjects and
44% in hypertensive subjects. The presence of plaque
(wall thickening with either mineralization or focal
protrusion in the lumen at least 50% greater than the
surrounding wall, usually >2 mm) was observed in 35% of
normotensive subjects and 44% of hypertensive subjects.
The prevalence of left ventricular hypertrophy was 13% in
normotensive subjects and 19% in hypertensive subjects


• Intima-media thickness in the common and bifurcation segments of
carotid arteries correlated well with LVMI (r=.20 and r=.19,
respectively; P<.01). Intima-media thickness and LVMI were both
positively related to 24-hour monitored BP (P<.01). However, in the
multivariate analysis, body mass index (P=.027), sex (P<.001), and
24-hour mean BP (P=.025) were the most significant determinants of
LVMI, whereas carotid artery intima-media thickness was found to be
associated best with age (P<.001), cigarette smoking (P=.009), serum
cholesterol (P=.025), serum glucose (P=.038), and nighttime systolic
BP (P=.006). Logistic regression analysis confirmed the association
between the presence of plaque and age (P<.001), nighttime systolic
BP (P<.05), and cigarette smoking (P<.05);


• a negative association between plaque and the decrease in
mean systolic BP from daytime to nighttime was also
observed (P<.001). In conclusion, in a general population
of unselected middle-aged subjects, carotid wall thickness
and LVMI were associated with each other and related to
24-hour BP levels although the major determinants of
carotid wall and cardiac structure were different.
•

IMT E FATTORI DI RISCHIO CV
• There is a strong association with various risk
factor for atherosclerosis.
Arterial wall thickening has a strong pronostic
value for cardiovascular events , in particular
stroke and myocardial infarction.
• IMT allows convenient stratification of patients at
risk for cardiovascular disease and has proved to
be a good marker of the efficacity of
antiatherogenic driugs.
• The ease and accuracy of computer -assisted IMT
measurement makes it a useful marker of
cardiovascular involvement in atherosclerosis.

CONCLUSIONI
• Forte associazione con vari fattori di rischio per
aterosclerosi (classici ed emergenti)
• Valore prognostico per eventi cardiovascolari- Stroke
e infarto miocardico.
• IMT = buon marker per l’effcacia di farmaci
antiaterogenici
• Notevole sensibilità per la stratificazione di pazienti
ad alto rischio per malattia cardiovascolare.

Stenosi Carotidea
Cosa significa

Stenosi carotidea significativa?

Emodinamicamente = > 50%

Clinicamente ?

TIA (VA CSP 309) Symptomatic PTS
(ECST) (NASCET)

Carotid endarterectomy symptomatic
stenosis >70% ipsilateral stroke/crescendo Carotid endarterectomy symptomatic Carotid endarterectomy symptomatic
stenosis >70% ipsilateral stroke stenosis >70% Ipsilateral stroke

5000 pts follow up 5 aa Mayo clinic
2518 pts 3 yars foolw up 662 pts five years follow up mean 2.7 y

•
ACAS TRIAL
1662 patients from more than 42 000

• 39 centers in North America between 1987 and 1993.

• age 40 to 79 year.

• Significant stenosis = 60% reduction in diameter by arteriography,

• Patients assigned to surgery then underwent preoperative cerebral arteriography.

• Arteriography was not mandatory in the medical arm, but 319 (37.5%) of the medical
patients had arteriography before randomization.

• NASCET Method (minimum residual lumen at the point of maximum stenosis referenced to
the diameter of the distal lumen of the internal carotid artery at the first point at which the
arterial walls became parallel).

• MEDICAL THERAPY : aspirin (325 mg/d)

• Primary end points included stroke and death, and those that occurred within 30 days
of surgery or 42 days (to account for the average of 12 days between randomization and
operation in the surgical arm)of medical randomization were considered perioperative.

ACAS trial

Asymptomatic carotid stenosis >60% Carotid endarterectomy asymptomatic
medical versus surgical therapy stenosis >60% relative risk reduction

2295 pts 5 years follow up
medical treatment: aspirin or another anti-platelet
drug, treatment of hypertension, and advice to stop
smoking.

ACST (3120 pts >60% US Stenosis); Lancet 2004

• In summary, patients younger than 80 years old and without
• major comorbidities, with low surgical risk and with a moderate
• to severe asymptomatic carotid stenosis, have an increased risk
• of stroke or death over a period of 5 years of 12%. CEA in such
• a selected population produces a modest absolute risk reduction
• of 5% to 6% over medical therapy alone, which translates into
• approximately 50% relative risk reduction for stroke and death
• over a 5-years period if the perioperative risk is contained at less
• than 3%.
• These RCT also show that, contrary to symptomatic
• CEA studies, the risk of stroke and the benefit from CEA is not
• predicted by the degree of stenosis.

