Chapter 5 - Intimal hyperplasia Flashcards
Stages of intimal hyperplasia development
Stage 1: hyperacute min-hours Stage 2: acute hours to weeks Stage 3: chronic weeks to months
Stage 1 intimal hyperplasia
FIGURE 5.1
Stage 2 intimal hyperplasia
FIGURE 5.1
Stage 3 intimal hyperplasia
FIGURE 5.1
Platelet adhesion requires the interaction of subendothelial collage with what
Platelet membrane glycoproteins: GPIb, GPIc/GPIIa, GPIa/GPIIa von Willebrand factor Fibronectin
Pathobiology of the injury response after angioplasty leading to intimal hyperplasia
FIGURE 5.1
Drive for the first phase of SMC proliferation
bFGF released from dead and damaged cells
Diabetes increases production of what in the vascular tissues
Advanced glycosylation end productsion also occurs with normal aging
4 categories of in-stent restenosis
1) Focal < 10 mm 2) diffuse > 10 mm 3) proliferative > 10 mm, extends outside 4) occlusion
Benefit of stenting over balloon only on a cellular level
Removes elastic recoin and negative remodelling cannot stop thrombus formation and intimal hyperplasia
Consequences and cures of angioplasty
FIGURE 5.3
DES on intimal hyperplasia
stops SMC proliferation but also stops endothelial cell migration and proliferation increase thrombogenic potential polymer can also increase thrombotic potential
Pathobiology of vein graft response to implantation
FIGURE 5.4
Factors associated with vein bypass intimal hyperplasia
1) dyslipidemia 2) high fibrinogen 3) high homocysteine 4) high antibodies to cardiolipin 5) smoking 6) platelet dysfunction 7) lipoprotein ?
Differing accelerated atherosclerosis from spontaneous atherosclerosis
Accelerated = diffuse, concentric, greater cellularity
Endothelialization of prosthetic bypass graft
limited to the first few CM near anastomoses rest is covered in thin irregular layer of organized fibrin (platelet, leukocyte) mostly collagen type III (no type II)
Two process of neo-endotehlium formation in prosthetic graft
1) from anastomosis 2) penetrating though graft pores with capillary ingrowth
6 stages of neoendothelial healing
STAGE 1: Platelet aggregation phase STAGE 2: fibrin network phase STAGE 3: bridging phase STAGE 4A: progression phase STAGE 4B:transmural migration phase STAGE 5: intimal closure phase STAGE 6: endothelial thromboresistance phase
Use of ASA in prosthetic grafts
prevent graft thrombosis at 2-4 weeks but does not prevent intimal hyperplasia
pathobiology of prosthetic graft after implantation
FIGURE 5.5
Most common regions of intimal thickening in dialysis access grafts
1) anastomotic site (worse with PTFE) 2) floor of artery
Most common stenosis in dialysis access
within 1 cm from venous anastomoses
