- 80 to 85% strokes are ischemic due to carotid artery stenosis (CAS).
peripheral arterial disease.
Risk factors for atherosclerosis:CAS is due to atherosclerosis. As the atherosclerosis progresses the atherosclerotic plaques rupture resulting in the formation of thrombus and arterial occlusion or dislodged materials from the plaques blocking the smaller branches of the carotid artery.
- Cigarette smoking
- Advanced glycation end products (AGEs) and its receptors (RAGE, soluble RAGE [sRAGE])
- Lack of exercise
- C-reactive protein (CRP)
Carotid artery atherosclerosis is mostly present at the carotid bifurcation into external and internal carotid artery. The ostium of the internal carotid artery is mostly affected. Intracranial internal carotid artery and its branches are less affected with atherosclerosis.
Extracranial symptomatic carotid stenosis:Typically seen at the carotid bifurcation extending to the intracranial internal carotid artery in a portion referred to as the cervical segment.
- Revascularization techniques for extracranial carotid atherosclerosis include carotid endarterectomy (CEA) or carotid angioplasty and stenting (CAS). Revascularization is discussed in more details below.
Intracranial symptomatic carotid stenosis:The intracranial carotid artery begins at the petrous segment and continues in the direction of blood flow to the lacerum, cavernous, clinoid, ophthalmic, and communicating segments where it ends at the carotid terminus.
- Intensive medical management has been demonstrated to be superior to revascularization in patients with severe (70–99%) intracranial stenosis.
Asymptomatic presentation:CAS is considered symptomatic when ipsilateral retinal or cerebral ischemia occurs and asymptomatic when these symptoms are absent.
Amaurosis fugax:Ipsilateral transient visual obscuration from retinal ischemia
Transient ischemic attacks (TIA) → Ischemic stroke:Approximately 30% of strokes are caused by carotid occlusive disease.
- Contralateral weakness/numbness of an arm, a leg, or the face, or of a combination of these sites
- Visual field defect
- Aphasia (in case of dominant (usually left) hemisphere involvement)
- Carotid artery disease is responsible for nearly 50% of all TIAs
- Risk of developing stroke after TIAs is as high as 20% within the 1st month. If untreated, TIAs result in development of stroke within 2 years. Risk of stroke events remains high for 10 to 15 years after TIAs.
Classic symptoms of TIA contrasted with vertebrobasilar symptoms:It is important to distinguish between these two types of symptoms because patients with transient ischemia of the vertebrobasilar system do not benefit from CEA.
- Carotid bruit: Turbulent flow in carotid artery
- Associated with increased risk of vascular disease, including stroke, myocardial infarction, and cardiovascular death
Doppler ultrasonography:First diagnostic imaging tool used to screen for carotid artery stenosis
Catheter angiography:Criterion standard for defining the degree of stenosis and the morphologic features of the offending plaque. However, catheter angiography is neither feasible nor recommended in every patient because of its risks and costs.
CT-angiography and MR-angiography (MRA):Confirmatory test after Doppler study suggestive of hemodynamically significant stenosis in an asymptomatic patient
Invasive treatment is considered for symptomatic patients with stenosis greater than 50%6 and for asymptomatic patients with stenosis greater than 60%.
Lifestyle changes:Slow the progression of CAS
- Cessation of smoking and use of tobacco products
- Diet low in saturated fats, cholesterol, and sodium
- Control of body weight
- Daily physical exercise
- Reduction of dietary calories intake
- Limitation of alcohol use
Pharmacological management:Recommended in asymptomatic patients with low-grade CAS (<50%)
- Lipid lowering agents: Statins
- Antihypertensive agents:
- Stage I HTN: Thiazide diuretics, angiotensin converting enzyme inhibitor (ACE-I), β blockers (BBs), angiotensin receptor blockers (ARBs), calcium channel blockers (CCBs) or combination.
- Stage II HTN: Thiazide diuretics + ACE-I/ARBs/BBs/CCBs.
- Anti-AGEs therapy: Aminoguanidine, pyrido-xanthine (natural vitamin 6), benfotiamine (a lipid-soluble derivative of thiamine), aspirin, metformin, candesartan, and orlistat, α-carbonyl compounds (alagebrium)
- Agents that increase levels of sRAGE: Antidiabetic agents (Insulin and rosiglitazone), Vitamin D, Statins, ACE-I (ramipril)
- CRP-lowering agents: Celecoxib, clopidogrel. Statins, rosiglitazone, carvedilol, antioxidants (α-tocopherol, vitamin C), ramipril, quinapril, valsartan, candesartan, calcium channel blockers (amlodipine), and combination of hydrochlorothiazide and amlodipine.
- Antiplatelet therapy: Aspirin, clopidogrel, or ticlopidine
Carotid endarterectomy (CEA):Recommended in asymptomatic patients with CAS of 50-60%.
Carotid angioplasty and stenting (CAS):