Lecture 17: Pathology of CAD

Question 1

Top three regions for atherosclerosis

Answer 1

1. Lower aorta; 2. Coronaries; 3. Femorals, popliteals

Question 2

Describe what happens to the monocytes…What causes all this?

Answer 2

Capture, roll, arrest and diapedesis into subendothelial space; cytokine production from damaged endothelial cells

Question 3

Once absorbed into endothelial space, a monocyte becomes a…how?

Answer 3

Macrophage foam cell; engulfing LDL particles

Question 4

What is the earliest recognizable form of atherosclerosis?

Answer 4

Fatty streaks

Question 5

What are the six (3 –> 3) key features of plaque progression?

Answer 5

Inflammation, neovascularization, intra-plaque hemorrhage –> lipid core expansion, oxidative stress, apoptosis

Question 6

Describe plaque neovascularization and three types

Answer 6

Vasa vasorum proliferate as neovessels: 1. Vasa vasorum interna, 2. Vasa vasorum externa, 3. Venous vasa vasorum

Question 7

What is the danger of plaque neovascularization (2)?

Answer 7

Neovessels are fragile –> intraplaque hemorrhage –> 1) larger plaque size and 2) free hemoglobin increases oxidative stress

Question 8

Type 1 AHA Class

Answer 8

Eccentric intimal thickening (no lipid), some isolated foam cells

Question 9

Type II AHA Class

Answer 9

Foam cells (intracellular lipids)

Question 10

Type III AHA Class

Answer 10

Type II lesion + some extracellular lipid pools

Question 11

Type IV AHA Class

Answer 11

Fibrous cap and lipid pool

Question 12

Type VA AHA Class

Answer 12

Larger cap, larger lipid core (lipid rich)

Question 13

Type VB AHA Class

Answer 13

Lipid core with dystrophic calcification (calcific)

Question 14

Type VC AHA Class

Answer 14

Lipid is replaced by fibro-collagenous tissue (fibrotic)

Question 15

Type VI AHA Class

Answer 15

Fibrous cap disrupted, thrombus associated, intra-plaque hemorrhage

Question 16

Which types can produce symptoms?

Answer 16

Type IV - VII (early)

Question 17

Which decade are Types I and II?

Answer 17

1st

Question 18

Which decade are Types III and IV?

Answer 18

3rd

Question 19

Which decade are Types V and VI?

Answer 19

4th

Question 20

Positive plaque remodeling: definition and associated with…

Answer 20

Increase in plaque size and External Elastic Membrane (EEM) area; Unstable lipid rich plaque, allowing considerable plaque expansion despite normal luminal size

Question 21

Negative plaque remodeling : definition and associated with…

Answer 21

Decrease in plaque size and External Elastic Membrane (EEM) area; Diminished plaque size with reduction in lumen size

Question 22

Three complications of plaque morphology

Answer 22

Rupture-thrombosis, erosion-thrombosis, calcific nodule

Question 23

Define plaque thrombosis

Answer 23

Thrombogenic necrotic lipid core gets exposed to the flowing blood and results in thrombus formation

Question 24

Define plaque erosion

Answer 24

The luminal thrombus overlies area that lacks surface endothelium but does not communicate with the lipid core

Question 25

Define calcific nodules

Answer 25

Plaques with calcified nodule protruding into the lumen through a disrupted thin fibrous cap (FC), with secondary thrombus formation

Question 26

Three clinical phase possibilities of coronary atherosclerosis

Answer 26

1. Wall weakening/mural thrombosis –> aneurysm and rupture; 2. Plaque rupture/hemorrhage –> occlusion by thrombus; 3. Plaque growth –> critical stenosis

Question 27

Stenting can lead to…

Answer 27

Restenosis via neoatherosclerosis due to deposition of ECM via myofibroblasts (from vessel wall injury)

Question 28

In vein grafts, atherosclerotic lesions are…They lack?

Answer 28

Densely fibrotic; lipid core