Doubts for Asymptomatic
This medical treatment is aimed at preventing stroke in any territory in the
previously asymptomatic patient (primary prevention) or preventing
recurrent stroke in a patient having suffered from either
a transient ischaemic attack (TIA) or previous stroke (secondary
prevention). In most cases, carotid endarterectomy will only prevent
stroke from the treated carotid stenosis. Medical treatment
has improved substantially since the randomised trials of surgery
versus medicine for carotid stenosis were completed. Hence,
particularly in asymptomatic patients, the thresholds for intervening
surgically or by endovascular treatment should almost
certainly be raised somewhat.
• Ederle J O, Brown MM, “The evidence for medicine versus surgery for carotid stenosis” European Journal of
Radiology 60(2006) 3–7.

Management of Carotid Stenosis
From the Division of Interventional Neurovascular Radiology and the Departments of
Radiology Neurology, Neurological Surgery, and Anesthesiology, University of California,
San Francisco, Medical Center, San Francisco. n engl j med 358;15, apr 2008

the 30-day rate of perioperative stroke or death was 1.1%, after exclusion
of the 1.2% rate-stroke from arteriography
• of Other strategies to treat this patient are possible, but none have been
shown to be as effective as carotid endarterectomy. The most
compelling
• alternative is intensive medical therapy with aggressive
• suppression of platelet function, targeted blood-pressure control
(possibly with the addition of beta-blockade and an angiotensin-
converting–
• enzyme inhibitor), and statin therapy. The argument
• has been made that the “best medical therapy” received by patients in
past clinical trials did not include widespread use of these current
therapies. This important question can be answered only by a proper
clinical trial comparing the two treatments. Until this is accomplished,

TACIT
TACIT (the Transatlantic Asymptomatic Carotid Intervention Trial),
controlled prospectic multicentric study, USA + Europe 2400 pts with
asymptomatic 70% carotid stenosis
• 3 branches : best medical therapy, BMT: terapia antiaggregante associata
• hypolipidemic. antihypertensive, glycemic and smoking control)
• vs BMT più EC vs
• BMT + stenting.
• Primary endpoint : evaluation and comparison of the peri –procedural risk off
stroke and death and at 3 yrs few secondary endpoints of which remarkable
is the effect on cognitive function.

Doppler flow measurement
Principle of blood flow measurement
US Doppler blood flow-meters
are based on the difference between the frequency of ultrasound
(US) waves emitted by the probe and those reflected (back-
scattered) by moving erythrocytes.

The frequency of reflected waves is (in comparison with the
emitted waves)
higher in forward blood flow (towards the probe)
lower in back blood flow (away from the probe)

The difference between the frequencies of emitted and reflected
US waves is proportional to blood flow velocity.
55

General principle of blood flow measurement

56

Doppler methods
Pulse wave (PW) systems
Aliasing – at high repetition frequency of pulses the upper part
of the spectral curve can appear in negative velocity range
- at velocity above 4m/s aliasing cannot be removed

Nyquist limit

57

∆F = 2 f x v x cos α ;
C

∆F = K x v x cos α

v = ∆F x K/ cos α

C = vel US nei tessuti
F = frequenza iniziale degli US


Dependence of velocity
overestimation on the incidence
angle α (if the device is adjusted
for
α = 0, i.e. cosα = 1)

α - angle made by axis of emitted US
beam and the velocity vector of the
reflector

59

Doppler flow measurementSystems
with pulsed wave - PW
1) Systems with continuous wave – CW. They are used for measurement on
superficial blood vessels. High velocities of flow can be measured, but without
depth resolution. Used only occasionally.
2) Systems with pulsed wave. It is possible to measure blood flow with accurate
depth localisation. Measurement of high velocities in depths is limited.

60

Doppler methods

DUPLEX method
is a combination
of dynamic B-mode imaging (the morphology of examined area
with blood vessels is depicted)
and the PW Doppler system (measurement of velocity spectrum
of blood flow).

