La placca vulnerabile

Savona 2015

Francesco Prati

San Giovanni Hospital, Rome

Rome Heart Research

Vulnerable plaque

Identify and measure: Lipid pool, FC thickness, local

inflammation

• Large plaque burden

• Large lipid pool

• Thin fibrous cap

Features of plaque vulnerability

• Thin fibrous cap

• Small lumen area

• Inflammation

Histopathologic Characteristics of Atherosclerotic Coronary Diseaseand Implications of the Findings for the Invasiveand Noninvasive Detection of Vulnerable Plaques

Narula et al JACC 2013

Histopathologic Characteristics of Atherosclerotic Coronary Disease and Implications of the Findings for the Invasiveand Noninvasive Detection of Vulnerable Plaques

Narula et al JACC 2013

IVUS NIRS-IVUS OCT

High Res. 15 µ

Small Penetration

Res. 150 µ

Identif. of lipid

components

Res. 150 µ

Good penetration

Male, 58 y/o

14thJuly 2014: inferolateral STEMI treated with a DES in the RCA

17thJuly 2014: PCI OCT-NIRS-IVUS study of non culprit lesion in LCx

NIRS-IVUSOCT

Combined assessment

The role of local The role of local

inflammation?

Histopathologic Characteristics of Atherosclerotic Coronary Disease and Implications of the Findings for the Invasiveand Noninvasive Detection of Vulnerable Plaques

Narula et al JACC 2013

• Vulnerable plaques are mainly located in the proximal segments

Some reasons for searching plaque

vulnerability

located in the proximal segments of the coronary tree

Spatial lesion distribution.

Lesions are Lesions are located in the prox. segments

Cheruvu et al JACC 2007

86,8%

1,5%10,5%1,2%

Non Atheroscl. Thin Fibrous capMedium-Thick Fibrous cap Ruptured plaques

Frequencies of ruptured plaque and fibrous cap atheroma in all hearts studied provided as a percentage of the total 3,639 coronary intervals of length 3 mm examined.

• Only a few vulnerable lesions progress to

an acute coronary events (less than 5% in

the PROSPECTS)

• Dynamic changes of plaque vulnerability

Some reasons not to search plaque

vulnerability

• Dynamic changes of plaque vulnerability

• Search for lesions causing ischemia

• Need to obtain a functional assessment of

coronary lesions- Local Inflammation

Lessons from IVUS- VH

The PROSPECTThe PROSPECT

The potential of NIRS-IVUS

tu study lesion vulnerabilitytu study lesion vulnerability

LIPISCAN: NIR-IVUS

Madder et al. JACC Int 2013

The IVUS-NIRS

S. Giovanni Registry. Rome

• 45 patients studied pre intervention• 45 patients studied pre intervention

• Preliminary Results

NSTEMI 43%

yes

yesyes

yesyes

YesYesYes

yesyes

yes

SA 20% STEMI 71%

MAX LCBI > 400

yesyes

S. Giovanni Registry. Rome

Case n 2 S. Giovanni H. August 2012

62 Y7O Male with Infero-lateral STEMI

Clinical Case OCT vs NIRS

• S. L.

• Male, 64 years old

• Cardiovascular Risk factors

– Hypertension

– Family History of CAD– Family History of CAD

– Previous Smoking Habit

• 12th August 2014: infero-postero-lateral STEMI treated with primary PCI and DES of LCX

• 18th August 2014: PCI OCT-NIRS-IVUS guided of non culprit lesion (Distal Right Coronary Artery)

• S. L.

• Male, 64 years old

• Cardiovascular Risk factors– Hypertension

– Family History of CAD

– Previous Smoking Habit

• 12th August 2014: infero-

Clinical Case OCT vs NIRS

• 12th August 2014: infero-postero-lateral STEMI treated with primary PCI and DES of LCX

• 18th August 2014: PCI OCT-NIRS-IVUS guidance ofnon culprit lesion (DistalRight Coronary Artery)

ACS. Non culprit RCA lesion

CalciumA

A

LP?

Inflammatory

cells?

