Morphological features of Atherosclerosis.

1)-ATHEROMATOUS PLAQUES-: A fully developed atherosclerotic lesion is called atheromatous plaque, also called fibrous plaque, fibrofatty plaque or atheroma. Unlike fatty streaks, atheromatous plaques are selective in different geographic locations and races and are seen in advanced age. Most often and most severely affected is the abdominal aorta, though smaller lesions may be seen in descending thoracic aorta and aortic arch. The major

branches of the aorta around the ostia are often severely involved, especially the iliac, femoral, carotid, coronary, cerebral artery.

2. GELATINOUS LESIONS. Gelatinous lesions develop in the intima of the aorta and other major arteries in the first few months of life. Like fatty streaks, they may also be precursors of plaques. They are round or oval, circumscribed grey elevations, about 1 cm in diameter.

4. COMPLICATED PLAQUES. Various pathologic changes that occur in fully-developed atheromatous plaques are

called the complicated lesions. These account for the most serious harmful effects of atherosclerosis and even death. These changes include calcification, ulceration, thrombosis, haemorrhage and aneurysmal dilatation. It is not uncommon to see more than one form of complication in a plaque.

i) Calcification.-: Calcification occurs more commonly in advanced atheromatous plaques, especially in the aorta and coronaries. The diseased intima cracks like an egg￾shell when the vessel is incised and opened.

ii) Ulceration.-: The layers covering the soft pultaceous material of an atheroma may ulcerate as a result of haemodynamic forces or mechanical trauma. This results in discharge of emboli composed of lipid material and debris into the blood stream, leaving a shallow, ragged ulcer with yellow lipid debris in the base of the ulcer.

Occasionally, atheromatous plaque in a coronary artery may suddenly rupture into the arterial lumen forcibly and cause thromboembolic occlusion.

iii) Thrombosis.-: The ulcerated plaque and the areas of endothelial damage are vulnerable sites for formation of superimposed thrombi. These thrombi may get dislodged to become emboli and lodge elsewhere in the circulation, or may get organised and incorporated into the arterial

wall as mural thrombi. Mural thrombi may become 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 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.