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F Prati
San Giovanni H. and CLI Foundation, Rome
Le espressioni della placca che
preoccupano il clinico: progressione o
vulnerabilità?
Euro Image Research
CardioLUCCA
Marzo 2017
Che cosa preoccupa il cardiologo clinico?
• Presenza di aterosclerosi • Vulnerabilità di placca/paziente • Progressione di malattia
First of all look carefully at the coronary angiogram ………….Absence of significant narrowing does not mean much !
Male 65 Years. Anterior NSTEMI with mild increase in Troponin and T wave inversion
Mild vesssel irregularities = Atherosclerosis
Male 63 Years Effort and rest chest pain. Angina?
Marked vessel irregularities = Advanced stage atherosclerosis
Female 81 Years NSTEMI triggered by high blood pressure
Smooth vessels = No Atherosclerosis
Date of download: 5/12/2016 Copyright © The American College of Cardiology. All rights reserved.
From: CORONARY ARTERY CALCIUM SCORE IS SUPERIOR TO CAROTID PLAQUE SCORE FOR PREDICTING
CARDIOVASCULAR DISEASE EVENTS: THE MULTI-ETHNIC STUDY OF ATHEROSCLEROSIS
J Am Coll Cardiol. 2016;67(13_S):1557-1557. doi:10.1016/S0735-1097(16)31558-3
At baseline, the 4955 participants were mean (standard deviation) 61.6 (10.1) years old and 52.8% female; 48.9% had
CAC and 50.8% had at least one carotid plaque. After 11.3 (3.0) years of follow-up, 709 CVD, 498 CHD, and 262
stroke/TIA events occurred. The CAC score was a stronger predictor of CVD and CHD and had better reclassification
statistics than carotid plaque score, except for stroke/TIA (Table).
A zero coronary artery calcium score
Hecht et al JACC 2010
Che cosa preoccupa il cardiologo clinico?
• Presenza di aterosclerosi • Vulnerabilità di placca/paziente • Progressione di malattia
What is the best way to detect atheroscerosis ?
• Should we rely on extension of CAD: 1,2 or 3 vessel
disease? • Should we rely on presence of peripheral
atherosclerosis ? • Should we try something new ?
• i.e. Assessment of the exact amount of plaque volume at CT scan for primary prevention
• i.e Assessment of plaque composition with IC imaging for secondary prevention
Why IC Imaging?
• Large plaque burden • Large lipid pool • Thin fibrous cap • Small lumen area • Inflammation
Features of plaque vulnerability
IVUS NIRS-IVUS OCT
High Res. 15 µ Small Penetration
Res. 150 µ Identif. of lipid components
Res. 150 µ Good penetration
The concept of plaque vulnerability
HRP was defined as plaque with PR (RI >1.1) and/or LAP ( > 30 HU).
Plaque Characterization by Coronary Computed Tomography Angiography and the Likelihood of Acute Coronary Events in Mid-Term Follow-Up Motoyama S et al. JACC 2015
Plaque characterisation by CTA
Motoyama S, et al. J Am Coll Cardiol 2015;66:337–46. CTA, computed tomography angiography; HRP, high-risk plaque;
LAP, low attenuation plaque; PR, positive remodelling; SS, significant stenosis.
HRP was defined as plaque with PR (RI >1.1) and/or LAP (>30 HU)
Histopathologic Characteristics of Atherosclerotic Coronary Disease
and Implications of the Findings for the Invasive and Noninvasive Detection of Vulnerable Plaques
Narula et al JACC 2013
Histopathologic Characteristics of Atherosclerotic Coronary Disease
and Implications of the Findings for the Invasive and Noninvasive Detection of Vulnerable Plaques
Narula et al JACC 2013
Local inflammation
Di Vito L, Agozzino M, Marco V, Ricciardi A, Concardi M, Romagnoli E, Gatto L,
Calogero G, Tavazzi L, Arbustini E, Prati F. Identification and quantification of
macrophages presence in aterosclerotic plaques by OCT. Eur Heart J Cardiovasc
Imaging. 2015;16:807-813
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-IVUS OCT
New trials
Catania,Ferratto
Siracusa Umberto I
Messina. G Martino
Roma S Giovanni Roma Pol Gemelli
Bologna Sant’Orsola
Milano, Monzino
Cotignola GVM Care and Research
Grosseto. Misericordia
Isernia. Veneziale
Siena. Sant’Anna
Caltanisetta, Sant’Elia
Brotzu Cagkiari
Madrid S. Carlos
Warsav Military Hosp.
