Atherosclerosis and Restenosis Flashcards
Review: Are thin fibrous caps or thick fibrous caps on plaques more likely to rupture?
Thin are more likely to rupture.
What did the COURAGE trial comparing percutaneous catheter intervention (PCI) to medical Rx for STABLE angina show? (2007)
No benefit from PCI over medical Rx.
Remember this is stable angina.
What’s a Type I atherosclerotic lesion?
Isolated macrophage / foam cells
What’s a Type II atherosclerotic lesion?
Fatty streak - still mostly intracellular lipids
What’s a Type III atherosclerotic lesion?
Extracellular lipid pools appear.
What’s a Type IV atherosclerotic lesion?
An atheroma - a lipid core develops in the neointima.
What’s a Type V atherosclerotic lesion?
A fibroatheroma - there’s a lipid core and fibrotic changes… can be multiple cores. Calcification can be present.
What’s a Type VI atherosclerotic lesion?
Complicated - surface defects, thrombus, hemorrhage
What’s one cytokine-receptor pair involved in recruiting monocytes to fatty streaks (Type I)?
CCR2 on monocytes sees MCP-1
Stable angina is most likely caused by what kind of lesions?
Fibrotic plaques with a thick cap, lots of SMC activity, partially occluding coronary arteries.
What limits the long-term effectiveness of stenting partially occluded arteries? What cell type mediates this process?
Restenosis.
SMCs mediate this process as a response to endothelial damage caused by the stend.
Does restenosis resemble atherosclerosis?
Nope. Restenosis is driven by SMCs and matrix deposition, not lipid accumulation.
4 vascular growth factors that mediate restenosis?
PDGF
basic FGF
A-II
TGFbeta
What does PDGF (platelet-derived growth factor) do in restenosis?
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.
What does basic FGF do in restenosis? What makes it, when is it made?
basic FGF is made by SMCs in response to stretch/damage (perhaps during balloon inflation), and causes proliferation of SMCs.