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CTCA - CT Coronary Angiography Plaque Characterization
- 1. Plaque Characterization Dr. Pankaj Saini ARTEMIS HOSPITALS Sr. Consultant MEDICAL IMAGING CT
- 2. Welcomeā¦
- 3. Plaque Characterization CORONARY IMAGING TECHNIQUES INVASIVE PROCEDURE Catheter Coronary Angiography Invasive Ultrasound Fractional Flow Reserve Optical Coherence Tomography NONVASIVE PROCEDURE ChestX-Ray Echocardiography
- 4. Invasive procedures Catheter Angiography (ICA) Minimally invasive Dr. Mason Sones Cleveland Clinic - 1958 Major epicardial vessels branches with the 2nd & 3rd order branches
- 5. Invasive procedures ā¢ Fractional Flow Reserve (FFR) ā¢ Physiological evaluation ā¢ Pressure sensitive wire ā¢ 2mm distal to stenosis ā¢ gradient to Aorta ā¢ < .80 Ischemia
- 6. Invasive procedures ā¢ Invasive Ultrasound ā¢ Lipid core thickness ā¢ Vulnerable Plaque characterization ā¢ Diagnostic modality superseded by Non Invasive ā¢ PROSPECT Trial
- 7. Non Invasive Procedures ā¢ X-Ray ā¢ Nuclear medicine ā¢ MPI - Myocardial perfusion imaging ā¢ Thallium 201/Technitium 99m ā¢ MRI and CT ā¢ Calcium scoring - surrogate marker of CAD
- 10. MDCT ā¢ Temporal Resolution ā¢ Contrast Resolution ā¢ Spatial Resolution ā¢ Voxel Size ā¢ Kv -120 / MAS - 800 ā¢ Contrast - 2 ml/kg - 80ml ļ§ High Pitch ļ§ 16 cm in a single beat ļ§ Iso-temporal Resolution ļ§ Rotation time ļ§ Over / Under Estimation
- 11. Image Acquisition MIP - Maximum Intensity Projection
- 13. Image Acquisition MPR - Multi-planar Reconstruction
- 17. RCA and Branches Originates from right coronary sinus of Valsalva Courses through the right AV groove between the right atrium and right ventricle to the inferior part of the septum
- 18. RCA and Branches ā¢ Conus Branch ā¢ Sinu Nodal Branch ā¢ Marginal Artery ā¢ Post Descending IV Artery ā¢ AVNodal Branch
- 19. RCA and Branches ā¢ Conus Branch ā¢ The first branch 50% ā¢ Arise from aorta ā¢ Supplies the RVOT
- 20. RCA and Branches ā¢ Sinu Nodal Branch ā¢ SecondBranch ā¢ Supplies the SANode ā¢ 40% originate from the LCA
- 21. RCA and Branches ā¢ Acute Marginal Artery ā¢ RV myocardial supply ā¢ Arise at an acute angle and runs along the margin of the right ventricle above the diaphragm
- 22. RCA and Branches ā¢ Post Descending Artery ā¢ Supplies lower part of the ventricular septum & adjacent ventricular wall of LV (inferior ventricular artā) ā¢ Dominance ā¢
- 23. LCA and Branches ā¢ Arises from left coronarycusp ā¢ Left main travels between RVOT anteriorly andleft atrium posteriorly ā¢ Length ā 5 to 10mm ā¢ Almost immediately bifurcate ā¢ left anterior descending ā¢ left circumflex artery ā¢ ramus intermedius
- 24. LCA and Branches ā¢ Ramus intermedius ā¢ Commonest variation ā¢ Trifurcation
- 25. LCA and Branches ā¢ Left anterior descending ā¢ Anterior inter-ventricular septum runningbehindthe auriculum ā¢ Diagonal Branches ā¢ Septal Perforators ā¢ Myocardial bridging ā¢ More commonly seenon CT
- 26. LAD - Bridging
- 27. LCA and Branches ā¢ Left Circumflex artery ā¢ Posterior AV groove ā¢ Obtuse Marginal Artery ā¢ Lateral wall of LV
- 28. Atherosclerosis
- 29. The āEvolutionā of Coronary Atherosclerosis Normal Artery Lesion Initiation Fibro-fatty Stage Vulnerable Plaque Plaque Rupture Fibrous, Calcified Plaque Endothelial Erosion Progression over time (yrs):
- 31. Type I - Initial Stage ā¢ Isolated macrophage ā¢ Foam cell accumulation ā¢ Diffuse intimal thickening ā¢ Atriskarteries ā¢ Risk factors ā¢ Hypertension ā¢ Smoking ā¢ Diabetesā¢ Endothelial dysfunction ā¢ Monocytes migrate into the endothelium differentiate into macrophages ā¢ Digest the low density lipoprotein to transform to foam cells
- 32. Type II - Fatty Streak ā¢ Intracellular Lipid accumulation ā¢ Fatty streak ā¢ Progress to ATHEROMA
