La placca vulnerabile Savona 2015 Francesco Prati San Giovanni Hospital, Rome Rome Heart Research
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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°
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