Pathology
- We divide the progression of atherosclerosis in different morphological states:
- Fatty streaks - begin as minute yellow flat spots that coalesce into elongated lesion. Consist of lipid-filled foamy macrophages
- Atherosclerotic plaque - here we see intimal thickening and lipid accumulation, the plaques are white to yellow raised lesions and larger than simple fatty streaks.
- Plaques consist of three parts 1) cells (smooth muscle, macrophages, T-cells), 2) ECM (collagen, elastic fibers, proteoglycans), 3) lipids
Atherosclerosis. Types of atherosclerotic microscopic & gross pathomorphological changes. Organ site damage in atherosclerosis. Complications.
Atherosclerosis generally affects large and medium size arteries (eg. aorta, carotid, coronary), the organs most likely to display symptoms are heart (MI), brain (stroke), limbs (gangrene of extremities) and the vessels themselves (aneurysms).
Remember: the vessels most heavily involved, in descending order: lower abdominal aorta, coronary arteries, popliteal arteries, internal carotid arteries and the circle of Willis. In the aorta the abdominal part is far worse than the thoracic part, and plaques gather around the ostia of branches.
As mentioned above, the early stage of a plaque is a fatty streak which then becomes an atherosclerotic plaque. A more complicated method of describing it is in the following categories:
- Initial lesions
- Fatty streak
- intermediate lesion
- Atheroma
- Fibroatheroma
- Complicated lesion
The outcome of the plaque depends on the size of the vessel, as well as the size and stability of the plaque. Possible outcomes are:
- Occlusion by plaque growth
- Damage to vessel wall causing aneurysm
- Plaque rupture causing thrombus to embolize
As a plaque grows, at 70% occlusion it typically causes limits to blood supply that are symptomatic (stable angina at 70%). There then comes a point where the plaque will have an acute change. Symptoms due to occlusion may come before this acute change, or the plaque may remain asymptomatic until one of the following:
- Rupture (exposing highly thrombogenic plaque elements)
- Erosion/ulceration (exposing thrombogenic subendothelial basement membrane)
- Hemorrhage into atheroma (expanding plaque volume)
Remember: a vulnerable plaque, the one that ruptures, has a thin fibrous cap, a large lipid-necrotic core and many inflammatory cells; a stable plaque has a thick, collagen-rich cap and a small core. Rupture with thrombosis turns stable angina into an acute coronary syndrome (unstable angina, myocardial infarction, sudden death).