- 33. Type III - Intermediate ā¢ Extracellular lipid pool ā¢ Pathological intimal thickening ā¢ Smooth muscle cells ā¢ Collagen matrix ā¢ Lipid pool ā¢ Clinically silent
- 35. Type IV - Atheroma ā¢ Additionally extracellular lipidcore ā¢ LD - NCP (<30 HU)
- 36. ā¢ Lipid core ā¢ Necrotic core with free cholesterol ā¢ Calcification - SC ā¢ Thick fibrous cap ā¢ > 0.25mm ā¢ Smooth muscle &Collagen Type IV - Atheroma
- 37. Stable Plaque
- 38. Type V - Fibroatheroma ā¢ Thin CappedFibroAtheroma ā¢ TCFA- <65 Ī¼m ā¢ Vulnerable Plaque
- 39. ā¢ Lipidcore ā¢ Fibroticlayer with calcification ā¢ Thin fibrous cap ā¢ Remodeling ā¢ Complex plaque ā¢ Accelerated smoothmuscle proliferation Type V - Fibroatheroma
- 40. Vulnerable Plaque ā¢ Potential to rupture ā¢ Macrophage ā¢ Necrotic core size ā¢ Intra-plaque hemorrhage ā¢ Positive remodeling
- 41. Napkin Ring Sign ā¢ Plaque Rupture Predictors ā¢ Fibrous cap thickness ā¢ Necrotic core size (>3.5mm) ā¢ Thin cap fibro-atheroma Vs. Stable lesion ā¢ Necrotic Core and Macrophage infiltrate ā¢ Central low attenuation in contact with lumen ā¢ Surrounding ring like higher attenuation plaque
- 42. Napkin Ring Sign
- 43. Type VI - Complicated ā¢ Calcification upto 69 % ā¢ Inflammatory cells ā¢ Ulcerated plaque
- 44. Type VI - Complicated ā¢ TCFA+ Rupture fibrous cap ā¢ Intra-luminal thrombus ā¢ Coagulationcascade activation ā¢ Occlusion ā¢ Acute coronary syndrome
- 45. ACS - Occlusion Ischemia ā Cell Death
- 46. Natural History of Coronary Atherosclerosis angina or ACSvulnerability likelihood of vulnerability or progression Quiescent, Stable plaque no symptoms Fibrotic/ Scarred plaque angina Vulnerable, Ruptured Plaque ACS ?
- 48. ā¢ 50% Stenosis - LAD ā¢ Positive remodeling ā¢ LAP + Calcified Plaque
- 49. Looking backā¦ ā¢ Large Plaque Volume ā¢ High risk plaque ā¢ Low attenuation (<30 HU) ā¢ Remodeling (and / or) ā¢ Napkin Ring sign ā¢ Spotty Calcification ā¢ Significant stenosis ā¢ CTCA detected plaque progression independent predictor of ACS ā¢ 38.98 % ACS ā¢ Non invasive Detection of vulnerable plaques by CTCA Motoyama et al ā JACC Vol 6, 2015
- 50. Looking forward ā¦ ā¢ Diffuse disease ā¢ Addressedin entirety ā¢ HRP burden ā¢ Plaque Character - ACS ā¢ Treatmentand followup ļ§ Atherosclerotic plaque characterization ļ§ Fractional flow reserve ā CT ļ§ Endothelial shear stress ā CT ļ§ 5% APV ā 50% risk of ischemia ļ§ LAP & SC ā Future ACS Hyung B Park et al ā JACC Vol 8, 2015
- 51. Thank Youā¦
Editor's Notes
- Despite significant advances in risk assessment and treatment coronary artery disease (CAD) remains the single leading cause of death with the majority of them being related to acute coronary syndrome (ACS) affecting to up to 19 million people world wide often in patients with low to intermediate risk profile.In the face of mounting evidence that interventional treatment of coronary stenosis does not significantly improve prognosis. It becomes imperative to prophylactically diagnose CAD.
- The composition of coronary atherosclerotic plaque ā CT atherosclerotic plaque characterization (APC) shows more predictive value for plaque rupture, thrombosis and ischemic event than the severity of luminal stenosis alone as predicted by the gold standard to lesion ischemia shown by fractional flow reserve (FFR).
- Fractional flow reserve (FFR) ā the physiological evaluation of coronary lesion at the time of invasive coronary angiography, being the gold standard. FFR is measured in 30 to 90% stenotic lesions by passing a pressure monitoring guide wire distal to the stenosis, after administration of nitroglycerine. Intraveinous or intracoronary adenosisne (140 Microgram/kg/min) is administered to induce hyperaemia and FFR is calculated by dividing mean distal coronary artery pressure by the mean aortic pressure in hyperaemia with the threshold of .80 or less being considered hemodynamically significant for causing ischemia.
