s.c. angiologia medica - messina. rosamond w, flegal k, furie k, et al. heart disease and stroke...

Placca carotidea e ictus ischemico

S.C. Angiologia Medica - Messina


Prevalence of Stroke

20-24 25-34 35-44 45-54 55-64 65-74 75+0

2

4

6

8

10

12

14

0.1 0.5 0.5

2.2

4

5.9

12.5

0.3 0 0.4 1

2.7

5.8

10.7

Prevalance of Stroke by Age and SexNHANES III: 1988-94

Men Women

Ages

% o

f Popula

tion

Rosamond W, Flegal K, Furie K, et al. Heart disease and stroke statistics--2008 update: a report from the American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Circulation 2008;117:e25-146.


European Journal of Neurology 2006, 13: 581–598


T. Willis (1621–1675)

J. Wepfer (1620–1695)

M. E. DeBakey (1908-2008)


20 to 30% of strokes are caused by atherosclerotic carotid artery disease1

Carotid artery disease increases the risk for stroke:

By plaque or clot breaking off from the carotid arteries and blocking a smaller artery in the brain By narrowing of the carotid arteries due to plaque build-upBy a blood clot becoming wedged in a carotid artery narrowed by plaque

Executive Committee for the Asymptomatic Carotid Atherosclerosis Study. Endarterectomy for Asymptomatic Carotid Artery Stenosis. JAMA 1995;273:1421


< 50 50-59 60-69 70-79 > 800

1

2

3

4

5

6

7

8 ≥ 50%

men women

Age (years)

Pre

vale

nce

(%

)

< 50 50-59 60-69 70-79 > 800

1

2

3

4

5

6 ≥ 70%

men women

Age (years)

Pre

vale

nce

(%

)

Stroke. 2010;41:1294-1297


Inzitari, D. et al. N Engl J Med 2000;342:1693-1700

No Disease <50% 50-59% 60-74% 75-94% 95-99% Occlusion0

5

10

15

20

25

30

4.6

7.8

12.914.8

18.5

14.7

9.4

18.720.2

25.827.1

17.2

No Symp-toms

Degree of Stenosis on Angiography

Ris

k o

f Ip

sil

ate

ral

Str

ok

e a

t 5

Yr

(%)


< 60 % stenosis 60 - 99 % stenosis0

2

4

6

8

10

12

1.22.11.9

65.4

9.9Cardioembolic Lacunar Large artery

Ris

k o

f st

roke a

t 5

years

(%

)


La placca carotidea “importante”………….è quella che darà dei sintomi cerebrali

ma anche MACEs (Major Adverse Cardiovascular events)

Come definirla ?• a rischio (embolico o emodinamico)• instabile• in progressione• vulnerabile


Placca carotidea a “rischio” o

“instabile” (fino al 1992)

Placca che determina una stenosi > 70 % (anche se di ecostruttura omogenea)Placca che determina una stenosi > 50%, disomogenea o con superficie microulcerata.Placca macro-ulcerataPlacca emorragica

De Fabritiis, Scondotto et al, 1988


Superficie fortemente irregolare

Capuccio fibroso sottile

Presenza di core anecogeno ampio

La percentuale di stenosi non è più rilevante

J.Willet Cerebrovasc Dis. 10 suppl. 5, 2000

Placca carotidea a “rischio” o

“instabile” (2000)


Stroke. 2006;37:2696-2701


Flogosi (la placca recentemente sintomatica presenta i nfiltrazioni di macrofagi e linfociti T)

Neovascolarizzazione (contiene microvasi immaturi)

Fattori plasmatici dell’angiogenesi e della flogosi nei pazienti sintomatici

Infezione (cellule correlate alla presenza di sostanze batteriche o virali)

Connessione fra infezione e placca sintomatica

Placca carotidea “instabile”

(2006-2007)


“Susceptibility of a plaque to rupture thus causing a clinical cardiovascular event.”