YES

Inflammatory

Cells + LP

B

B

MACE (20 pts) No MACE (20 pts) P

AGE 69.94±12.31 69.40±13.46 0.89

Female 3 (15%) 3 (15%) 0.65

STEMI 4 (20%) 5 (25%) 1

NSTEMI 3 (15%) 3 (15%) 0.65

Stable Angina 13 (65%) 12 (60%) 1

Current Smoker 7 (35%) 2 (10%) 0.12

Hypertension 17 (85) 16 (80%) 1

Dyslipidemia 11 (55%) 13 (65%) 0.74

CLIMA Trial. Clinical and Demographic data

Dyslipidemia 11 (55%) 13 (65%) 0.74

Family History of

CAD

2 (10%) 5 (25%) 0.40

Diabetes 4 (20%) 5 (25%) 1

Prior MI 5 (25%) 3 (15%) 0.69

Prior PCI 3 (15%) 8 (40%) 0.15

Prior CABG 0 0 ns

Creatinine pre 1.13±0.48 1.02±0.38 0.43

Creatinine post 1.30±0.56 1.09±0.39 0.22

LVEF 49.47±11.05 55.81±12.3 0.18

Multivessel Dis. 16 (80%) 11 (55%) 0.17

Left Main Disease 1 (5%) 1 (5%) ns

Clinical Case OCT vs NIRS 1

• T.D.

• Male, 58 years old

• Cardiovascular Risk factors

– Hypertension

– Dyslipidaemia– Dyslipidaemia

– Smoking Habit

• 14thJuly 2014: inferolateral STEMI treated withprimary PCI and DES of RCA

• 17thJuly 2014: PCI OCT-NIRS-IVUS guided of non culprit lesion (Marginal branch of Left Circumflex)

Ulceration NON Ulceration

OCT to address the mechanism of ACS

Calcific NoduleNo TCFA

CLIMA Registry

PreliminaryResults• 500 pts with OCT assessment of the LAD

– Segment lenght : 50 mm of prox LAD

• Mean clinical FU lenght of 2,7 y

• Correlation between plaque composition at OCT and • Correlation between plaque composition at OCT and

hard clinical end-point (cardiac death and anterior

MI)

• One to one comparison with matching process

(demographic and clinical) between the coronary

anatomy of 20 pts with MACE vs 20 pts of the

control arm

Firenze. Conoscere e Curare il Cuore 2015

Thrombogenic Plaque Vulnerable Plaque

A new classification

Conoscere e Curare il Cuore 2013

Vulnerable Plaques. Presence of all of the following 4 features.

TCFA<84 µ, LP arc>180 degrees, MLA <4mm2, Macrophages

60

MACE No MACE

% P<0.05

15

LP Arch > 180

MLA

<4mm2, TCFA

< 84 µ

Macrophages

%

55

40

50

60

MACE No MACE

%

Vulnerable Plaques. Calcific Nodules

P=0.06

25

0

10

20

30

40

Calcific Nodule

35

25

30

35

40

Thrombogenic Plaques.

MACE No MACE

%

P=NS

10

25

10

0

5

10

15

20

25

Layered Pl. Ulcerated Pl.

P=NS

Ulcerated Pl.Layered Pl.

Presence of at least one lesion with the following features.

TCFA<84 µ, LP arc>200µ, MLA <5mm2, Macrophages, Chol Crystals

MACE No MACE

9095

60

70

605555

P= 0.002P= 0.007

P= 0.20

P= 0.51

P= 0.055

40 4035

25 25

MLA < 4 TFC < 84 Lipid Arc >

180 0

Macroph. Chol. Crystals Calcif.