It allows to examine blood flow inside heart or in deep blood
vessels (flow velocity, direction and character)

61

Doppler methods DUPLEX method

Scheme: sector image Image of carotid with spectral
with sampling volume analysis of blood flow velocity

62

Doppler methods
Pulse wave (PW) systems
Aliasing – at high repetition frequency of pulses the upper part
of the spectral curve can appear in negative velocity range
- at velocity above 4m/s aliasing cannot be removed

Nyquist limit

63

Doppler methods
Colour Doppler imaging

The image consists of black-white and colour part.
The black-white part contains information about reflectivity and
structure of tissues.
The colour part informs about movements in the examined
section. (The colour is derived from average velocity of flow.)
The apparatus depicts distribution and direction of flowing blood
as a two-dimensional image.
BART rule – blue away, red towards. The flow away from the
probe is coded by blue colour, the flow towards the probe is coded
by red colour. The brightness is proportional to the velocity,
turbulences are depicted by green patterns.

64

Doppler methods
Colour Doppler imaging

Carotid bifurcation

65

Doppler methods TRIPLEX method

A combination of duplex method (B-mode imaging with PW
Doppler) and color flow mapping
Normal finding of blood flow in a. carotis communis (left) and
about 90%-stenosis of a. carotis interna (right)

66

Doppler methods
POWER DOPPLER method
- the whole energy of the Doppler signal is utilised
- mere detection of blood flow only little depends on the
so-called Doppler incidence angle
- imaging of even very slow flows (blood perfusion of tissues and
organs)
- flow direction is not shown

67

Absolute velocity?
• Table I. Hemodynamic parameters described by Zwiebe111. and Strandness 12 for
duplex
• assessment of internal carotid artery stenosis
• Percent stenosis Zwiebel criteria Percent stenosis Strandness criteria
• 0-39 PSV < 110 cm/sec, EDV <40 crn/sec 1-15 No flow reversal in bulb
• 40-59 PSV < 130 cm/sec, EDV < 40 crn/sec 16-49 Spectral broadening
• 60-79 PSV > 130 cm/sec, EDV >40 crn/sec 50-79 PSV >25 cm/sec, EDV < 140
cm/sec
• 80-99 PSV > 250 cm/sec, EDV > 100 cm/sec 80-99 EDV > 140 cm/sec
• Occlusion No flow detected Occlusion No flow detected
• PSV, Peak systolic velocity; EDV, end diastofic velocity.
• *Zwiebel also describes the use of velocity ratios. Only the systolic velocity and end
diastolic velocity have been used here.

Reappraisal of duplex criteria to assess significant carotid stenosis with
special reference to reports from the North American Symptomatic Carotid
Endarterectomy Trial and the European Carotid Surgery Trial
ML. Neale, et al, j vasc surg 1994 20:642-9

• Conclusions: The accuracy of duplex studies
compared with angiography in the assessment
• of extracranial vascular disease depends on the
method of angiographic determination of
• carotid stenosis. Vascular laboratories should
validate the duplex criteria they use against
• a standard method of angiographic assessment of
carotid artery stenosis, with special reference to the
recently reported studies noting the significance of a
stenosis greater than 70% in patients with
symptoms. (J VAsc SURG 1994;20:642-9.)

Changes in area are not equal to
changes in diameter
• 2-1.4 cm = 70%
• 2- 1,4 = 0.6 cm D Area : 3.14 x 2

• 1x 1 x 3.14 =3.14

• 0.3 x 0.3 = 0.09 X
3.14 = 0.28

• 3.14 – 0.28 : 100 =
92%

Ultrasonography
Harmonic imaging
An impulse with basic frequency f0 is
emitted into the tissue. The receiver,
however, does not detect the reflected US
with this same frequency but with the second
harmonic frequency 2f0. Its source is tissue
itself (advantage in patients „difficult to
examine“). The method is also used with
echocontrast agents – source of the second
harmonic are oscillating bubbles.
Advantageous when displaying blood supply
of some lesions.
Conventional (left) and
harmonic (right) images
of a kidney with a stone.
87

Ultrasonography
Echocontrast agents
- increase echogenity of streaming blood
Gas microbubbles
(mainly air or volatile
hydrocarbons)
- free
- enclosed in
biopolymer
envelope

A SEM micrograph of
encapsulated
echocontrast agent
88

Ultrasound pitfalls
• Carotid duplex ultrasound has several limitations:
• It is user dependent. If the duplex is not performed in a meticulous,
standardized and thorough fashion, results can be misleading.
• Heavy calcifications cause acoustic shadows that preclude
interpretation.
• Duplex ultrasound can not visualize the carotid arteries intracranially
or beyond the jaw. Visualization of the common carotid origin from
the Aorta is also difficult.
• PSV in tortuous vessels may be measured as high, thus mimicking
stenosis.
• Although duplex can characterize plaque according to various
characteristics, it has not been very successful in predicting which
plaque is more vulnerable to embolization. The same is true for carotid
artery imaging with CT and MR.

