Although there are many causes of cerebral artery stenosis, atherosclerosis is the leading cause. Stroke kills approximately 160,000 patients each year in the United States and accounts for 1 in every 15 deaths. Currently, stroke is the number one leading cause of death in China, surpassing heart disease and cancer. Each year, approximately 600,000 new or recurrent strokes occur, of which approximately 500,000 are first-episode strokes and 100,000 are recurrent strokes.
In the Framingham Study, the most common type of stroke was atherosclerotic cerebral infarction, which accounted for 61% of all cerebral infarctions, excluding transient ischemic attacks (TIAs). In the International Heart, Lung, and Blood Institute’s Community Study of Atherosclerosis Risk Factors, ischemic strokes accounted for 83% of all strokes, of which 38% were lacunar, 14% were thrombo-embolic, and the remainder were large arterial strokes.
Cerebral atherosclerosis occurs mainly at the bifurcations and turns of the great arteries, such as the beginning of the internal carotid artery and the siphon, the bifurcation of the middle cerebral artery trunk, the beginning of the basilar artery, the beginning of the vertebral artery and the entry to the skull.
The diagnosis of cerebral artery stenosis should include: nature, e.g., atherosclerotic, arteritis, post-radiotherapy, fibromuscular dysplasia, etc.; location, e.g., internal carotid artery stenosis, basilar artery stenosis, etc.; degree, e.g., mild stenosis, moderate stenosis, severe stenosis, or note the rate of stenosis; presence or absence of cerebral ischemic symptoms, e.g., symptomatic or asymptomatic stenosis, TIA, mini-stroke, major stroke, etc. When surgical intervention is to be performed for cerebral artery stenosis, an evaluation regarding risk-benefit evaluation and predicted outcome is yet to be performed.
Section I. Risk factors
The formation of cerebral atherosclerosis is an insidious process that is manifested by thickening of the arterial wall and a decrease in elasticity. Risk factors are divided into modifiable and non-modifiable factors. The former can be controlled or eliminated through lifestyle changes and pharmacological interventions. The latter are inherent to the individual and have unchangeable characteristics.
I. Non-modifiable risk factors.
These include age, sex, and race. In adults, the risk of stroke increases 2-fold every 10 years, and the risk is greater in men than in women. The incidence of stroke is higher in blacks. The incidence of atherosclerotic stenosis of intracranial arteries is higher in Asians and blacks than in extracranial internal carotid arteries, and vice versa in Caucasians.
II. Modifiable risk factors.
Hypertension: Studies suggest that hypertension is a major risk factor for cardiovascular and cerebrovascular diseases. Analysis of different hypertension trials has shown that elevated systolic blood pressure alone is strongly associated with the degree and progression of carotid artery stenosis; a 6-7 mmHg decrease in diastolic blood pressure is associated with a 42% decrease in the 5-year incidence of stroke.
Hyperlipidemia: It is well established that cholesterol levels significantly influence the extent and rate of progression of atherosclerosis formation, particularly elevated low-density lipoprotein (LDL) levels and elevated LDL to high-density lipoprotein (HDL) ratios; reductions in LDL and total cholesterol levels reduce carotid plaque and stenosis.
Diabetes mellitus: Whether type I or type II diabetes mellitus, intensive treatment to bring blood glucose levels down to around normal levels can significantly reduce microvascular complications such as retinopathy and peripheral neuropathy. However, the final treatment should reduce the microvascular complication – stroke.
Smoking: Smoking is a risk factor for stroke and may be associated with an increased risk of atherosclerosis formation from smoking. A subgroup analysis of a cardiovascular health program showed that the thickness of the internal and common carotid artery walls increased significantly with increased smoking.
Inflammation and chronic infection: Recent evidence suggests that inflammatory responses and systemic infections play a role in atherosclerosis formation. In a clinical study on asymptomatic carotid atherosclerosis, chlamydial pneumonia was found to be a possible pathogenic mechanism leading to carotid atherosclerosis formation.
Multiple risk factors increase the chance of developing severe carotid stenosis.
Section II Clinical manifestations
I. Carotid artery stenosis.
This includes stenosis of the internal carotid artery in the extracranial segment, stenosis of the subclavian and vertebral arteries, and stenosis of the innominate and common carotid arteries.
Clinical manifestations: arterial murmur and symptoms caused by cerebral ischemia; may also be asymptomatic.
Carotid artery stenosis.
Carotid murmurs were present in half of the patients in a study of 331 individuals with neurologic symptoms, and only 37% had high stenosis by Doppler ultrasound scan. In the North American Symptomatic Carotid Endarterectomy Trial (NASCET), the sensitivity of the ipsilateral localized carotid murmur was 63%, of which 75% were moderate to severe stenoses.
Cerebral ischemia or embolism manifests as.
(TIA: usually <24 hours in duration).
Reversible neurological deficit (RIND): symptoms last from 1 day to 3 weeks.
Progressive stroke: progressive or stepwise worsening of neurological deficit symptoms over 48h after onset.
Complete stroke: symptoms of neurological deficit are more severe and complete after onset, often within a few hours.