Pathophysiology of carotid artery disease and related clinical syndromes

The severity of internal carotid artery lesion per se is a poor indicator of the cerebral haemodynamic status of the brain. Positron emission tomography (PET) of the brain allows to study the different pathophysiological changes related to carotid artery disease. Several stages of impairment of cerebral blood flow and metabolism can be shown such as the compensatory phases by the haemodynamic and the metabolic reserve, the transition to reversible (penumbra) and irreversible ischaemia and the phase of luxury perfusion. Distinct PET patterns correlate with certain clinical outcomes. PET studies found evidence for an embolic origin rather than for a low-flow status as most frequent cause of stroke in severe carotid artery disease. Except for deep borderzone infarcts in the centrum semi-ovale, most cortical borderzone infarcts are not due to chronic misery perfusion. Recent silent and recurrent infarcts can be demonstrated with Cobalt-55 PET, which is of importance for the therapeutical decision. The PET studies argue that carotid endarterectomy is successful probably by removing the source of emboli rather than by restoring the cerebral perfusion in severe carotid artery stenosis.