Transcranial ECD
.
Can U. Et Al Stroke. 1997 Oct;28(10):1966-71

the strongest indicators of a residual lumen diameter < 1.5 mm
• transorbital , :
• reversed flow in the ipsilateral ophthalmic artery (spec 100% S = 31%)
• a > 50% peak systolic velocity difference between the carotid siphons (distal ICAs) in patients
with unilateral ICA origin stenosis. (Spec 100% S 26% ) .
• transtemporal (no controlateral stenosis)
• in patients with a unilateral stenosis,
• > 35% difference in ipsilateral MCA PSV relative to the contralateral MCA. (SP 100/% S =
32%)

• > 50% difference in contralateral (ACA) PSV relative to the ipsilateral ACA. (SP 100%; S
43%).

• Irrespective of contralateral stenosis, a > 35% difference in ipsilateral MCA peak systolic velocity
relative to the ipsilateral PCA (Spec = 100% S = 23%)
• CONCLUSIONS:
• Although the TCD sensitivity for detecting a hemodynamically significant stenosis is relatively
low, it can be highly specific (up to 100%). We conclude that TCD enhances the specificity of
highly sensitive CDUS criteria for detecting a hemodynamically significant ICA stenosis.

AORTA

ascendente
Toracica
discendente

sovrarenale
Addominale
sottorenale

Aneurismi
• Dissecante A o B

• Fusiformi o sacciformi (4.5 o 6 cm)

• Patologia stenosante congenita o acquisita
• (cong= coartazione aortica; acq. Leriche)

Vengono valutati tutti gli studi grandi emulticentrici
(DRASTIC, STAR, ASTRAL) che concludono tutti per una
scarsa efficacia globale dello stenting rispetto alla terapia
medica. Tutti gli studi hanno importanti lacune sul numero e
sulla metodologia (spesso stenosi non significative o creatinina
normale etc) E in corso lo studio CORAL (USA) che dovrebbe
essere più rigoroso.

3. Hirsch AT, Haskal ZJ, Hertzer NR, et al. ACC/AHA Guidelines
for the Management of Patients with Peripheral
Arterial Disease (Lower Extremity, Renal, Mesenteric,
and Abdominal Aortic): A Collaborative Report from the
American Association of Vascular Surgery/Society for
Vascular Surgery, Society for Cardiovascular Angiography
and Interventions, Society for Interventional Radiology,
Society for Vascular Medicine and Biology and the
American College of Cardiology/American Heart Associa-

Gli autori suggeriscono :
1)Stenosi di almeno il 70% all’angiografia o all’ultrasonografia intravascolare

2)ipertensione rapidamente instaurantesi, resistente a terapia o maligna.

3)Ipertensione rapida e d IRA in pts con stenosi bilaterale o monorene

4)Episodi di insufficienza cardiaca congestizia o edema polmonare

5)Intervento controindicato per IR (peak- end diastolic vel)/ peak elevati (>0.8)

ARTERIOSCLEROSI
MANIFESTAZIONI CLINICHE

 CORONAROPATIA

 INSUFFICIENZA CEREBRO-VASCOLARE

 IPERTENSIONE RENO-VASCOLARE

 INSUFFICIENZA CELIACO-MESENTERICA

 MALATTIA ANEURISMATICA



DEFINIZIONE

LESIONI OSTRUTTIVE LOCALIZZATE A VALLE
DELLE ARTERIE RENALI CHE,
INDIPENDENTEMENTE DALLA LORO NATURA,
COMPORTANO UNA RIDUZIONE
DELLA PERFUSIONE DEGLI ARTI INFERIORI

CLASSIFICAZIONE

 DIFFUSE
 DEGENERATIVE
O ARTERIOSCLEROTICHE  SEGMENTARIE

 INFIAMMATORIE
 NON DEGENERATIVE
 INFETTIVE

NON DEGENERATIVE

 MALATTIA DI HORTON

 INFIAMMATORIE  MALATTIA DI TAKAYASU

 MALATTIA DI BUERGER

 BATTERICHE (salmonelle, cocchi)

 INFETTIVE  VIRALI (influenza, herpes)

 RICKETTSIE (burneti, moseri)

DEGENERATIVE
 ATEROSCLEROSI
(ACCUMULO DI LIPIDI E STENOSI VASALE)