- The multicentre Providing Regional Observations to Study Predictors of Events in the Coronary Tree (PROSPECT) trial strongest predictor of future events was the IVUS-derived plaque burden of ā„70%
- CT plaque characterization and quantification is limited by temporal, spatial and contrast resolution of the current equipment. Volume scanners ā increasing the z-axis in a high pitch scanner to cover the 16cm in the shortest scan time (single beat) and decrease the contrast media attenuation gradient (isotemporal resolution) and faster rotation time by dual source scanners. Voxel size ā limitations are evident as overestimation of calcified plaque and underestimation of a soft plaque by volume averaging especially when surrounded by high density contrast.
- It is a type of Arteriosclerosis that most commonly affects the aorta and the coronary arteries causing them to become less flexible, weak and narrow occurring by fatty build up in the inner lining of the vessels that is called plaque. It thus reduces the amount of oxygenated blood delivery.
- A lot of work has been done on plaque characterization of the aorta and the carotid arteries in vivo however the imaging of coronary artery is limited by respiratory and cardiac motion, the tortuous course and the small size of the vessels.
- Type I and II AHA Classification cause minor morphologic changes which may be present as early as the first decade and are invisible on the current resolution of clinical CT and MRI.
- spotty calcification is defined as a small, dense (&gt;130 HU) plaque component surrounded by noncalcified plaque tissue a small calcification in CCTA as spotty is &lt;3 mm.16,36,53 Spotty calcifications have been further differentiated into small (&lt;1 mm), intermediate (1ā3 mm), and large (&gt;3 mm) calcifications. Small spotty calcification has the strongest association with vulnerable plaque features
- (A) Multiplanar reformat and short-axis view of the CTA in the proximal left anterior descending coronary artery. CTA demonstrates mild diameter stenosis with PR (remodelling index 1.15) and LAP (yellow circle, 24 HU). Corresponding images of ICA (B) and OCT (C and D). (D) Yellow arrow shows macrophage infiltration (superficial high-intensity signal band underlying a low signal area), and yellow circle shows thin fibrous cap, indicating TCFA with macrophage. CTA, coronary CT angiography; LAP, low attenuation plaque; OCT, optical coherence tomography; PR, positive arterial remodelling.
- Type III and IV occur from the 3rd decade.
- Positive remodeling is associated with abundance of macrophages and large necrotic core. A remodelling index threshold of ā„1.1 was suggested for the definition of positive remodelling visualized by CCTA which correlates well with IVUS and CCTA shows trend towards overestimation.
- Stable plaque. Optical coherence tomography (A), coronary angioscopy (B), intravascular ultrasound (C), angiography (D), volume-rendered (E), and curved multiplanar reformation (F) images were obtained from a culprit lesion with a stable plaque in a 57-year-old male presenting with stable angina. Optical coherence tomography revealed a thick fibrous cap (A) with smooth lumen. Coronary angioscopy (B) showed a pale white and smooth surface to the plaque. Intravascular ultrasound (C) revealed focal calcium deposits in the plaque. Angiography (D) and volume-rendered computed tomographic images (E) disclose a significant stenosis in the distal segment of the left anterior descending coronary artery (yellow arrow in D and E). The curved multiplanar reformation computed tomographic image (F) indicates the absence of positive remodelling with focal calcium deposits (yellow arrow in F).
- The limited spatial resolution of current CT scanners (ā 400 Ī¼m) precludes the morphometric analysis of fibrous cap by CCTA In TCFAs the necrotic core length is ~2ā17 mm (mean 8 mm) and the area of the necrotic core in 80% of cases is &gt;1.0 mm
- The limited spatial resolution of current CT scanners (ā 400 Ī¼m) precludes the morphometric analysis of fibrous cap by CCTA In TCFAs the necrotic core length is ~2ā17 mm (mean 8 mm) and the area of the necrotic core in 80% of cases is &gt;1.0 mm
- Vulnerable plaque ā due to potential to rupture with morphological and biological characterization ā inflammatory activity, necrotic core size, neovascularization, intraplaque hemorrhage and positive vessel wall remodeling.
- The napkin-ring sign is a qualitative plaque feature, whereāØthe central area of low CT attenuation is apparently in contact with the lumen.
