Page 415 - Textbook of Pathology, 6th Edition

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Figure 15.8 Histologic appearance of a fully-developed atheroma.

i) Calcification. Calcification occurs more commonly in in discharge of emboli composed of lipid material and
advanced atheromatous plaques, especially in the aorta debris into the blood stream, leaving a shallow, ragged
and coronaries. The diseased intima cracks like an egg- ulcer with yellow lipid debris in the base of the ulcer.
shell when the vessel is incised and opened. Occasionally, atheromatous plaque in a coronary artery
Microscopically, the calcium salts are deposited in the may suddenly rupture into the arterial lumen forcibly and CHAPTER 15
vicinity of necrotic area and in the soft lipid pool deep in cause thromboembolic occlusion.
the thickened intima (Fig. 15.9). This form of athero- iii) Thrombosis. The ulcerated plaque and the areas of
sclerotic intimal calcification differs from Mönckeberg’s endothelial damage are vulnerable sites for formation of
medial calcific arteriosclerosis that affects only the tunica superimposed thrombi. These thrombi may get dislodged
media (page 392). to become emboli and lodge elsewhere in the circulation,
ii) Ulceration. The layers covering the soft pultaceous or may get organised and incorporated into the arterial
material of an atheroma may ulcerate as a result of wall as mural thrombi. Mural thrombi may become
haemodynamic forces or mechanical trauma. This results occlusive thrombi which may subsequently recanalise.
iv) Haemorrhage. Intimal haemorrhage may occur in an
atheromatous plaque either from the blood in the vascular
lumen through an ulcerated plaque, or from rupture of
thin-walled capillaries that vascularise the atheroma from The Blood Vessels and Lymphatics
adventitial vasa vasorum. Haemorrhage is particularly a
common complication in coronary arteries. The
haematoma formed at the site contains numerous
haemosiderin-laden macrophages.
v) Aneurysm formation. Though atherosclerosis is
primarily an intimal disease, advanced lesions are
associated with secondary changes in the media and
adventitia. The changes in media include atrophy and
thinning of the media and fragmentation of internal elastic
lamina. The adventitia undergoes fibrosis and some
inflammatory changes. These changes cause weakening
in the arterial wall resulting in aneurysmal dilatation.

Clinical Effects
The clinical effects of atherosclerosis depend upon the size
and type of arteries affected. In general, the clinical effects
result from the following:
Figure 15.9 Complicated atheromatous plaque lesion. There is 1. Slow luminal narrowing causing ischaemia and atrophy.
narrowing of the lumen of coronary due to fully developed atheromatous
plaque which has dystrophic calcification in its core. 2. Sudden luminal occlusion causing infarction necrosis.