N 700 pts
OCT vulnerable plaque criteria
Lesion presenting all of the
following four features:
• TCFA <65 μm
• Lipid pool arc >180º
• MLA <4.0 mm2
• Macrophages
Clinical outcome
Composite of cardiac death and/or target vessel MI (STEMI/NSTEMI)
F Prati et al. LP, lipid pool.
LP arc
>180º
MLA
<4 mm2, TCFA
<70 µm
Macrophages
ClinicalTrials.Gov
Distal
Prox
Mixed plaque with
irregular surface
Lipid pool Thin FC
Lipid pool Thin FC
Small LA
LP Plaque with
irregular surface
Lipid pool
REF
The pt died 4 years
after The OCT
study
Che cosa preoccupa il cardiologo clinico?
• Presenza di aterosclerosi • Vulnerabilità di placca/paziente • Progressione di malattia
EEMCSA is the external elastic membrane cross-sectional area ,
LUMENCSA is the luminal cross-sectional area.
PAV Reduct. 1%
Change in percent atheroma volume (PAV) = PAV (end of treatment) − PAV (baseline).
Improvement of lipid
profile
Regression of atherosclerosis
Clinical benefit
PROVE-IT N Engl J Med 2004
20
21
22
23
24
25
26
27
Primary end-point
Pravastatin 40
mgAtorvastatin
80 mg
20
21
22
23
24
25
26
27
Primary end-point
Pravastatin 40
mgAtorvastatin
80 mg
Euroimage Research
How to identify lesions that
progress vs vulnerable lesions
I doubt it can be done
Kolodgie et al. Heart 2004
Ruptured and healed plaques are
more severely narrowed
G Souteyrand1, P Motreff1, L Di Vito2, V Marco2, N Amabile3, A Chisari2, T Kodama4, L
Tavazzi5, Jagat Narula6, F Crea , E Arbustini4, F Prati2
Post intervention
and FU assessment
Eurointervention 2014
EROSION
The healing process after rupture
often leads to plaque progression
…..yet 88.2% of patients with similar plaques did not have a major adverse cardiovascular event in a nonculprit lesion during 3.4 years of follow-up.
Attilio Maseri, Enrico Ammirati, Francesco Prati
Corerspondence N Engl J Med 2011
• In many ACS studies it is difficult to
distinguish events related to plaque
rupture/erosion from those caused by plaque
progression
• Soft end-point are included like
hospitalization due to angina that may be
due to plaque progression
Take Home Message – Identification of atherosclerosis is key for primary
prevention
– Recent studies showed that it is rationale to identify pts at higher risk of coronary event and put them on a more agrresive anti-thrombotic therapy
– Imaging modalities (CT for primary prevention) and IC imaging modalities (OCT for secondary prevention) potentially better identify patients with a more aggressive atherosclerosis
– 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.
– Plaque progression is related to a worse clinical outcome and can be caused by plaque healing after rupture
Madder et al. JACC Int 2013
• S. L. • Male, 64 years old • Cardiovascular Risk factors
– Hypertension – 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 guidance of non culprit lesion (Distal Right Coronary Artery)
Clinical Case OCT vs NIRS
ACS. Non culprit RCA lesion
LP?
Inflammatory cells?
Calcium
YES
Inflammatory Cells + LP FC Thick 0,07 mm
Ulceration NON Ulceration
OCT to address the mechanism of ACS
Calcific Nodule No TCFA
Take Home Messages
– 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 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
– 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)