- Cross-sectional CT showing coronary plaque with napkin-ring sign and spotty calcification. The napkin-ring sign is a qualitative plaque feature, wherethe central area of low CT attenuation is apparently in contact with the lumen. The circumferential outer rim (red dashed line) of the noncalcified plaque has a higherCT attenuation. a | Non-contrast-enhanced cross-sectional CT. b | Contrast-enhanced cross sectional CT. c | Histopathology reveals a thin-cap fibroatheroma with spotty calcification. The necrotic core (stars) correlates with the low-attenuation plaque core on the CT images. The outer-rim attenuation (red dashed line) corresponds to the fibrous plaque tissue. Abbreviation: L, coronary lumen.
- Unlike plaque rupture erosive plaques are characterized by fewer inflammatory cells and non occlusive thrombus. Plaque calcification is present in 69% of ruptured plaques versus 23% of the superficially eroded plaques. Main cellular components characterizing atherosclerotic plaque formation and destabilization are illustrated as well as biological and morphological features occurring in vulnerable plaque. SMCs: Smooth muscle cells; LDL: Low density lipoprotein; MMPs: Matrix metalloproteases.
- Plaque rupture or endothelial erosion activate and accelerate the coagulation cascade causing the rapid development of intraluminal thrombus and occlusion causing the acute coronary syndrome. In a majority of cases it may remain subclinial and silent with the necrotic core being washed to become an ulcerated plaque or Extended plaque calcification (Type VI) with calcification (Type VII) fibrocalcific plaque and may be associated with moderate to sever stenosis. Type IV, V and VI may be clinically silent or overt with ACS. Type V and VI appear from the 4th decade of life.
- Progression of the Atherosclerotic plaque and characterization Aim is to replicate the plaque classification achieved by the American Heart Association as closely as the histo-pathological grading by radiological imaging.
- The morphology and functional characteristics of stable and vulnerable plaques. a | Stable fibrocalcific lesion with calcification and small lipid pools.The plaque leads to mild narrowing of the lumen; however, there is no ischaemia after the lesion (FFR &gt;0.8; green). ESS near the plaque is in the normal physiological range indicating undisturbed flow. b | Rupture prone vulnerable plaque with a large lipid-rich necrotic core, thin fibrous cap, neovascularization, spotty calcium and presence of inflammatory cells. Despite the positively remodelled vessel wall at the site of the plaque, the lesion causes severe luminal narrowing and ischaemia (FFR &lt;0.8; red). The downstream plaque region with low and oscillatory ESS promotes plaque growth, whereas the upstream low ESS at the shoulder regions is more inflamed (indicated by presence of macrophages), which might lead to plaque destabilization. High ESS at the most stenotic part can trigger plaque rupture. Abbreviations: ESS, endothelial shear stress; FFR, fractional flow reserve.
- Stenosis &gt;50%: severe stenosis of the mid left anterior descending coronary artery(red arrow). Positive remodeling: Noncalcified plaque with positive remodeling in the distal right coronary artery. The 2 dotted red lines demonstrate the vessel diameters at the proximal and distal references (both 1.8 mm), and the solid red line demonstrates the maximal vessel diameter in the mid portion of the plaque (2.7 mm). The remodeling index is 1.5. Low Hounsfield units (HU) plaque: partially calcified plaque in the mid right coronary artery with low &lt;30 HU plaque. The red circles demonstrate the 3 regions of interest, with mean computed tomography (CT) numbers of 22 HU, 19 HU, and 20 HU. Napkin-ring sign: napkin-ring sign plaque in the mid left anterior descending coronary artery. Schematic cross-sectional view of the napkin-ring sign. The red line demonstrates the central low HU area of the plaque adjacent to the lumen (yellow ellipse) surrounded by a peripheral rim of the higher CT attenuation (red arrows). Spotty calcium: partially calcified plaque in the mid right coronary artery with spotty calcification (diameter &lt;3 mm in all directions;red circles). ACS 1ā4 acute coronary syndromes; RR 1ā4 relative risk.
- High risk plaque ā Low attenuation (&lt;=30 HU) and or positively remodeled plaques on CTA with significant (70%) stenosis correlate with 38.98% ACS and without stenosis to 14.9% ACS in a prospective trial with 3158 subjects(Ref Motoyama et al ā JACC Vol 6, 2015) Additionally CTA detected Plaque progression was an independent predictor of ACS.
- Here we will discuss the possibilities and limitations of CTCA in the evaluation of atheromatous coronary artery plaques, including aggregate plaque volume (%APV), positive remodeling (PR), low attenuation plaque (LAP) and spotty calcification (SC) with future coronary syndrome however their relationship to lesion ischemia remains unclear (JACC 2015, vol 8). % APV association with 50% increased risk of ischemia per 5% increase APV. PR, LAP and SC associated with 3 to 5 times higher with ischemic lesion. PR remained an indicator for ischemia when examined with stenosis severity. %APV and LAP are indicators in &gt;50% stenosis and not below that. FFR has shown the poor correlation of stenosis severity to ischemia, with almost half of severe stenosis causing no ischemia.