Atheroscleroticplaquesdevelopandgrowslowlyoverdecades.Stableplaquescanproducesymptomsrelatedtochronicischemiabynarrowingvessels,whereasunstableplaquescancausedramaticandpotentiallyfatalischemiccomplicationsrelatedtoacuteplaquerupture,thrombosis,orembolization.
Stableplaquestendtohaveadensefibrouscap,minimallipidaccumulation,andlittleinflammation,whereas“vulnerable”unstableplaqueshavethincaps,largelipidcores,andrelativelydenseinflammatoryinfiltrates.
B. True aneurysm (saccular)
C. True aneurysm (fusiform)
Aneurysms are congenital or acquired dilations of blood vessels or the heart (
Fig. 10.17 ). “True” aneurysms involve all three layers of the artery (intima, media, and adventitia) or the attenuated wall of the heart; these include atherosclerotic and congenital vascular aneurysms, as well as ventricular aneurysms resulting from transmural myocardial infarctions. By comparison, a false aneurysm (pseudoaneurysm) results when a wall defect leads to the formation of an extravascular hematoma that communicates with the intravascular space (“pulsating hematoma”). Examples are ventricular ruptures contained by pericardial adhesions and leaks at the junction of a vascular graft with a natural artery. In arterial dissections, pressurized blood gains entry to the arterial wall through a surface defect and then pushes apart the underlying layers. Aneurysms and dissections are important causes of stasis and subsequent thrombosis; they also have a propensity to rupture—often with catastrophic results.
Fig. 10.17 ). Saccular aneurysms are discrete outpouchings ranging from 5 to 20 cm in diameter, often with a contained thrombus. Fusiform aneurysms are circumferential dilations up to 20 cm in diameter; these most commonly involve the aortic arch, the abdominal aorta, or the iliac arteries.
Arteries are dynamic tissues that must withstand the constant mechanical stress of pulsatile blood flow. Aneurysms occur when alterations in SMCs or ECM compromise the structural integrity of the arterial media. Among the implicated factors in aneurysm formation are the following: • Inadequate or abnormal connective tissue synthesis. Several rare inherited diseases provide insight into the types of abnormalities that can lead to aneurysm formation. As discussed earlier, TGF-β regulates SMC proliferation and matrix synthesis. Thus, mutations in TGF-β receptors or downstream signaling pathways result in defective elastin and collagen synthesis; aneurysms in affected
D. False aneurysm E. DissectionA. Normal vessel
Fig. 10.17 Aneurysms.(A)Normalvessel.(B)Trueaneurysm,sacculartype.Thewallbulgesoutwardandmaybeattenuatedbutisotherwiseintact.(C)Trueaneurysm,fusiformtype.Thereiscircumferentialdilationofthevessel.(D)Falseaneurysm.Thewallisruptured,creatingacollectionofblood(hematoma)boundedexternallybyadherentextravasculartissues.(E)Dissection.Bloodhasenteredthewallofthevesselandseparated(dissected)thelayers.
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Fig. 10.18 Cysticmedialdegeneration.(A)Cross-sectionofaorticmediafromapatientwithMarfansyndrome,showingmarkedelastinfragmentationandareasdevoidofelastinthatresemblecysticspaces(asterisks). (B)Normalmediaforcomparison,showingtheregularlayeredpatternofelastictissue.Inboth (A)and(B),elastinisstainedblack.