Placca carotidea “vulnerabile”

(2012)

% stenosi > 70% pressione parietale/shear stress basso e incostante infiammazione/neovascolarizzazione cappuccio fibroso sottile fissurazione cappuccio fibroso denudazione endoteliale ampia presenza di lipidi


Radiology 2009 251:2 583-9


Carotid EndarterectomySYMPTOMATIC PATIENTS

NASCET ≥ 70 NASCET 50-69 ECST ≥ 80-5%

0%

5%

10%

15%

20%

25%

30% 26.0%

22.2%20.6%

9.0%

15.7%

6.8%

MED SURG

p < .001

p < .001

p = .045


CASANOVA VA ACAS ACST0

5

10

15

20

25

10.7

8

5.16.4

11.3

20.6

11 11.7

CEA MEDICAL

ns

p <0.01

p <0.01p <0.001

CEA vs MEDICALAsymptomatic Stenosis


Relationship Between Severity of Stenosis and Stroke Rate

Stenosis NASCET (2 year) ECST (3 years) ACAS (3 years)

60%-69% 428 13% 137 11% 131 6%

70%-79% 43 21% 170 9% 94 5%

80%-89% 33 27% 159 21% NS

90%-99% 24 35% 60 32% NS

80%-99% 57 31% 219 24% 88 3%

Stroke. 2000;31:774-781


Estimates of NNT with CEA to prevent 1 stroke in 2 years by age and degree of

stenosis

Patient group NNT

Symptomatic

≥ 70% stenosis age < 75 yr 6

≥ 70% stenosis age ≥ 75 yr 3

50%-69% stenosis 15

< 50% No benefit

Asymptomatic

> 60% stenosis 83

CMAJ • AUG. 31, 2004; 171 (5)


Stroke. 2010;41:e11-e17.


“I pazienti con una stenosi carotidea in progressione sono ad alto rischio per eventi maggiori alle coronarie ed alla circolazione periferica e cerebrale (MACE : IMA, Stroke, Amputazione, Morte)”

“L’infiammazione al centro della disfunsione endoteliale e della crescita della placca”

“Ripetuti controlli ECD dovrebbero essere eseguiti nei pazienti con placche e stenosi moderate alla ricerca di una malattia progressiva”


Number of Events in Patients With and Without CAS (during follow up)

Asynt CAS (n 221)

No Asyntom (n 2463)

Non vascular death 8% 3%

Vascular death 15% 5%

MI 13% 6%

Ischemic Stroke 3% 2%

All first vascular events 20% 9%

CEA 6% 0%

Endovascular interventation 2%

Stroke. 2007;38:1470-1475.


From: Screening for Carotid Artery Stenosis: U.S.Preventive

Services Task Force Recommendation Statement

http://www.ahrq.gov/


Comment: The perceived effectiveness and cost-effectiveness of carotidduplex ultrasound surveillance programs should be questioned. Thestudy raises a significant question: Do carotid duplex surveillance programs primarily benefit physicians, vascular laboratories, or patients? The fact that 40% of the patients had only two duplex ultrasound scans performed during the surveillance period is a serious study limitation. Follow-up was, however, comparable to other studies in the literature and therefore the results likely can be generally applied to other practices. The personal and economic impact of stroke is huge, but this report still calls into serious question the use of limited health care resources to fund carotid duplex surveillance programs.

Conclusion: Carotid duplex ultrasound surveillance programs are costly and inefficient.


Despite these advances in understanding the pathophysiology of atherosclerotic plaque, the utility of morphological, pathological, and biochemical features in predicting the occurrence of TIA, stroke, or other symptomatic manifestations of ECVD has not been established clearly by prospective studies.


Conceptually, the presence of a vulnerable plaque is, by definition, a probabilistic entity. It does not denote the occurrence of an event at present but rather a higher risk for such occurrence in the future relative to a non vulnerable or less vulnerable plaque. As such, before it is widely adopted by clinicians, plaque vulnerability (if validated) should be able to provide incremental predictive value on top of currently available methods of risk stratification, which may be less expensive and less invasive than the methods proposed to detect vulnerable plaques.


Moreover, the complex implications of such a probabilistic diagnosis are exemplified in the observation that not all plaques that rupture (the basis for the classic definition of the term) actually result in a clinical cardiovascular event. Some plaques would rupture and then become quiescent and heal without causing a myocardial infarction or stroke (so called silent plaque rupture). Conversely, not all acute cardiovascular events are the result of plaque rupture because non ruptured plaques have been implicated as culprit lesions nearly one third of the time in autopsy series.

s.c. angiologia medica - messina. rosamond w, flegal k, furie k, et al. heart disease and stroke...

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