 ARTERIOSCLEROSI
(ISPESSIMENTO INTIMALE DA MIGRAZIONE CELL.
MUSC. LISCE DELLA MEDIA SENZA ACCUMULO DI
LIPIDI)

 SCLEROSI DELLA MEDIA DI MONCKEBERG
(DEGENERAZIONE CELLULE MUSCOLARI LISCE
E DEPOSIZIONE DI CALCIO NELLA MEDIA)
(ARTERIE MUSCOLARI DI MEDIO CALIBRO)

STADI CLINICI

FONTAINE NUOVA CLASSIFICAZIONE

I: PARESTESIE, IPOTERMIA

II: CLAUDICATIO INTERMITTENS ISCHEMIA RELATIVA
a) se maggiore di 200 m
b) se minore di 200 m

III: DOLORI A RIPOSO
ISCHEMIA CRITICA
IV: LESIONI TROFICHE, GANGRENA

CLAUDICATIO INTERMITTENS
 DOLORE
 CRAMPO
SINTOMO DESCRITTO COME:
 STANCHEZZA
 RIGIDITA’
 INTERESSA SEMPRE I GRUPPI MUSCOLARI
SITUATI A VALLE DELLA LESIONE
 PROVOCATO SEMPRE DALL’ATTIVITA’
 SCOMPARE IN POCHI MINUTI CON IL RIPOSO
 LA RIPRESA DELL’ATTIVITA’ PROVOCA IL DISTURBO
DOPO UNO STESSO PERCORSO E SEMPRE
CON LE STESSE CARATTERISTICHE

CLAUDICATIO INTERMITTENS
LOCALIZZAZIONE DEL DOLORE

LESIONE CLAUDICATIO

AORTO-ILIACA
GLUTEO

ILIACO-FEMORALE
COSCIA

FEMORO-POPLITEA
POLPACCIO

INFRA-POPLITEA
PIEDE

CARATTERIZZAZIONE CLAUDICATIO

 SEDE

 MODALITA’ D’INSORGENZA

 AUTONOMIA DI MARCIA

 TEMPO DI RECUPERO

 RICOMPARSA ALLA RIPRESA DELL’ATTIVITA’

 EVOLUZIONE NEL TEMPO


SEDE OSTRUZIONE ERRORE
ARTERIOSA Zona
DIAGNOSTICO
claudicatio

LOMBALGIA
AORTO-ILIACA ARTRITE DELL’ANCA
LOMBOSCIATALGIA

DISCOPATIA
ILIACO-FEMORALE MIOSITE
NEURITE LOMBARE

FEMORO-POPLITEA ARTRITE DEL GINOCCHIO

NEUROMA PLANTARE
INFRA-POPLITEA OSTEOPOROSI
NEUROPATIA DIABETICA

MODELLO IDRAULICO DELLA CIRCOLAZIONE

NORMALE

MODELLO IDRAULICO DELLA CIRCOLAZIONE

CLAUDICATIO

CIRCOLO COLLATERALE

 PREFORMATO
(ARTERIE MESENTERICHE,
LOMBARI, IPOGASTRICHE, FEMORALE
PROFONDA)

 NEOFORMATO
(ARTERIE MUSCOLARI)


DISTRETTO AORTO-ILIACO NORMALE

CIRCOLO COLLATERALE
OSTRUZIONE ARTERIA
ILIACA COMUNE DX

DISTRETTO
ARTERIOSO
NORMALE

RIABITAZIONE A VALLE

CIRCOLO COLLATERALE
OSTRUZIONE ARTERIA
FEMORALE COMUNE

RIABITAZIONE
BIFORCAZIONE FEMORALE

CIRCOLO COLLATERALE
OSTRUZIONE ARTERIA
FEMORALE SUPERFICIALE

RIABITAZIONE A VALLE

CIRCOLO COLLATERALE

STENO-OSTRUZIONI
MULTIPLE
ARTERIA
FEMORALE
SUPERFICIALE

OTTIMO CIRCOLO
COLLATERALE

CIRCOLO COLLATERALE

OSTRUZIONE
ARTERIA POPLITEA

CIRCOLO COLLATERALE
FATTORI FAVORENTI

 EMODINAMICI
GRADIENTE PRESSORIO
RIDUZIONE VISCOSITA’
RIDUZ. RESISTENZE
PERIFERIFERICHE
 NERVOSI VASOMOTORI
VASOCOSTRIZIONE
VASODILATAZIONE

 METABOLICI
CATABOLITI ACIDI
(CO2, AC. PIRUVICO,
AC. LATTICO, LDH, CPK)

