Large Artery Ischaemic Stroke

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Learning objectives

  • Risks factors for those at risk of large vessel atherosclerosis
  • Mechanisms of stroke
  • Identify arteries at risk
  • Appropriate management of risks

Causes of Atherosclerosis and artery to Artery stroke

Atherosclerosis is only one of the causes of disease of the large arteries. In young patients, alternative causes may be sought e.g. dissection possibly related to fibromuscular dysplasia. Vessels at risk include the Intra and extracranial vessels including carotid artery, vertebral, basilar and the proximal major branches of the circle of Willis. However, the formation of large plaques of atheroma in these arteries can progressively lead to luminal stenosis and resultant ischaemia e.g. carotid disease which may be worsened further with systemic hypotension. Approximately 35% of all ischaemic strokes are thrombotic due to large and small vessel disease with the remainder embolic. However, there is some overlap with large vessel disease as plaque ulceration may cause thrombosis and overlying clot either embolises or occludes the artery. Atherosclerotic plaques are seen in post-mortem studies of the aorta and other large and medium-sized vessels of patients even from their 20's. This can be found in aortic or subclavian or internal carotid atheroma. Aortic atheroma is even detectable by TOE is significantly more common in stroke patients than healthy controls. Atheromatous plaques may be a source of embolic material through rupture and thrombus formation. Watershed infarction can occur at the edges of vascular territories due to luminal stenosis and hypotensive episode.

Epidemiology

  • Large vessel atherosclerosis accounts for about 20% of all ischaemic stroke
  • Extracranial atherosclerosis is commoner in Europe and the USA
  • Intracranial atherosclerosis is commoner in China and Thailand and in the Afro-Caribbean population.

Clinical

  • Transient vessel occlusion and corresponding TIA syndrome
  • Acute stroke which may be thrombotic +/- embolic in character
  • A carotid bruit may be heard
  • Coexisting coronary artery disease
  • Smoker, diabetes or have hyperlipidaemia or hypertension.

Aetiology

  • Disease may be seen both in the large and medium-sized arteries from the aorta to carotids and subclavian and vertebral vessels as well as extracranial and intracranial vessels which are commoner in those of Afro-Caribbean origin.
  • Lesions may be seen at typical sites such as bifurcation of the carotid (branching), aortic arch, carotid syphon (tortuous) and the basilar artery (confluence).
  • Atheroma seems to accumulate at sites of haemodynamic shear stress. Usually, rupture of an unstable atherosclerotic plaque leads to overlying platelets activation and clot formation which embolises. The first sign of the disease is the formation of fatty streaks and with time smooth muscle cells proliferate and there is a local accumulation of lipid.
  • The plaques have a fibrous cap which can become unstable and fissure and crack and rupture with the release of prothrombotic matter. The plaques can also cause luminal obstruction and narrowing. Close relationship with age, male sex, smoking, cholesterol, hypertension, diabetes, obesity, lack of exercise

Investigations

  • FBC, U&E, LFTs, ESR, CRP and standard investigations
  • Lipid profile
  • Doppler Carotids may shown increased velocities suggesting stenois and plaque formation
  • CTA/MRA may show both intracranial and/or extracranial stenosis

Management

  • General Best Medical therapy: smoking cessation, antiplatelet, control diabetes and hypertension, encourage weight loss and exercise. Commence Statin.
  • Carotid disease: If there is > 50% carotid stenosis which is symptomatic and the likely source of emboli then carotid endarterectomy (or stenting) should be considered.


<img src="220px-Carotid_Plaque.jpg" hspace="10" width=100 align = "right">Carotid plaque</a>