Nodules

P= 0.20 P= 0.055

P= 0.06

13,1

10,7

6060

70

P=0.17

P=0.019P=0.47

P=0.52

%

Vulnerable Plaques. Sites with Maximum LP extension

MACE No MACE

4,3

2,52

0,94

6,2

1,8 1,44

MLA Lenght Max LP arc TCFA

4545

20

0

10

20

30

40

50

P=0.17

P=0.009

P=0.011

Mm2 Mm Quadrants 100µ

4,8

10,7

5,86,4

55

45

40

50

60P=0.33

P=0.06

P=0.75

%

Vulnerable Plaques. Sites with Minimum FC Thickness

MACE No MACE

4,8

2,06

0,63

1,560,87

MLA Lenght Max LP arc TCFA

30

15

0

10

20

30

40

P=0.44

P=0.09

P=0.008

Mm2 Mm Quadrants 100µ

CLIMA Study

MACE group

FA: case n 8

FA. Male. 66 years

RF: None

November 2010: Admitted to S.Giovanni H for an Inferior

NSTEMI.

•OCT assessment of LAD for an intermediate lesion

November 2010:

• Admitted to S.Giovanni H for an

Inferior NSTEMI.

•OCT assessment of LAD for an

intermediate lesion

•Many plaques with features of

vulnerability

CLIMA Study

MACE group

MC: case n 15

October 2014: Sudden death

Prox

Mixed plaque

with

irregular surface

Lipid pool

Thin FC

Lipid pool

Thin FC

Small LA

LP Plaque

with

irregular surface

Lipid pool

Distal

Lipid pool

REF

The pt died

4 years

after

The OCT

study

MLA

4.3 mm2

FA. Male. 61 years

RF: Hypertension, Smoker

June 2010: Admitted to S.Giovanni H

June 2010: OCT studyVulnerable Plaques.

Lipid-necrotic plaque with

TCFA<84 µ, LP arc>200µ, MLA

<5mm2, Macrophages

June 2010: Admitted to S.Giovanni H

for an anterior STEMI.

OCT guided intervention

March 2012: New Anterior STEMI

March 2012

Acute thrombosis

CLIMA Study

MACE group

GR: case n 11

GR. Male. 61 years

RF: Hypertension, Smoker

2010: Admitted to S.Giovanni

Metti post ptca

CLIMA Study

MACE group

GR: case n 11

2010: Admitted to S.Giovanni

H for an anterior STEMI.

OCT guided intervention

FA. Male. 66 years

RF: None

2007: Admitted to S.Giovanni H

CLIMA Study

MACE group

FA: case n 8

2007: Admitted to S.Giovanni H

for an Inferior NSTEMI.

OCT assessment of LAD for an

intermediate lesion

Lipid pool

Old

Ulceration

Layered tissue

CLIMA Study

MACE group

FA: case n 8

Year 2007: OCT Study

Lipid pool

Calcific nodule with

regular surface

Calcific nodule

with

irregular surface2014: Sudden death

I nuovi trialsI nuovi trials

Prox

Mixed plaque

with

irregular surface

Lipid pool

Thin FC

Lipid pool

Thin FC

Small LA

LP Plaque

with

irregular surface

Lipid pool

Distal

Lipid pool

REF

The pt died

4 years

after

The OCT

study

Prox

January

OCT study. Dic 2009

for Stable Angina

Distal

January

2015

NO MACE

Take Home Message

– IVUS, NIRS-IVUS and OCT have recently offered new insights on the composition of vulnerable plaques

– Large superficial plaques with local inflammation and clacific nodules are features related to plaque and clacific nodules are features related to plaque vulnerabilty

– Pheraps in the next future IC imaging will be used to identify vulnerable plaques to be treated with stenting or vulnerable patients to be treated with a more aggressive drug treatment.

Clinical Case OCT vs NIRS 2

• S. L.

• Male, 64 years old

• Cardiovascular Risk factors

– Hypertension

– Family History of CAD– Family History of CAD

– Previous Smoking Habit

• 12th August 2014: infero-postero-lateral STEMI treated with primary PCI and DES of LCX

• 18th August 2014: PCI OCT-NIRS-IVUS guided of non culprit lesion (Distal Right Coronary Artery)

• non culprit

lesion of RCA

De vecchis fu

°

FC THICKNESS

MIN: 73µ

MACROPHAGES

LIPID POOL LENGHT 20.2mm

MAX

LIPID POOL ARC: 237°

CALCIFIC PLAQUE

MAX CALCIFIC PLAQUE ARC: 36°