LESIONI MULTIPLE


DOLORE A RIPOSO

 SI VERIFICA O SI ACCENTUA DI NOTTE

 E’ PERSISTENTE TANTO DA IMPEDIRE IL SONNO

 SI ATTENUA CON LA POSIZIONE ORTOSTATICA


DOLORE A RIPOSO
IMBIBIZIONE
INTERSTIZIO

> ESTRAZIONE O2 EDEMA
E METABOLITI

DIFFUSIONE O2
RISTAGNO SANGUE
E METABOLITI

PEGGIORAMENTO
ISCHEMIA

LESIONI ISCHEMICHE

GRAVE RIDUZIONE APPORTO EMATICO

INCAPACITA’ A
MANTENERE
METABOLISMO

NECROSI
TESSUTALE

LESIONE TROFICA (GANGRENA)

TIPI DI GANGRENA

 GANGRENA SECCA

 GANGRENA UMIDA

 GANGRENA GASSOSA


GANGRENA SECCA
 RAPIDA EVAPORAZIONE TESSUTI
 DIFFUSIONE E DECOMPOSIZIONE Hb
(COLORAZIONE NERASTRA)
 REAZIONE INFIAMMATORIA
LIMITANTE (DEMARCAZIONE)
 “MUMMIFICAZIONE”

GANGRENA UMIDA

 SUPERINFEZIONE BATTERICA
(PUTREFAZIONE)

 CUTE CIANOTICA  BRONZINA
(FLITTENE SIEROEMORRAGICHE)

 REAZ. INFIAM. NON LIMITANTE
(DEMARCAZIONE MENO NETTA)

 ODORE “SUI GENERIS”


GANGRENA GASSOSA

 INFEZIONE GERMI ANAEROBI

 RAPIDA DIFFUSIONE
AI TESSUTI CIRCOSTANTI
(PRODUZIONE DI GAS)
 CREPITIO ALLA PALPAZIONE
(ENFISEMA SOTTOCUTANEO)


MAL PERFORANTE
PLANTARE

DIABETE MELLITO

EVOLUZIONE CLINICA
LESIONE CIRCOLO COLLAT.
FATTORI ANATOMICI
PROGRESSIONE LESIONE

RIDUZ. PORTATA CARDIACA
FATTORI EMODINAMICI DISTURBI RITMO CARDIACO
IPOTENSIONE ARTERIOSA

IPERVISCOSITA’ EMATICA
FATTORI COAGULATIVI
SINDROMI TROMBOFILICHE

EVOLUZIONE CLINICA

LESIONE
CIRCOLO COLLATERALE

EVOLUZIONE CLINICA
A. FEMORALE SUPERFICIALE

PROGRESSIONE
LESIONE

STENOSI NON STENOSI
EMODINAMICHE EMODINAMICHE

EVOLUZIONE CLINICA

DISTRETTO AORTO-ILIACO

PROGRESSIONE
LESIONE

G. A. 3. 4. 71 G. A. 6. 12. 71
CLAUDICATIO DOLORI A RIPOSO
400 mt

EVOLUZIONE CLINICA

STENOSI POPLITEEE STENOSI POPLITEEE
NON EMODINAMICHE EMODINAMICHE

EVOLUZIONE CLINICA

PROGRESSIONE
LESIONE

OSTRUZIONE BIFORCAZIONE
AORTICA
(SINDROME DI LERICHE)

SINDROME DI LERICHE
DEFINIZIONE

OSTRUZIONE CRONICA DELLA BIFORCAZIONE
AORTICA AD ETIOLOGIA ARTERIOSCLEROTICA
CON TENDENZA DELLA TROMBOSI ALLA
PROGRESSIONE IN SENSO PROSSIMALE SINO
A COINVOLGERE L’ORIGINE DELLE ARTERIE
VISCERALI (RENALI, MESENTERICHE)

SINDROME DI LERICHE
ESAME OBIETTIVO

 DISTROFIE CUTANEE E PERDITA ANNESSI

 IPOTONIA E IPOTROFIA MASSE MUSCOLARI

 ASSENZA BILATERALE POLSO FEMORALE

 LESIONI TROFICHE (RARE)

SINDROME DI LERICHE
SINTOMATOLOGIA

 CLAUDICATIO INTERMITTENS
A LUNGA AUTONOMIA DI MARCIA
(POLPACCIO, COSCIA E GLUTEO)

 IMPOTENTIA ŒRIGENDI

 ANGINA ABDOMINIS

INSUFFICIENZA RENALE ACUTA ED ANURIA

SINDROME DI LERICHE

SINDROME DI LERICHE
CIRCOLI COLLATERALI
ARTERIE VISCERALI
A. PANCR.-DUODEN. SUP. A. PANCR.-DUODEN. INF.
(TRONCO CELIACO) (A. MESENTERICA SUP.)

