Le espressioni della placca che preoccupano il clinico: progressione o vulnerabilità? CardioLUCCA Marzo 2017 F Prati San Giovanni H. and CLI Foundation, Rome Euro Image Research
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
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). Date of download: 5/12/2016 Copyright The American College of Cardiology. All rights reserved.
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?
Features of plaque vulnerability Large plaque burden Large lipid pool Thin fibrous cap Small lumen area Inflammation
The concept of plaque vulnerability IVUS NIRS-IVUS OCT Res. 150 µ Good penetration Res. 150 µ Identif. of lipid components High Res. 15 µ Small Penetration
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 HRP was defined as plaque with PR (RI >1.1) and/or LAP ( > 30 HU).
Plaque characterisation by CTA HRP was defined as plaque with PR (RI >1.1) and/or LAP (>30 HU) 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.
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 14 th July 2014: inferolateral STEMI treated with a DES in the RCA 17 th July 2014: PCI OCT-NIRS-IVUS study of non culprit lesion in LCx OCT NIRS-IVUS
New trials
Milano, Monzino Bologna Sant Orsola Cotignola GVM Care and Research Grosseto. Misericordia Siena. Sant Anna Roma S Giovanni Roma Pol Gemelli Isernia. Veneziale Warsav Military Hosp. Madrid S. Carlos Brotzu Cagkiari Caltanisetta, Sant Elia Messina. G Martino Catania,Ferratto Siracusa Umberto I
ClinicalTrials.Gov 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 mm 2 Macrophages Clinical outcome Macrophages MLA <4 mm 2, TCFA <70 µm Composite of cardiac death and/or target vessel MI (STEMI/NSTEMI) LP arc >180º F Prati et al. LP, lipid pool.
Lipid pool Thin FC Small LA Lipid pool Thin FC Mixed plaque with irregular surface LP Plaque with irregular surface Prox Lipid pool The pt died 4 years after The OCT study Distal REF
Che cosa preoccupa il cardiologo clinico? Presenza di aterosclerosi Vulnerabilità di placca/paziente Progressione di malattia
EEM CSA is the external elastic membrane cross-sectional area, LUMEN CSA is the luminal cross-sectional area. Change in percent atheroma volume (PAV) = PAV (end of treatment) PAV (baseline). PAV Reduct. 1%
Improvement of lipid profile 27 26 25 24 23 Euroimage Research 27 Clinical benefit 22 21 20 Regression of atherosclerosis 26 25 24 Primary end-point 23 22 21 20 Primary end-point Pravastatin 40 mg Atorvastatin 80 mg Prava mg Atorv 80 m PROVE-IT N Engl J Med 2004
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 Souteyrand 1, P Motreff 1, L Di Vito 2, V Marco 2, N Amabile 3, A Chisari 2, T Kodama 4, L Tavazzi 5, Jagat Narula 6, F Crea, E Arbustini 4, F Prati 2 Eurointervention 2014 EROSION Post intervention and FU assessment 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
Clinical Case OCT vs NIRS S. L. Male, 64 years old Cardiovascular Risk factors Hypertension Family History of CAD Previous Smoking Habit 12 th August 2014: inferopostero-lateral STEMI treated with primary PCI and DES of LCX 18 th August 2014: PCI OCT- NIRS-IVUS guidance of non culprit lesion (Distal Right Coronary Artery)
ACS. Non culprit RCA lesion Calcium YES Inflammatory cells? FC Thick 0,07 mm LP? Inflammatory Cells + LP
OCT to address the mechanism of ACS Ulceration NON Ulceration No TCFA Calcific Nodule
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 12 th August 2014: infero-postero-lateral STEMI treated with primary PCI and DES of LCX 18 th August 2014: PCI OCT-NIRS-IVUS guided of non culprit lesion (Distal Right Coronary Artery)