Fig. 10.12 Atheroscleroticlesions.(A)Aortawithmildatherosclerosiscomposedoffibrousplaques,onedenotedbythearrow.(B)Aortawithseverediffusecomplicatedlesions,includinganulceratedplaque(open arrow), andalesionwithoverlyingthrombus(closed arrow).
Fig. 10.13 Atheroscleroticplaque,coronaryartery.(A)Overallarchitecturedemonstratingfibrouscap(F) andacentralnecrotic(largelylipid)core(C); collagen(blue) isstainedwithMassontrichrome.Thelumen(L) ismoderatelynarrowedbythiseccentriclesion,whichleavespartofthevesselwallunaffected(arrow). (B)Moderate-powerviewoftheplaqueshowninA, stainedforelastin(black); theinternalandexternalelasticmembranesareattenuated,andthemediaofthearteryisthinnedunderthemostadvancedplaque(arrow). (C)High-powerviewofthejunctionofthefibrouscapandcore,showingscatteredinflammatorycells,calcification(arrowheads), andneovascularization(small arrows).
http://ebooksmedicine.net (2) ECM, including collagen, elastic fibers, and proteoglycans; and (3) intracellular and extracellular lipid (see
Fig.
10.13AandB ).Theproportionandconfigurationofeachcomponentvariesfromlesiontolesion.Mostcommonly,plaqueshaveasuperficialfibrouscapcomposedofSMCsandrelativelydensecollagen.Wherethecapmeetsthevesselwall(the“shoulder”)isamorecellularareacontainingmacrophages,Tcells,andSMCs.Deeptothefibrouscapisanecroticcore,containinglipid(primarilycholesterolandcholesterolesters),necroticdebris,lipid-ladenmacrophagesandSMCs(foam cells), fibrin,variablyorganizedthrombus,andotherplasmaproteins.Theextracellularcholesterolfrequentlytakestheformsofcrystallineaggregatesthatarewashedoutduringroutinetissueprocessing,leavingbehindempty“cholesterolclefts.”Theperipheryofthelesionsshowsneovascularization (proliferatingsmallbloodvessels)(see
Fig.10.13C ).Themediadeeptotheplaquemaybeattenuatedandexhibitfibrosissecondarytosmoothmuscleatrophyandloss.Typicalatheromascontainrelativelyabundantlipid,butsomeso-calledfibrous plaques arecomposedalmostexclusivelyofSMCsandfibroustissue.
Plaquesgenerallyprogressivelyenlargeovertimethroughcelldeathanddegeneration,synthesisanddegradationofECM(remodeling),andthrombusorganization.Atheromasalsooftenundergocalcification(see
Fig.10.13C
Atherosclerotic plaques are susceptible to several clinically important changes:
Rupture, ulceration, or erosion of the luminal surface of atheromatous plaques exposes highly thrombogenic substances and induces thrombus formation. Thrombi may partially or completely occlude the lumen, leading to tissue ischemia (e.g., in the heart) (Chapter 11) (
Fig.
10.14 ). If the patient survives, thrombi become organized and incorporated into the growing plaque.
Hemorrhage into a plaque. Rupture of the overlying fibrous cap or of the thin-walled vessels in the areas of neovascularization can cause intra-plaque hemorrhage; the resulting hematoma may cause rapid plaque expansion or plaque rupture.
Atheroembolism. Ruptured plaque can discharge debris into the blood, producing microemboli composed of plaque contents.