Microscopic of aorta wall shows fragmentation of elastic fibers and cleft-like spaces known as cystic medial degeneration
The changes are referred to as “cystic medial degeneration” rather than the old term “cystic medial necrosis.” The changes are not specific for Marfan’s and are also seen as an ageing change. The cleft-like spaces contain amorphous extracellular material and are not true, epithelial lined cysts.
Partially occlude the lumen ? unstable angina, subendocardial infarct, sudden death
Organize contribute to growth of plaque
The most dangerous plaques are moderately stenotic (50 – 75%) with a relatively large, soft lipid core and a thin cap. More stenotic lesions may actually be more stable. More stenotic lesions may actually protect the myocardium against MI by preconditioning (mechanism unknown).
For a good review of vulnerable plaque change, see Circulation 108:1664, 2003
What causes acute plaque change?
Mechanisms are uncertain; may include:
Adrenergic stimulation – accounts for more MI’s in AM or when stressed (increased MI's after earthquakes, 9/11 attacks)
Vasoconstriction may contribute to plaque fracture
Inflammation may play a role in destabilizing the plaque
~90% due to disrupted plaque platelet adhesion occlusive thrombus