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Imaging of Vulnerable Plaque — 60 FAQs (5 Points Each)

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1. What is a vulnerable plaque?

1. Plaque prone to rupture or erosion
2. Characterized by thin fibrous cap
3. Large lipid/necrotic core
4. High inflammatory activity
5. Often non-obstructive angiographically

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2. Why is stenosis severity a poor predictor of MI?

1. Most MIs arise from <50% lesions
2. Angiography shows lumen, not wall
3. Positive remodeling masks severity
4. Biology outweighs geometry
5. Proven in pathology–angiography studies

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3. What defines thin-cap fibroatheroma (TCFA)?

1. Fibrous cap <65 µm
2. Lipid-rich necrotic core
3. Macrophage infiltration
4. Rupture-prone morphology
5. Best visualized by OCT

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4. Which modality best identifies TCFA?

1. OCT has highest axial resolution
2. Measures cap thickness directly
3. Identifies rupture vs erosion
4. Detects macrophages
5. Superior to IVUS and CT

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5. Why is OCT not used to guide preventive PCI?

1. TCFA often heals spontaneously
2. Many TCFAs never rupture
3. Vulnerability is dynamic
4. No outcome-driven trial support
5. Guidelines discourage prophylactic stenting

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6. What is plaque burden and why is it important?

1. Total atherosclerotic volume
2. Assessed best by IVUS
3. Strong predictor of future events
4. More important than stenosis
5. Proven in PROSPECT trial

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7. Key findings of the PROSPECT trial?

1. Events arise from non-culprit plaques
2. Plaque burden ≥70% is high risk
3. MLA ≤4 mm² increases risk
4. Most events are non–STEMI
5. Did not support preventive PCI

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8. What did PROSPECT II add?

1. Integrated NIRS with IVUS
2. Identified lipid-rich plaques
3. High LCBI predicts risk
4. Confirmed patient-level vulnerability
5. Still no lesion-directed therapy

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9. What is NIRS imaging?

1. Spectroscopic lipid detection
2. Measures lipid core burden index
3. No structural imaging
4. Often combined with IVUS
5. Risk marker, not treatment guide

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10. What is LCBI?

1. Quantifies lipid signal intensity
2. Expressed per 4-mm segment
3. LCBI ≥400 considered high risk
4. Predicts future events
5. Does not indicate PCI necessity

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11. Limitations of NIRS?

1. No cap thickness assessment
2. No plaque geometry
3. Cannot detect inflammation directly
4. Lesion-level prediction weak
5. Adjunctive tool only

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12. What is the role of IVUS in vulnerable plaque?

1. Quantifies plaque burden
2. Detects positive remodeling
3. Assesses vessel size
4. Guides stent sizing
5. Cannot detect TCFA

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13. Why can IVUS not detect TCFA?

1. Limited axial resolution
2. Cap thinner than ultrasound limits
3. Lipid–fibrous interface indistinct
4. Inflammation poorly visualized
5. Structural, not biological tool

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14. What is positive remodeling?

1. Outward vessel expansion
2. Preserves lumen size
3. Masks disease severity
4. Associated with vulnerability
5. Detected by IVUS or CCTA

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15. What is the CLIMA study?

1. OCT-based observational study
2. Identified four high-risk features
3. TCFA, macrophages, lipid arc, MLA
4. Predicted adverse events
5. Did not justify preventive PCI

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16. What did CLIMA NOT prove?

1. That TCFA requires intervention
2. That OCT-guided PCI prevents MI
3. That vulnerability equals culprit lesion
4. That morphology predicts timing
5. That stenting improves outcomes

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17. Role of CCTA in plaque vulnerability?

1. Non-invasive whole-vessel assessment
2. Detects high-risk plaque features
3. Identifies positive remodeling
4. Guides preventive therapy
5. Best population-level tool

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18. High-risk plaque features on CCTA?

1. Low attenuation plaque (<30 HU)
2. Napkin-ring sign
3. Spotty calcification
4. Positive remodeling
5. High total plaque burden

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19. What is napkin-ring sign?