ARCATA DI RIOLANO
A. COLICA MEDIA A. COLICA SINISTRA
(A. MESENTERICA SUP.) (A. MESENTERICA INF.)

ARCATA MARGINALE O DI DRUMMOND
A. MESENTERICA SUP. A. MESENTERICA INF.
(RAMI BORDO MESOCOLICO) (RAMI BORDO MESOCOLICO)

SINDROME DI LERICHE
CIRCOLI COLLATERALI
AORTO-IPOGASTRICI
VISCERALI
A. EMORROIDARIA SUP. A. EMORROIDARIA MEDIA
(A. MESENTERICA INF.) (A. MESENTERICA INF.)
A. OMBELICALE
A. SPERMATICA INTERNA A. VESCICOLO-DEFER.
A. OVARICA A. UTERINA

PARIETALI
A. INTERCOSTALI A. ILEOLOMBARE
A. LOMBARI A. GLUTEA SUP.
A. SACRALI LATERALI
A. SACRALE MEDIA A. PUDENDA INTERNA

SINDROME DI LERICHE
CIRCOLI COLLATERALI
AORTO-ILIACA ESTERNA, FEMORALE

VISCERALI
A. SPERMATICA INTERNA
STERNA
A. VESCICOLO-DEFEREN.
INF.)
(A. OMBELICALE)

PARIETALI
A. MAMMARIA INT. A. EPIGASTRICA INF.
A. INTERCOSTALI A. EPIGASTRICA SUPERF.
A. FRENICHE A. CIRCONFL. ILIACA PROF.
A. LOMBARI A. CIRCONFL. ILIACA SUPERF.

SINDROME DI LERICHE
CIRCOLI COLLATERALI
AORTO-ILIACA ESTERNA, FEMORALE
PARIETALI
A. OTTURATORIA A. EPIGASTRICA INFERIORE

A. ILEO-LOMBARE A. ILIACA ESTERNA
(RAMI M. PSOAS) (RAMI M. PSOAS)

A. PERINEALE SUPERF. A. PUDENDA ESTERNA
(A. PUDENDA INTERNA) (RAMI SCROTALI E LABIALI)

AA. CIRCONFLESSE ILIACHE
A. GLUTEA SUP.
(SUPERFICIALE E PROFONDA)

A. GLUTEA SUP. E INF. AA. CIRCONFLESSE FEMORALI
A. OTTURATORIA (MEDIALE E LATERALE)
A. PUDENDA INT. I, II, E III A. PERFORANTE

SINDROME DI LERICHE

TROMBOSI AORTICA A LIVELLO
DELLE ARTERIE RENALI

DIAGNOSI

 CLINICA
 ANAMNESI
 ESAME OBIETTIVO

 STRUMENTALE
 NON INVASIVA
 INVASIVA

DIAGNOSI CLINICA
ESAME OBIETTIVO

RE
 ISPEZIONE TA I
LU TT TI
 PALPAZIONE VA TU ET
TR
IS
 PERCUSSIONE
ID
 AUSCULTAZIONE

ESAME OBIETTIVO

ISPEZIONE

 COLORE CUTE
 TROFISMO ANNESSI CUTANEI
 TROFISMO MASSE MUSCOLARI
 PRESENZA LESIONI TROFICHE

ESAME OBIETTIVO

PALPAZIONE
 TEMPERATURA CUTANEA
 TROFISMO MASSE MUSCOLARI
 EVENTUALI MASSE PULSANTI
 VALUTAZIONE DEI POLSI
 ARTI
 COLLO
INFERIORI
 ARTI SUPERIORI
RITMO  ADDOME
CARDIACO

PALPAZIONE
POLSO FEMORALE

Due cm medialmente al punto medio tra spina
iliaca anteriore-superiore e tubercolo del pube

PALPAZIONE
POLSO POPLITEO

Lungo la bisettrice della losanga poplitea,
nel cavo popliteo

PALPAZIONE
POLSO TIBIALE POSTERIORE

Nella doccia retromalleolare mediale

PALPAZIONE
POLSO PEDIDIO

Lateralmente al tendine dell’estensore lungo dell’alluce
(molte variazioni anatomiche di decorso)

