Atherosclerosis and Restenosis Flashcards

0
Q

Review: Are thin fibrous caps or thick fibrous caps on plaques more likely to rupture?

A

Thin are more likely to rupture.

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1
Q

What did the COURAGE trial comparing percutaneous catheter intervention (PCI) to medical Rx for STABLE angina show? (2007)

A

No benefit from PCI over medical Rx.

Remember this is stable angina.

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2
Q

What’s a Type I atherosclerotic lesion?

A

Isolated macrophage / foam cells

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3
Q

What’s a Type II atherosclerotic lesion?

A

Fatty streak - still mostly intracellular lipids

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4
Q

What’s a Type III atherosclerotic lesion?

A

Extracellular lipid pools appear.

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5
Q

What’s a Type IV atherosclerotic lesion?

A

An atheroma - a lipid core develops in the neointima.

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6
Q

What’s a Type V atherosclerotic lesion?

A

A fibroatheroma - there’s a lipid core and fibrotic changes… can be multiple cores. Calcification can be present.

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7
Q

What’s a Type VI atherosclerotic lesion?

A

Complicated - surface defects, thrombus, hemorrhage

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8
Q

What’s one cytokine-receptor pair involved in recruiting monocytes to fatty streaks (Type I)?

A

CCR2 on monocytes sees MCP-1

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9
Q

Stable angina is most likely caused by what kind of lesions?

A

Fibrotic plaques with a thick cap, lots of SMC activity, partially occluding coronary arteries.

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10
Q

What limits the long-term effectiveness of stenting partially occluded arteries? What cell type mediates this process?

A

Restenosis.

SMCs mediate this process as a response to endothelial damage caused by the stend.

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11
Q

Does restenosis resemble atherosclerosis?

A

Nope. Restenosis is driven by SMCs and matrix deposition, not lipid accumulation.

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12
Q

4 vascular growth factors that mediate restenosis?

A

PDGF
basic FGF
A-II
TGFbeta

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13
Q

What does PDGF (platelet-derived growth factor) do in restenosis?

A

PDGF (which here comes from endothelial cells and macrophages, not just platelets) is a chemoattractant for SMCs to migrate to the intima from the media.

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14
Q

What does basic FGF do in restenosis? What makes it, when is it made?

A

basic FGF is made by SMCs in response to stretch/damage (perhaps during balloon inflation), and causes proliferation of SMCs.

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15
Q

How might A-II be involved in restenosis?

A

Promotes proliferation of SMCs.

in rats… ACE inhibition has been shown to decreased restenosis in rats, but not in humans

16
Q

In restenosis, what makes TGFbeta, and what does it do?

A

SMCs, endothelial cells, and platelets make TGFbeta.

TGFbeta stimulates SMCs to lay down ECM.

17
Q

How do rapamycin and paclitaxel-eluting stents help reduce restenosis?

A

By inhibiting SMC proliferation.

18
Q

Major risk with drug-eluting stents?

A

Late thrombosis - (perhaps because atherosclerotic plaques can’t form a strong fibrous cap w/o SMC activity)

19
Q

Why is restenosis considered “predictable”?

A

If it doesn’t happen in the first 6mo post PCI, it’s probably not going to happen.