1. Central low attenuation core
2. Peripheral higher density rim
3. Surrogate of necrotic core
4. Associated with ACS
5. Seen only on CCTA

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20. Key findings of SCOT-HEART trial?

1. CT improves diagnosis of CAD
2. Identifies high-risk plaques
3. Leads to preventive intensification
4. Reduces MI incidence
5. Benefits driven by medical therapy

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21. Why is CCTA superior to invasive imaging for risk?

1. Assesses entire coronary tree
2. Non-invasive and reproducible
3. Captures total plaque burden
4. Guides statin escalation
5. Suitable for screening

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22. Limitations of CCTA?

1. Cannot visualize fibrous cap
2. Limited inflammation detection
3. Motion artifacts
4. Contrast exposure
5. Radiation dose

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23. Role of PET imaging in vulnerable plaque?

1. Detects biological activity
2. FDG shows inflammation
3. NaF shows microcalcification
4. Strong research signal
5. Not clinically routine

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24. Why is PET not used routinely?

1. Poor coronary spatial resolution
2. Cardiac motion issues
3. High cost
4. Limited availability
5. No outcome-guided strategies

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25. What is plaque erosion?

1. Endothelial denudation
2. Intact fibrous cap
3. Common in younger patients
4. Better visualized by OCT
5. Often treated conservatively

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26. OCT role in ACS?

1. Differentiates rupture vs erosion
2. Guides antithrombotic strategy
3. Assesses residual thrombus
4. Optimizes stent deployment
5. Improves mechanistic understanding

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27. Why does plaque vulnerability not equal culprit lesion?

1. Multiple plaques vulnerable
2. Rupture may be silent
3. Healing occurs frequently
4. Inflammation is systemic
5. Proven by PROSPECT

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28. What is healed plaque rupture?

1. Previous rupture with repair
2. Layered fibrotic appearance
3. Seen on OCT
4. Contributes to plaque growth
5. Indicates chronic instability

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29. Why do statins stabilize plaques?

1. Reduce lipid core volume
2. Decrease inflammation
3. Thicken fibrous cap
4. Improve endothelial function
5. Reduce clinical events

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30. Effect of PCSK9 inhibitors on plaque?

1. Further lipid reduction
2. Decrease lipid-rich plaques
3. Reduce necrotic core
4. Additive to statins
5. Evidence from imaging substudies

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31. Why PCI fails to prevent MI in stable CAD?

1. Treats focal stenosis only
2. Does not modify biology
3. Leaves non-culprit plaques untreated
4. Proven in COURAGE
5. Reinforced by ISCHEMIA

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32. ISCHEMIA trial key message?

1. No mortality benefit of early PCI
2. Symptom relief only
3. Optimal medical therapy critical
4. Anatomy alone insufficient
5. Reinforced systemic approach

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33. Why vulnerable plaque imaging did not change guidelines?

1. Lack of interventional benefit
2. Dynamic plaque behavior
3. High false-positive risk
4. Systemic disease dominance
5. Absence of RCTs

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34. Current guideline position?

1. No screening for vulnerable plaque
2. No preventive PCI
3. IVUS/OCT for PCI optimization
4. CCTA for risk stratification
5. Medical therapy cornerstone

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35. What is “vulnerable patient”?

1. Systemic inflammatory milieu
2. High plaque burden
3. Multiple unstable plaques
4. Elevated clinical risk
5. Better predictor than single plaque

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36. Why is vulnerability a patient-level phenomenon?

1. Plaques behave synchronously
2. Inflammation is systemic
3. Multiple silent ruptures
4. Risk factors act globally
5. Proven by longitudinal studies

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37. Best imaging to assess vulnerable patient?

1. CCTA for burden
2. IVUS for plaque volume
3. NIRS for lipid burden
4. Clinical risk integration
5. Not single-lesion OCT

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38. Common exam trap regarding vulnerability?

1. Equating severe stenosis with MI risk
2. Assuming TCFA mandates PCI
3. Overvaluing OCT findings
4. Ignoring systemic therapy
5. Confusing ischemia with instability

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39. Vulnerable plaque vs ischemic plaque?

