The normal vessel wall comprises:
^^ Intima: a single endothelial cell lining.
Media: fibroblasts and smooth muscle with collagen support and elastic tissue.
Adventitial mainly composed of thick collagen fibres.
Within brain and spinal cord tissue the adventitia is usually very thin and the elastic lamina between media and adventitia less apparent.
The intima is an important barrier to leakage of blood and constituents into the vessel wall. In the development of the atherosclerotic plaque, damage to the endothelium of the intima is the primary event.
The atherosclerotic plaque
Following intimal damage:
Smooth muscle cells laden with build up cholesterol, lipids, phospholipids subintimally.
Haemorrhage may occur within the plaque or the plaque — may ulcerate into the lumen of the vessel forming an intraluminal mural thrombus. Either way, the lumen of the involved vessel is narrowed (stenosed) or blocked (occluded).
The plaque itself may give rise to emboli. Cholesterol is present partly in crystal form and fragments following plaque rupture may be sufficiently large to occlude the lumen of distal vessels. The cholesterol esters, lipids and phospholipids each play a role in the aggregation of such emboli.
The carotid bifurcation in the neck is a frequent site at which the atheromatous plaque causes stenosis or occlusion.
When stenosed by more than 80%, reduction of blood flow to brain occurs
When occluded, the clinical outcome depends on speed of occlusion and the state of collateral circulation
When plaque has ulcerated - may result in cholesterol emboli or platelet emboli
Platelet emboli arise from thrombus developed over the damaged endothelium. This thrombus is produced partly by platelets coming into contact with exposed collagen fibres. Endothelial cells synthesise PROSTACYCLIN which is a potent vasodilator and inhibitor of platelet aggregation. THROMBOXANE A2, synthesised by platelets, has opposite effects. In thrombus formation these two PROSTAGLANDINS actively compete with each other.
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