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