1. Vulnerable = rupture-prone
2. Ischemic = flow-limiting
3. Not synonymous
4. Different imaging targets
5. Different treatments

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40. Why is OCT excellent but limited?

1. Superb resolution
2. Limited penetration
3. Requires contrast
4. Focal assessment only
5. Not predictive alone

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41. What predicts future events better: TCFA or plaque burden?

1. Plaque burden
2. Reflects total disease
3. Supported by PROSPECT
4. TCFA is common
5. Burden correlates with outcomes

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42. Role of inflammation in plaque rupture?

1. Weakens fibrous cap
2. Activates macrophages
3. Promotes matrix degradation
4. Increases thrombogenicity
5. Target of future therapies

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43. Why anti-inflammatory therapy is attractive?

1. Targets root cause
2. Systemic benefit
3. Complements lipid lowering
4. Supported by CANTOS
5. Addresses vulnerable patient

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44. Why imaging predicts risk but not timing?

1. Plaques evolve rapidly
2. Triggers are unpredictable
3. Healing–rupture cycles
4. External stressors involved
5. Biology exceeds resolution

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45. Best single-line summary of vulnerable plaque imaging?

1. Risk marker
2. Not treatment trigger
3. Improves prevention
4. Does not guide PCI
5. Patient-focused insight

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46. Why dense calcification indicates stability?

1. Represents healed plaque
2. Low inflammation
3. Thick fibrous cap
4. Reduced rupture risk
5. Seen in chronic disease

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47. Spotty vs dense calcification?

1. Spotty = active disease
2. Dense = stable plaque
3. Spotty linked to ACS
4. Dense linked to chronic CAD
5. Seen on CT/OCT

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48. OCT feature of inflammation?

1. High backscattering spots
2. Macrophage clusters
3. Surface irregularity
4. Thin cap association
5. Rupture risk indicator

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49. Why whole-vessel assessment matters?

1. MI may arise anywhere
2. Culprit lesions unpredictable
3. Multiple plaques unstable
4. Supports CT use
5. Guides prevention

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50. Why prophylactic stenting is harmful?

1. Treats wrong target
2. Adds procedural risk
3. Ignores systemic disease
4. No outcome benefit
5. Guideline Class III

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51. PCI improves outcomes when?

1. ACS setting
2. Flow-limiting ischemia
3. Left main disease
4. Refractory angina
5. Not for vulnerability

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52. Future of vulnerable plaque imaging?

1. Better risk stratification
2. Therapy monitoring
3. Drug response assessment
4. Patient-level prediction
5. Not lesion stenting

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53. Imaging surrogate of plaque stabilization?

1. Reduced lipid core
2. Increased cap thickness
3. Less inflammation
4. Reduced remodeling
5. Seen after statins

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54. Why multiple imaging modalities are used?

1. Each sees different biology
2. No single gold standard
3. Complementary information
4. Improves understanding
5. Does not change PCI rules

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55. Vulnerable plaque imaging in daily practice?

1. Not routine screening
2. Research and selected cases
3. PCI optimization
4. Risk discussion
5. Prevention focus

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56. Best therapy for vulnerable plaque?

1. High-intensity statins
2. Risk factor control
3. Antiplatelet therapy
4. Lifestyle modification
5. Systemic approach

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57. Why is OCT popular despite limitations?

1. Visual clarity
2. Mechanistic insight
3. PCI optimization
4. Academic value
5. Teaching utility

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58. Vulnerable plaque imaging in NEET SS exams?

1. Focus on concepts
2. Trials over technology
3. Patient vs plaque distinction
4. Guideline alignment
5. Avoid intervention bias

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59. One sentence integrating all trials?

1. PROSPECT showed risk source
2. CLIMA showed morphology
3. ISCHEMIA showed futility of routine PCI
4. COURAGE reinforced medical therapy
5. All favor systemic treatment

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60. Final exam takeaway?

1. Vulnerable plaques exist
2. Most never cause MI
3. Imaging predicts risk
4. Statins save lives
5. Treat the patient, not the plaque

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