ESAME OBIETTIVO
AUSCULTAZIONE

 AORTICO

 RENALE
CAROTIDEO
FOCOLAI SUCCLAVIO
 ILIACO (VERTEBRALE)

 FEMORALE

SOFFIO VASCOLARE

STENOSI SOFFIO

VIBRAZIONE
FLUSSO PARETE
TURBOLENTO ARTERIOSA
PARETE ARTERIOSA CALCIFICA SOFFIO ASSENTE
CIRCOLO IPERCINETICO
(ANEMIA, FAV, IPERTIROIDISMO) SOFFIO PRESENTE
SOFFIO CARDIACO TRASMESSO

IL SOFFIO E’ SPESSO ESPRESSIONE DI
LESIONE STENOSANTE

SOFFIO CERVICALE
INCIDENZA

ETA’ > 45 ANNI
3,5-7%

I. V. A. I. 20%

DIAGNOSI

 CLINICA
 ANAMNESI
 ESAME OBIETTIVO

 STRUMENTALE
 NON INVASIVA

 INVASIVA

DIAGNOSTICA STRUMENTALE

NON INVASIVA
DOPPLER
ECOCOLORDOPPLER
PLETISMOGRAFIA
RISONANZA MAGNETICA E ANGIO-RM

INVASIVA

ANGIOGRAFIA
TOMOGRAFIA COMPUTERIZZATA

DOPPLER

 PERVIETA’ VASI

 SEDE E GRAVITA’ LESIONI (DATO GROSSOLANO)

 MISURAZIONE PRESSIONI DISTALI (I. W.)

 COMPENSO EMODINAMICO (I. C. P. P.)

INDIRIZZO DIAGNOSTICO

DOPPLER
TERRITORIO AD ALTE RESISTENZE

1 ONDA SFIGMICA
1
2 ONDA REVERSE

3 SECONDA ONDA POSITIVA

3 4 RITORNO ALLA LINEA ZERO

4
2
ASSENZA DI
VELOCITOGRAMMA NORMALE FLUSSO DIASTOLICO

DOPPLER
TERRITORIO AD ALTE RESISTENZE

A
AUMENTO
PROGRESSIVO
DEL GRADO
DI LESIONE

H
VELOCITOGRAMMI PATOLOGICI

DOPPLER
RILEVAZIONI PRESSORIE

 MISURAZIONE A VARI LIVELLI
(COSCIA, 1/3 SUPERIORE GAMBA, CAVIGLIA)

 INDICE PRESSORIO O DI WINSOR PC
IW = ≥1
P. A. CAVIGLIA / P. A. OMERALE PO
(VALORE NORMALE ≥ 1)

 INDICE DI COLLATERALITA’ PROFUNDO-POPLITEA
P. A. COSCIA – P. A. GAMBA / P. A. COSCIA
PC – PG
ICPP =
PC

ECOCOLORDOPPLER
ECODOPPLER
IMMAGINE ANATOMICA +
INFORMAZIONE FLUSSIMETRICA
SENSIBILITA’ 77-82%
SPECIFICITA’ 92-98%

ECOCOLORDOPPLER PER STENOSI
IMMAGINE DI FLUSSO DI > 50%
IMMEDIATA COMPRENSIONE
SENSIBILITA’ 76-92%
SPECIFICITA’ 93-99%

ECOCOLORDOPPLER

IMMAGINE
ANATOMICA

INFORMAZIONE
FLUSSIMETRICA

RISONANZA MAGNETICA E ANGIO-RM

VANTAGGI SVANTAGGI
 ASSENZA DI INVASIVITA’  CLAUSTROFOBIA
O RISCHIO
 VISUALIZZAZIONE VASI  SOVRASTIMA STENOSI
E TESSUTO PERIVASALE
 INFORMAZIONI  NON ESEGUIBILE IN PAZIENTI
ANATOMO-FUNZIONALI CON PROTESI METALLICHE
 GRANDE POTENZIALITA’  COSTI ELEVATI
(“TECNICA IDEALE”)


Angio-RM: STENOSI ILIACA COMUNE SN

Messaggio Finale
• Eccetto il dubbio per trattare le stenosi
carotidee asintomatiche ( e gli aneurismi) ,
l’indicazione agli esami invasivi ed
all’eventuale terapia invasiva
(endovascolare o chirurgica) è guidata dal
sintomo (e/o dalla logica rischio-beneficio)

Aterosclerosi il danno d'organo: vasculopatia periferica - di P. Buonamico

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